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PubMed1983

Activation of potassium transport induced by secretagogues in superfused submaxillary gland segments of rat and mouse.

In order to investigate the actions of acetylcholine (ACh), catecholamines and substance P on K transport in the submaxillary gland, measurements of net K flux to and from the gland tissue using flame photometry, Na efflux from the tissue using radioactive 22Na, and membrane potential and input resistance using micro-electrodes were carried out on isolated superfused segments of rat and mouse submaxillary glands. ACh (5.5 X 10(-8) to 5.5 X 10(-4) M), phenylephrine (5 X 10(-7) to 5 X 10(-4) M) or substance P (10(-9) to 10(-5) M) stimulation for 5 min induced a transient K release followed by a small K uptake after the cessation of stimulation. The K release was markedly enhanced by the simultaneous addition of ouabain (10(-3) M). On the other hand, isoprenaline (2.5 X 10(-9) to 2.5 X 10(-5) M) induced a transient K uptake without any preceding K release. The K uptake was completely blocked by the addition of ouabain. Noradrenaline induced only K uptake at a low concentration (3 X 10(-7) M), but induced transient K release followed by marked K uptake at higher concentrations (3 X 10(-6) to 3 X 10(-4) M). The K release induced by noradrenaline was suppressed by the addition of phentolamine (10(-5) M), while the K uptake was suppressed by propranolol (5 X 10(-6) M). The K release induced by ACh, phenylephrine, noradrenaline or substance P was severely reduced by Ca omission from the superfusing solution and restored by the re-admission of Ca. The isoprenaline- or noradrenaline-induced K uptake was, however, little affected by Ca omission. Application of isoprenaline (2.5 X 10(-6) M) induced an increase in 22 Na efflux. The increase in 22Na efflux was completely abolished in the presence of ouabain. Local application to the tissue bath of isoprenaline (4.7 X 10(-13) to 4.7 X 10(-12) mole) or noradrenaline (5.7 X 10(-12) to 5.7 X 10(-11) mole) in the presence of phentolamine (10(-5) M) induced membrane hyperpolarization without any appreciable change in input resistance. The hyperpolarization was abolished in the presence of ouabain (10(-3) M) or propranolol (5 X 10(-6) M) or in a K-free or low Na solution. Higher doses of both agonists, however, induced depolarization or biphasic responses (initial depolarization followed by hyperpolarization). The depolarizations were accompanied by a moderate reduction in input resistance. It is concluded that in the rat and mouse submaxillary gland acinar cells cholinergic, alpha-adrenergic or substance P stimulation causes K release (and perhaps Na uptake) resulting in activation of the Na-K pump, while beta-adrenergic receptor stimulation might directly activate the Na-K pump resulting in K uptake, or might cause Na uptake resulting in activation of the Na-K pump.

Acetylcholine↗
PubMed1984

The reflex effects of changes in carotid sinus pressure upon renal function in dogs.

In chloralose-anaesthetized and artificially ventilated dogs, the carotid sinuses were vascularly isolated and perfused with arterial blood. Mean aortic pressure was held constant at 100 +/- 2 mmHg (mean +/- S.E. of mean, n = 19) by means of a pressure bottle connected to the aorta. Both vagus nerves were sectioned in the neck and propranolol hydrochloride (0.5 mg kg-1) was administered every 30 min. The left renal blood flow was measured by an electromagnetic flowmeter (wrap-round probe), glomerular filtration rate by creatinine clearance and urinary sodium by flame photometry. Decreasing pressure in the isolated carotid sinuses from 186 +/- 10 to 63 +/- 5 mmHg resulted in significant decreases in renal blood flow from 281 +/- 35 to 177 +/- 30 ml min-1 100 g-1 renal mass; glomerular filtration rate from 40.0 +/- 7.8 to 12.3 +/- 4.4 ml min-1 100 g-1; urine flow from 0.31 +/- 0.05 to 0.12 +/- 0.03 ml min-1 100 g-1 and sodium excretion from 21.7 +/- 7.2 to 8.2 +/- 3.0 mumol min-1 100 g-1. Increasing carotid sinus pressure back to 188 +/- 11 mmHg resulted in increases in all the variables to values not significantly different from their initial values. Tying renal sympathetic nerves at low carotid sinus pressure (73 +/- 11 mmHg) caused an increase in all of the variables. After denervation there was no response to changes in carotid sinus pressure. These results show that changes in carotid sinus pressure can result in significant reflex effects on renal function and that these effects are mediated by renal sympathetic nerves.

Animals↗
PubMed1985

The luminance origin of the pattern electroretinogram in man.

Electroretinograms (e.r.g.s) and visually evoked potentials (v.e.p.s) to pattern stimuli were recorded simultaneously from healthy subjects. The stimuli were produced by a configuration in which the luminance of two sets of spatial elements (checks) could be modulated independently. Experiments were designed to distinguish between contrast responses and non-linear luminance responses. In the first of two basic experiments, the luminance of only one set of checks was modulated, at a constant level in every trial. The other set was not modulated, but its luminance was set at various levels. Under these conditions the local luminance stimulation was kept equal for every trial whereas the contrast stimulation varied. Therefore, local luminance responses in these experiments were expected to be constant and contrast responses were expected to vary. The e.r.g.s were identical for all luminance settings of the unmodulated checks, suggesting that luminance rather than contrast determines the response. The v.e.p.s showed, on the contrary, the behaviour expected for contrast responses. In the second basic experiment the local luminance stimulation was also kept constant, but the phase difference between the modulations of the two sets of checks was varied between 0 deg (pure luminance stimulation) and 180 deg (pattern reversal). In this type of experiment the second harmonic responses to local luminance modulation are expected to decrease to a minimum as phase difference goes from 0 to 90 deg and increase again as phase difference goes to 180 deg. Contrast responses are expected to increase monotonically from zero to maximal at phase difference shifts from 0 deg (no contrast stimulation) to 180 deg (contrast reversal). The e.r.g.s decreased to a minimum at 90 deg phase difference and increase again with phase difference going to 180 deg. At 0 and 180 deg the same value was recorded. Consequently, the e.r.g. behaviour suggests a luminance origin of the responses. The v.e.p.s monotonically increased as phase difference went from 0 to 180 deg, thus suggesting a contrast origin of the responses. Two additional control experiments were performed. The first experiment compared the responses to homogeneous field red/green exchange and pattern red/green exchange, with the luminances of the red and green sources matched by heterochromatic flicker photometry. The exchange of luminance-matched red and green checks (pattern reversal) did not produce different e.r.g. responses from those recorded in response to homogeneous field red/green exchange. The v.e.p. showed a significant increase for the pattern stimulus.(ABSTRACT TRUNCATED AT 400 WORDS)

Color Perception↗
PubMed1985

Acetylcholine-evoked potassium release in the mouse pancreas.

Mouse pancreatic segments were superfused with physiological saline solutions and the K+ concentration in the effluent was measured by flame photometry. Acetylcholine (ACh) evoked a dose-dependent and transient increase in the K+ concentration in the effluent (K+ release). The removal of calcium (Ca2+) from the superfusing solution and addition of 10(-4) M-EGTA (ethyleneglycol-bis-(beta-amino-ethylether)N,N'-tetraacetic acid) caused a significant reduction in the ACh-elicited K+ outflow. Pre-treatment of pancreatic segments with the 'loop diuretics' (furosemide, piretanide and bumetanide; all 10(-4) M) resulted in uptake of K+ into the tissue segments. The diuretics also caused a marked reduction in the ACh-induced K+ release. Replacement of chloride (Cl-) in the physiological salt solution by nitrate (NO3-), sulphate (SO42-) or iodide (I-) caused K+ uptake and a significant reduction in the ACh-evoked K+ release. However, when Cl- was replaced by bromide (Br-) the response to ACh was virtually unaffected. When sodium (Na+) was replaced by lithium (Li+) ACh did not evoke K+ release but instead K+ uptake was observed. However, when Tris+ was substituted for Na+ ACh evoked a very small K+ release. Pre-treatment of pancreatic segments with 10(-3) M-ouabain resulted in a marked sustained K+ release. In the continuing presence of ouabain ACh induced a further increase in K+ outflow. Pre-treatment of the preparation with 10 mM-tetraethyl-ammonium (TEA) caused a small transient increase in K+ efflux, but TEA had virtually no effect on the secretagogue-evoked changes in effluent K+ concentration. The results suggest the presence of a diuretic-sensitive Na+-K+-Cl- co-transport system in the mouse pancreatic acinar membrane.

Acetylcholine↗
PubMed1987

The effects of stimulating carotid chemoreceptors on renal haemodynamics and function in dogs.

1. Dogs were anaesthetized with chloralose and artificially ventilated. The carotid chemoreceptors were stimulated by changing the perfusion of vascularly isolated carotid sinus regions from arterial to venous blood. The mean carotid sinus pressure and the mean arterial blood pressure were held constant at 124 +/- 3 and 122 +/- 3 mmHg, respectively. Both vagosympathetic trunks were sectioned in the neck and propranolol (17 micrograms kg-1 min-1 I.V.) and gallamine triethiodide (0.2-2.0 mg kg-1 30 min-1 I.V.) were infused. Renal blood flow was measured by an electromagnetic flow probe, glomerular filtration rate by creatinine clearance, sodium excretion by flame photometry and solute excretion by osmometry. 2. In sixteen tests in thirteen dogs perfusion of the carotid sinus regions with venous blood resulted in significant decreases in renal blood flow from 271 +/- 24 to 198 +/- 21 ml min-1 100 g-1 renal mass; glomerular filtration rate from 41.0 +/- 4.8 to 22.1 +/- 3.1 ml min-1 100 g-1; filtration fraction from 0.25 +/- 0.02 to 0.19 +/- 0.02; urine flow from 0.48 +/- 1.0 to 0.21 +/- 0.03 ml min-1 100 g-1; sodium excretion from 18.1 +/- 4.1 to 12.9 +/- 4.2 mumol min-1 100 g-1; and osmolar excretion 327 +/- 42 to 171 +/- 26 mu osmol min-1 100 g-1. The right atrial pressure did not change significantly from 4.6 +/- 1.2 cmH2O. 3. In seven dogs, tying renal sympathetic nerves abolished all the responses except that of sodium excretion which was now reversed; sodium excretion increased from 68 +/- 19 to 116 +/- 38 mumol min-1 100 g-1 without significant change in right atrial pressure from 7.4 +/- 1.9 cmH2O. Crushing the carotid bodies, however, abolished all the responses. 4. The results show that carotid chemoreceptor stimulation can cause significant reflex effects on renal haemodynamics and function which are mediated via renal sympathetic nerves. They also show that the chemoreceptor stimulation can cause natriuresis in the absence of haemodynamic changes, in the denervated kidney, presumably via a humoral factor.

Animals↗
PubMed1988

Taste responses in the nucleus tractus solitarius of sodium-deprived rats.

1. Maintenance of sodium balance is crucial to mammals and is expressed in the innate salt appetite. With depletion, sodium preference is exaggerated, hypertonic solutions accepted and salt balance restored. This compensatory behaviour is thought to result from a centrally induced change in taste responsiveness. This proposal was tested by recording taste activity from ninety-four single neurones in the nucleus tractus solitarius of sodium-replete (N = 44) and of deprived (N = 50) rats. Twelve Wistar rats were given a nominally sodium-free diet for 10-13 days, and the resulting sodium depletion confirmed by flame photometry of their urine. Nine rats provided control data. Taste stimuli included five concentrations of NaCl (0.003-0.3 M) plus eight other salts, acids, sugars and alkaloids. 2. Taste responsiveness was generally reduced in sodium-depleted rats. Spontaneous activity was 33% lower while responses to sodium salts lagged by a mean of 30%, to acids by 25% and to bitter salts and quinine by 17%. Mean activity to sugars was 60% higher in the deprived group. 3. Activity in sugar- and salt-profile neurones was most affected. In deprived animals responses to sodium salts were lower by 80% among salt-profile cells while among sugar-profile neurones activity to these stimuli was nearly 10 times greater than in controls. These changes in activity resulted in a dramatic shift in the participation of sodium- and sugar-profile cells in the afferent signal for NaCl. In replete animals 60% of sodium-induced activity was transmitted through salt-profile cells while only 1% occurred in sugar-profile neurones. In deprived subjects this situation was nearly reversed as 7% of the total NaCl response was conveyed through salt-profile cells while the contribution of neurones with sugar-profiles rose to 46%. 4. Multidimensional stimulus spaces based on average activity in each of four identifiable neurone subgroups demonstrated a shift in the affiliation of sodium salts away from bitter and acid stimuli and towards sugars. 5. These results confirm earlier findings from the chorda tympani that sodium deprivation suppresses activity evoked by sodium salts. However the application of more recent analytical procedures permits quite a different interpretation of this finding. The overall decrease is merely the net effect of a shift in the major responsibility for encoding sodium from salt-profile neurones to those whose primary sensitivity is to sugars.(ABSTRACT TRUNCATED AT 400 WORDS)

Acids↗
PubMed1989

Sympathetic nerves in the mediation of renal response to localized stimulation of atrial receptors in anaesthetized dogs.

1. Dogs were anaesthetized with chloralose and artificially ventilated. Localized stimulation of left atrial receptors for 23-25 min was achieved by distension of three small balloons at the pulmonary vein-atrial junctions and one in atrial appendage. Renal blood flows were measured by electromagnetic flow probes, glomerular filtration rate by creatinine clearance, urinary sodium excretion by flame photometry and solute excretion by osmometry. The mean aortic pressure was held constant at 92.2 +/- 2.4 mmHg (mean +/- S.E.M., n = 27) by means of a pressure bottle connected to the aorta and beta-adrenergic receptor activity was blocked by continuous infusion of propranolol (17 micrograms kg-1 min-1, I.V.). 2. In twelve dogs stimulation of left atrial receptors resulted in significant increases of 11.8 +/- 2.4% (P less than 0.001) in renal blood flow; 32.5 +/- 7.2% (P less than 0.001) in glomerular filtration rate; 19.5 +/- 5.0% (P less than 0.005) in filtration fraction: 36.3 +/- 9.0% (P less than 0.001) in urine flow: 32.7 +/- 9.2% (P less than 0.005) in sodium excretion: 36.6 +/- 9.9% (P less than 0.005) in osmolar excretion and a decrease of 31.3 +/- 11.2% (P less than 0.025) in free water clearance. Left atrial pressure and heart rate did not change significantly. In eight of the dogs ligation of the renal nerves resulted in similar changes in all of the renal variables; subsequent stimulation of atrial receptors did not cause significant changes in the renal variables. 3. In five additional dogs, in which heart rate and aortic pressure were allowed to change, stimulation of left atrial receptors for the same period resulted in significant increases in heart rate (4.3 +/- 0.7%. P less than 0.001) and mean aortic pressure (2.0 +/- 0.6%, P less than 0.025). Under this condition both the intact right kidneys and the denervated left kidneys showed significant responses in urine flow, sodium excretion, osmolar excretion and free water clearance. 4. The results show that the renal sympathetic nerves mediate the primary renal responses to atrial receptor stimulation, at least in the short term. The influence of any humoral factor in this reflex seems to be secondary to changes in heart rate and systemic blood pressure, possibly via arterial baroreceptors.

Animals↗
PubMed1989

Effects of small changes in carotid sinus pressure on renal haemodynamics and function in dogs.

1. In dogs anaesthetized with chloralose and artificially ventilated, the carotid sinuses were vascularly isolated and perfused with arterial blood. Mean aortic pressure was held constant at 111 +/- 2 mmHg (mean +/- S.E.M., n = 18) by means of a pressure bottle connected to the aorta and a Starling resistance. Both vagus nerves were sectioned in the neck and propranolol hydrochloride (1 mg kg-1 h-1) or atenolol (0.5-4 mg kg-1 h-1) was administered. The left and right renal blood flows were measured by electromagnetic flowmeters (wrap-round probes), glomerular filtration rate by creatinine clearance, urinary sodium by flame photometry and solute excretion by osmometry. 2. In six dogs decreasing pressure in the isolated carotid sinuses from 119 +/- 4 to 78 +/- 3 mmHg (n = 9) resulted in significant decreases in renal blood flow by 18 +/- 3% (P less than 0.01), glomerular filtration rate by 41 +/- 9% (P less than 0.01), filtration fraction by 30 +/- 11% (P less than 0.05), urine flow by 46 +/- 6% (P less than 0.001), sodium excretion by 46 +/- 9% (P less than 0.001) and osmolar excretion by 44 +/- 6% (P less than 0.001). Fractional sodium excretion did not change significantly. Increasing carotid sinus pressure back to 120 +/- 4 mmHg (n = 6) resulted in increases in all the variables to values not significantly different from those at initial high carotid pressure. 3. Ligation of left renal nerves at low carotid sinus pressure (83 +/- 3 mmHg, n = 5) caused significant increases in all of the variables in the left kidney. After ligation, changes in carotid sinus pressure produced no effect on the denervated left kidney, but in the three dogs in which the responses of the right kidney were also tested, the usual responses after denervation of the left kidney were seen. 4. The results show that changes in carotid sinus pressure around the normal range can result in significant reflex effects on renal haemodynamics and function and that these effects are mediated solely by renal sympathetic nerves. The influence of any extrarenal humoral factors seems to be minimal.

Animals↗
PubMed1990

The physiological basis of the minimally distinct border demonstrated in the ganglion cells of the macaque retina.

1. The minimally distinct border method involves setting the relative radiances of two adjacent, differently coloured fields until the border between them is minimally distinct. At these radiance settings, the two fields are found to be of equal luminance. The task shares with flicker photometry all the requirements of a photometric method. 2. We have recorded responses of macaque ganglion cells to such borders moved back and forth across the receptive field; the size of the luminance step across the border was systematically varied. 3. Phasic ganglion cells gave transient responses to such borders, consisting of an increase or decrease in firing rate depending on direction of luminance contrast and cell type (on- or off-centre). Tonic ganglion cells gave sustained responses dependent on chromatic contrast across the border. 4. An analysis of phasic cell responses showed a minimum near equal luminance, suggesting their signal could readily support the minimally distinct border task. We could not devise a scheme whereby tonic cells could support the task. 5. Spectral sensitivity of phasic cells, determined from their minima, closely resembled the 10 deg luminous efficiency function, as required of a mechanism underlying the psychophysical performance. 6. For phasic cells, the minimum was independent of movement speed, and hence of eye movement velocity under natural viewing conditions. 7. Proportionality, additivity and transitivity are found psychophysically with the minimally distinct border method. All these properties were also exhibited by phasic cell responses. 8. Residual responses were present in individual phasic cells to equal-luminance borders, probably due to a non-linearity of M- and L-cone summation. The amplitude of residual response depended on the wavelengths on either side of the border, and was zero for pairs of lights lying along a tritanopic confusion line. These residual responses could be correlated with residual border distinctness at equal luminance as reported psychophysically. 9. There was some variability in spectral sensitivity among phasic cells, and this could be described in terms of variability in weighting of the middle- and long-wavelength cone inputs to each cell. With equal-luminance borders, the residual response of the phasic cell population will thus be made up of the residual responses from individual cells and a contribution due to variation in spectral sensitivity among cells. 10. The responses of phasic ganglion cells thus form the physiological substrate of psychophysical performance on the minimally distinct border task. These cells also provide a residual signal to equal-luminance borders which correlates with residual distinctness.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1991

Inhibition of atrial receptor-induced renal responses by stimulation of carotid baroreceptors in anaesthetized dogs.

1. Dogs were anaesthetized with chloralose and artificially ventilated. The receptors at three pulmonary vein-atrial junctions and in the left atrial appendage were stimulated by distension of small balloons. The carotid sinuses were vascularly isolated and perfused with arterial blood. A volume reservoir was connected to the aorta via the common carotid and femoral arteries to keep the mean aortic pressure constant (78.8 +/- 2.9 mmHg at low and 87.1 +/- 4.3 mmHg at high carotid sinus pressure, CSP). Propranolol and atropine were infused (i.v.) at 17 and 13 micrograms kg-1 min-1 respectively in order to block beta-adrenergic and cholinergic receptor activities. The renal blood flow was measured by an electromagnetic flow meter (wrap-round probe), glomerular filtration rate by creatinine clearance, urinary sodium excretion by flame photometry and osmolar excretion by osmometry. 2. In twelve tests in eight dogs, stimulation of the left atrial receptors for 13 min, at a mean CSP of 68.6 +/- 2.3 mmHg, resulted in significant increases in renal blood flow from 216 +/- 20.0 to 230 +/- 22.1 ml min-1 (100 g renal mass)-1 (P less than 0.005), glomerular filtration rate from 33.9 +/- 3.2 to 42.1 +/- 4.1 ml min-1 100 g-1 (P less than 0.005), filtration fraction from 0.23 +/- 0.02 to 0.26 +/- 0.02 (P less than 0.005), urine flow rate from 0.21 +/- 0.03 to 0.26 +/- 0.03 ml min-1 100 g-1 (P less than 0.001), sodium excretion from 12.9 +/- 4.0 to 16.4 +/- 4.8 mumol min-1 100 g-1 (P less than 0.01), osmolar excretion from 196 +/- 27.8 to 246 +/- 32.9 muosmol min-1 100 g-1 (P less than 0.005), whilst free water clearance decreased from -0.39 +/- 0.07 to -0.50 +/- 0.09 ml min-1 100 g-1 (P less than 0.005). However, the fractional excretion of sodium did not change. 3. In nine tests in seven dogs, stimulation of the left atrial receptors at a constantly high CSP (161 +/- 11.3 mmHg) did not produce significant change in any of the renal variables. 4. The results show that high level excitation of carotid baroreceptors can completely inhibit the reflex renal haemodynamic and functional responses to atrial receptor stimulation.

Animals↗
PubMed1991

The renal response to electrical stimulation of renal efferent sympathetic nerves in the anaesthetized greyhound.

1. The effect of direct electrical stimulation of the renal efferent nerves upon renal haemodynamics and function was studied in greyhounds anaesthetized with chloralose and artificially ventilated. The left kidney was neurally and vascularly isolated, and perfused with blood from one of the femoral arteries at a constant pressure of 99 +/- 1 mmHg. Renal blood flow was measured with a cannulating electromagnetic flow probe placed in the perfusion circuit, glomerular filtration rate by creatinine clearance, urinary sodium excretion by flame photometry and solute excretion by osmometry. Beta-Adrenergic receptor activation was blocked by the infusion of dl-propranolol (17 micrograms kg-1 min-1). The peripheral ends of the ligated renal nerves were stimulated at 0.5, 1.0, 1.5 and 2.0 Hz. 2. At 0.5 Hz frequency only osmolar excretion was significantly reduced (10.3 +/- 3.2%, P less than 0.05, n = 6). Reductions in sodium excretion (53.6 +/- 8.5%, P less than 0.01, n = 6) and water excretion (26.9 +/- 8.0%, P less than 0.05, n = 6) and further reductions of osmolar excretion (20.7 +/- 3.7%, P less than 0.01, n = 6) were observed at 1.0 Hz; however, these were observed in the absence of significant changes in renal blood flow and glomerular filtration rate. Significant reductions were observed in glomerular filtration rate at 1.5 Hz (16.3 +/- 4.1%, P less than 0.02, n = 5) and in renal blood flow at 2.0 Hz (13.1 +/- 4.0%, P less than 0.05, n = 5). Further reductions in urine flow and sodium excretion were also observed at these higher frequencies. 3. These results clearly show that significant changes in renal tubular function can occur in the absence of changes in renal blood flow and glomerular filtration rate when the renal nerves are stimulated electrically from a zero baseline activity up to a frequency of 1.5 Hz. Higher frequencies caused significant changes in both renal haemodynamics and function.

Anesthesia↗
PubMed1991

Glucose stimulation of ouabain-resistant efflux of Na+ from rat pancreatic islets.

1. Integrating flame photometry was employed for measuring the mobilization of sodium from rat pancreatic islets after substitution of extracellular Na+ by N-methylglucamine. 2. Glucose accelerated the initial loss of sodium both in the absence and presence of ouabain (1 mM). In the latter case the effect was maximal at 5 mM of the sugar. 3. Amiloride (0.1 mM), an inhibitor of Na(+)-H+ exchange, prevented the effect of glucose on the ouabain-resistant Na+ efflux, increasing the rate of outward transport in the absence of the sugar. 4. Extracellular K+ and arginine (10 mM) mimicked the action of glucose in promoting a ouabain-resistant mobilization of sodium. 5. Whereas the hypoglycaemic sulphonylurea tolbutamide (100 microM) did not modify the outward transport of Na+, the ouabain-resistant component of this process was partially suppressed after bumetanide (100 microM) inhibition of the chloride-dependent co-transport of Na+ and K+. 6. It is suggested that the glucose-induced lowering of the steady-state content of islet sodium involves an increased outward transport mediated at least in part by mechanisms other than stimulation of the Na(+)-K+ pump.

Animals↗
PubMed1991

The effect of discrete stimulation of carotid body chemoreceptors on atrial natriuretic peptide in anaesthetized dogs.

1. In seven chloralose-anaesthetized and artificially ventilated beagles, the carotid sinus regions were vascularly isolated and perfused with either arterial or mixed (arterial and venous) blood (PO2 46.4 +/- 1.5 mmHg, mean +/- S.E.M.) to stimulate the chemoreceptors at constant flow and pressure. Cervical vagosympathetic trunks were ligated in all dogs, and gallamine triethiodide (2.0 mg kg-1 h-1, I.V.) was given in five dogs. Right atrial pressure was measured in all dogs, and left atrial pressure in four dogs. Mean aortic pressure was held constant (91.0 +/- 3.0 mmHg) by means of a reservoir connected to the animal via the common carotid and femoral arteries. Plasma atrial natriuretic peptide (ANP) was measured by radioimmunoassay and urinary sodium by flame photometry. 2. In seven dogs with mean carotid sinus pressure maintained at 96.0 +/- 4.3 mmHg, stimulation of the carotid chemoreceptors for 25 min produced significant increases in left atrial pressure of 41.2 +/- 3.3% (n = 4; P less than 0.005) from 5.4 +/- 0.6 cmH2O and of 30.9 +/- 4.5% (n = 7; P less than 0.002) in ANP from 31.6 +/- 2.1 pg ml-1. However, chemoreceptor stimulation produced significant decreases in urine flow rate of 26.1 +/- 1.9% (n = 9; P less than 0.001) from 0.29 +/- 0.03 ml min-1 (100 g kidney weight)-1 and sodium excretion of 29.0 +/- 2.3% (P less than 0.001) from 8.5 +/- 1.7 mumol min-1 (100 g kidney weight)-1 but right atrial pressure and heart rate did not change significantly. In three of the dogs, beta-adrenoceptor blockade by atenolol (2 mg kg-1, I.V.) greatly reduced the effects of chemoreceptor stimulation on plasma levels of ANP. 3. The results show, for the first time, that discrete stimulation of the carotid chemoreceptors caused an increase in plasma ANP levels, probably due to the reflex increase in atrial pressure that results from an inhibition of the cardiac sympathetic nerves, and an increase in venous return from a reduction of peripheral vascular capacitance.

Anesthesia↗
PubMed1992

Calcium gradients and buffers in bovine chromaffin cells.

1. Digital imaging and photometry were used in conjunction with the fluorescent Ca2+ indicator, Fura-2, to examine intracellular Ca2+ signals produced by depolarization of single adrenal chromaffin cells. 2. Depolarization with a patch pipette produced radial gradients of Ca2+ within the cell, with Ca2+ concentration highest in the vicinity of the plasma membrane. These gradients dissipated within a few hundred milliseconds when the voltage-gated Ca2+ channels were closed. 3. Dialysis of Fura-2 into the chromaffin cell caused concentration-dependent changes in the depolarization-induced Ca2+ signal, decreasing its magnitude and slowing its recovery time course. These changes were used to estimate the properties of the endogenous cytoplasmic Ca2+ buffer with which Fura-2 competes for Ca2+. 4. The spatially averaged Fura-2 signal was well described by a model assuming fast competition between Fura-2 and an endogenous buffer on a millisecond time scale. Retrieval of calcium by pumps and slow buffers occurs on a seconds-long time scale. No temporal changes indicative of buffers with intermediate kinetics could be detected. 5. Two independent estimates of the capacity of the fast endogenous Ca2+ buffer suggest that 98-99% of the Ca2+ entering the cell normally is taken up by this buffer. This buffer appears to be immobile, because it does not wash out of the cell during dialysis. It has a low affinity for Ca2+ ions, because it does not saturate with 1 microM-Ca2+ inside the cell. 6. The low capacity, affinity and mobility of the endogenous Ca2+ buffer makes it possible for relatively small amounts of exogenous Ca2+ buffers, such as Fura-2, to exert a significant influence on the characteristics of the Ca2+ concentration signal as measured by fluorescence ratios. On the other hand, even at moderate Fura-2 concentrations (0.4 mM) Fura-2 will dominate over the endogenous buffers. Under these conditions radiometric Ca2+ concentration signals are largely attenuated, but absolute fluorescence changes (at 390 nm) accurately reflect calcium fluxes.

Adrenal Glands↗
PubMed1992

Primary effects of carotid chemoreceptor stimulation on gracilis muscle and renal blood flow and renal function in dogs.

1. In chloralose-anaesthetized and artificially ventilated dogs, the carotid sinus regions were vascularly isolated and perfused either with arterial or mixed (arterial and venous) blood (partial pressure of O2 (PO2) 43.8 +/- 2.4 mmHg, mean +/- S.E.M. n = 14) to stimulate the carotid chemoreceptors. The carotid sinus pressure was held constant at 142.0 +/- 2.8 mmHg. Measurements were made of renal and gracilis muscle blood flow by wrap-round electromagnetic flow probes placed around the renal and gracilis arteries, glomerular filtration rate by creatine clearance, urinary sodium excretion by flame photometry and solute excretion by osmometry. 2. In ten dogs, with intact cervical vagosympathetic trunks, carotid chemoreceptor stimulation produced significant increases in aortic pressure (AoP) of 12.7 +/- 1.1% (n = 10, P < 0.001), in glomerular filtration rate (GFR) of 14.7 +/- 4.1% (P < 0.001), urine flow rate (V) of 16.5 +/- 3.5% (P < 0.002), in urinary sodium excretion (UNaV) of 17.5 +/- 2.5% (P < 0.005) and in urinary osmolar excretion (UosmV) of 13.2 +/- 2.2% (P < 0.001), but a significant decrease in renal blood flow (RBF) of 5.8 +/- 1.8% (P < 0.02). In six of these dogs in which gracilis muscle blood flow (MBF) was also recorded, carotid chemoreceptor stimulation caused significant increases in AoP of 12.8 +/- 1.4% (n = 6, P < 0.001) and in MBF of 10.0 +/- 1.6% (P < 0.002), and a small but significant decrease in RBF of 3.6 +/- 1.5% (P < 0.02). 3. In fourteen dogs, with sectioned cervical vagosympathetic trunks, carotid chemoreceptor stimulation produced increases in AoP of 22.0 +/- 2.6% (n = 14, P < 0.001), in GFR of 36.9 +/- 4.2% (P < 0.001), in V of 30.1 +/- 4.4% (P < 0.001), in UNaV of 31.4 +/- 5.3% (P < 0.001), and in UosmV of 25.7 +/- 5.8% (P < 0.001). However, it produced a greater decrease in RBF of 10.5 +/- 1.9% (P < 0.001). In ten of these dogs, where MBF was recorded, carotid chemoreceptor stimulation caused greater increase in AoP of 22.4 +/- 3.0% (n = 10, P < 0.001) and in MBF of 32.8 +/- 3.7% (P < 0.001), and a greater decrease in RBF of 9.8 +/- 1.9% (P < 0.001).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Effects of left atrial receptor stimulation on carotid chemoreceptor-induced renal responses in dogs.

1. Dogs were anaesthetized with thiopentone sodium and alpha-chloralose and artificially ventilated. The carotid sinus regions were vascularly isolated and perfused with arterial or venous blood to stimulate the chemoreceptors. Left atrial receptors were stimulated by distending four balloons, three in the left pulmonary vein-atrial junctions and one in the left atrial appendage. Mean aortic pressure was held constant by means of a pressure control device. Atenolol and atropine (2.0 and 0.5 mg kg-1, respectively), and gallamine triethiodide (3.0 mg kg-1 h-1) were given I.V. Renal blood flow was measured by an electromagnetic flowmeter, glomerular filtration rate by creatinine clearance, urinary sodium by flame photometry and solute excretion by osmometry. 2. In fifteen tests in eight dogs (in one dog responses of both left and right kidneys were determined), at a constant aortic pressure (AoP) of 92.0 +/- 3.2 mmHg, and carotid sinus pressure (CSP) of 95.0 +/- 2.0 mmHg, stimulation of left atrial receptors with balloon inflation resulted in significant increases in renal blood flow (RBF) by 8.3 +/- 0.9 from 255.0 +/- 14.6 ml min-1 (100 g kidney weight)-1 (n = 9), in glomerular filtration rate (GFR) by 4.1 +/- 0.6 from 21.2 +/- 1.9 ml min-1 (100 g)-1, in filtration fraction (FF) by 0.04 +/- 0.003 from 0.20 +/- 0.01, in urine flow rate (V) by 0.08 +/- 0.02 from 0.33 +/- 0.05 ml min-1 (100 g)-1, in sodium excretion (UNaV) by 4.4 +/- 0.9 from 27.7 +/- 4.2 mumol min-1 (100 g)-1, in osmolar excretion (UosmV) by 62.0 +/- 5.6 from 303.0 +/- 28.3 mu osmol min-1 (100 g)-1, and in a decrease in free water clearance (CH2O) by 0.13 +/- 0.03 from -0.63 +/- 0.04 ml min-1 (100 g)-1. Left atrial pressure (LAP) and heart rate (HR) did not change significantly from 6.9 +/- 0.3 cmH2O, and 133.0 +/- 3.4 beats min-1 respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1996

Ca2+ clearance mechanisms in isolated rat adrenal chromaffin cells.

1. Intracellular Ca2+ clearance mechanisms were studied in rat adrenal chromaffin cells, by measuring slow tail currents through small-conductance Ca(2+)-activated K+ channels and using indo-1 photometry following depolarization-induced Ca2+ loading. 2. Following several-hundred millisecond depolarizations, [Ca2+]i decayed in three phases. An initial fast decay was followed by a long-lasting, low plateau, then [Ca2+]i returned to the resting level slowly. 3. Replacement of external Na+ moderately slowed [Ca2+]i decay, indicating a contribution of plasma membrane Na(+)-Ca2+ exchange. 4. Raising external pH or application of extracellular Eosin of La3+ prolonged slow tail currents, indicating a contribution of plasma membrane Ca(2+)-ATPase to Ca2+ clearance. 5. Ca(2+)-induced Ca2+ release from caffeine-sensitive stores occurred during depolarization. 6. Inhibition of endoplasmic reticulum Ca(2+)-ATPase had little effect on Ca2+ clearance. 7. Slow tail currents and [Ca2+]i decay following 0.2 - 2 s depolarizations were much prolonged by mitochondrial inhibition with carbonyl cyanide m-chlorophenylhydrazone (CCCP) or Ruthenium Red, which abolished the initial rapid decay and plateau of [Ca2+]i. 8. In conclusion, mitochondrial Ca2+ uptake plays a major role in Ca2+ clearance by rapidly and reversibly sequestering Ca2+ during depolarization-evoked Ca2+ loads.

Adrenal Glands↗
PubMed2005

Mitochondrial redox state and Ca2+ sparks in permeabilized mammalian skeletal muscle.

Intact skeletal muscle fibres from adult mammals exhibit neither spontaneous nor stimulated Ca(2+) sparks. Mechanical or chemical skinning procedures have been reported to unmask sparks. The present study investigates the mechanisms that determine the development of Ca(2+) spark activity in permeabilized fibres dissected from muscles with different metabolic capacity. Spontaneous Ca(2+) sparks were detected with fluo-3 and single photon confocal microscopy; mitochondrial redox potential was evaluated from mitochondrial NADH signals recorded with two-photon confocal microscopy, and Ca(2+) load of the sarcoplasmic reticulum (SR) was estimated from the amplitude of caffeine-induced Ca(2+) transients recorded with fura-2 and digital photometry. In three fibre types studied, there was a time lag between permeabilization and spark development. Under all experimental conditions, the delay was the longest in slow-twitch oxidative fibres, intermediate in fast-twitch glycolytic-oxidative fibres, and the shortest in fast-twitch glycolytic cells. The temporal evolution of Ca(2+) spark frequencies was bell-shaped, and the maximal spark frequency was reached slowly in mitochondria-rich oxidative cells but quickly in mitochondria-poor glycolytic fibres. The development of spontaneous Ca(2+) sparks did not correlate with the SR Ca(2+) content of the fibre, but did correlate with the redox potential of their mitochondria. Treatment of fibres with scavengers of reactive oxygen species (ROS), such as superoxide dismutase (SOD) and catalase, dramatically and reversibly reduced the spark frequency and also delayed their appearance. In contrast, incubation of fibres with 50 microm H(2)O(2) sped up the development of Ca(2+) sparks and increased their frequency. These results indicate that the appearance of Ca(2+) sparks in permeabilized skeletal muscle cells depends on the fibre's oxidative strength and that misbalance between mitochondrial ROS production and the fibre's ability to fight oxidative stress is likely to be responsible for unmasking Ca(2+) sparks in skinned preparations. They also suggest that under physiological and pathophysiological conditions the appearance of Ca(2+) sparks may be, at least in part, limited by the fine-tuned equilibrium between mitochondrial ROS production and cellular ROS scavenging mechanisms.

Animals↗