Biomedical subjects

J Schnermann

Publications and source records attributed to J Schnermann.

At least 73 records · Page 4Linked to original sources

PubMed1990

Inhibition of tubuloglomerular feedback during adenosine1 receptor blockade.

Experiments were performed in anesthetized rats to study the effect of the selective adenosine1 (A1) receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (CPX) on tubuloglomerular feedback (TGF) responses assessed as the maximum change of stop-flow pressure (PSF). Compared with control, PSF responses were reduced during luminal application of CPX at 10(-4) and 10(-5)M (-4.9 +/- 0.44 vs. + 0.9 +/- 0.42 mmHg and -6.8 +/- 0.69 vs. -1.4 +/- 0.7 mmHg, respectively), during peritubular administration of CPX at 10(-4)M (-6.2 +/- 0.44 vs. -2.8 +/- 0.42 mmHg), and during infusion of CPX at 10(-4) M into the lumen of a neighboring nephron (-5.6 +/- 0.6 vs. -1.98 +/- 0.51 mmHg). Selectivity of CPX was tested by studying its effect on the PSF reduction produced by the A1-receptor agonist N6-cyclohexyladenosine (CHA). CHA at 10(-5)M reduced PSF when infused into the peritubular blood (-11.8 +/- 3.7 mmHg), and this effect was blunted by luminal application of CPX (-1.5 +/- 0.6 mmHg). CHA also reduced PSF when infused into a neighboring nephron, and this effect was blunted by infusing CPX at 10(-4)M into the same neighboring nephron, a different neighboring nephron, or a peritubular capillary. These results are consistent with the concept that activation of A1-receptors on vascular cells of the afferent arterioles participates in the mediation of TGF responses.

Adenosine↗

PubMed1990

Effect of dopamine on the tubuloglomerular feedback mechanism.

Experiments were performed in anesthetized rats to examine whether infusion of dopamine is associated with a reduction in the tubuloglomerular feedback (TGF) response of stop-flow pressure (PSF) and early proximal flow rate (VEP) to increases of loop of Henle flow. The purpose of these studies was to test further the validity of the proposal that renal vasodilation is a nonspecific cause for diminished TGF responsiveness. When femoral arterial pressure was kept constant with a suprarenal aortic clamp, intravenous infusion of dopamine at rates of 4, 15, 35, and 75 micrograms.kg-1.min-1 induced a 10.9, 23.4, 31.3, and 30.1% decrease in renal vascular resistance. Maximum PSF and VEP responses were significantly reduced at all dose levels of dopamine, whereas V1/2, the flow rate required to produce the half-maximum response, was not altered. TGF blunting occurred within less than 10 min after starting the dopamine infusion. Peritubular infusion of dopamine reduced maximum PSF responses from 8.8 +/- 0.7 to 4.6 +/- 0.53 mmHg at 10(-4) M (P less than 0.01) and from 6.0 +/- 1.19 to 3.6 +/- 0.55 mmHg at 10(-3) M (P less than 0.05). The results are consistent with the notion that renal vasodilatation may modify TGF responses by preventing the full vasoconstrictor response to changes in luminal NaCl concentration.

Animals↗

PubMed1990

Characterization of the macula densa stimulus for renin secretion.

These studies utilize the isolated perfused rabbit juxtaglomerular apparatus (JGA) to study the macula densa signal for renin secretion in the absence of the confounding influences of intravascular pressure and renal nerve activity. In the first experimental series, JGAs were perfused alternately with high- and low-NaCl solutions to determine the reversibility of the renin response to changes in NaCl concentration. Compared with high-NaCl controls, perfusion with a low-NaCl solution resulted in a fivefold increase in renin secretion rate (RSR) [2.1-10.0 nano-Goldblatt hog units (nGU)/min], and this response was largely reversible. When the solutions were presented in the reverse order, a similar inhibition by high NaCl was observed. In the second series, JGAs were perfused with high-, medium-, and low-NaCl solutions to determine the sensitive range of the renin response to NaCl concentration changes. The full renin response (3.2-16.6 nGU/min), similar in magnitude to that seen in series 1, was found to occur between 80 and 24 mM for Na+ and 61 and 7 mM for Cl-. In the third series, the NaCl concentration and flow rate of the perfusate were altered independently to separate the effects of flow rate, NaCl delivery, and NaCl concentration on RSR. Although a decrease in perfusate flow rate slightly increased RSR (3.4-8.1 nGU/min), a comparable decrease in NaCl concentration resulted in a much higher RSR (26.3 nGU/min). We conclude that in this preparation 1) RSR responds equally to both increases and decreases in macula densa NaCl concentration, and these changes are rapid and largely reversible, 2) the full renin response occurs within the concentration range normally occurring at the macula densa, i.e., below 80 mM Na+ and 61 mM Cl-, and 3) RSR responds with a larger change to alterations in NaCl concentration than in NaCl delivery or fluid flow rate.

Animals↗

PubMed1990

Restoration of tubuloglomerular feedback in volume-expanded rats by angiotensin II.

Experiments were performed in anesthetized rats to examine whether angiotensin II corrects the attenuation of tubuloglomerular feedback (TGF) responses produced by acute extracellular volume expansion. Volume expansion was achieved by an infusion of isotonic saline at a rate of 9 ml/h. When urine flow had stabilized, an increase in loop of Henle flow from 0 to 45 nl/min caused a fall in stop-flow pressure (PSF) by 3.7 +/- 0.3 mmHg and in single-nephron glomerular filtration rate (SNGFR) by 5.1 +/- 1.7 nl/min. During continued saline administration angiotensin II was infused at 16, 48, or 96 ng.kg-1.min-1 while renal arterial pressure was held constant by suprarenal aortic clamping. The mean responses of PSF increased to 5.9 +/- 0.6, 9.8 +/- 0.7, and 14.9 +/- 1.7 mmHg. Angiotensin II infused at 54 ng.kg-1.min-1 increased the SNGFR response to 15.1 +/- 2.1 nl/min, whereas kidney GFR and distal SNGFR fell. Subcapsular pressure was not significantly altered by angiotensin II infusion (16 ng.kg-1.min-1). Plasma angiotensin (y, pg/ml) as a function of angiotensin II infusion rate (x, ng.kg-1.min-1 for approximately 20 min) was found to fit the function y = 2.89 + 3.53x. An infusion of approximately 15 ng.kg-1.min-1 restored plasma angiotensin levels in the volume-expanded rats to hydropenic values. These data confirm that angiotensin II may play a role as a physiological regulator of TGF sensitivity.

Angiotensin II↗

PubMed1990

Effect of adenosine1-receptor blockade on renin release from rabbit isolated perfused juxtaglomerular apparatus.

Adenosine has been proposed to act within the juxtaglomerular apparatus (JGA) as a mediator of the inhibition of renin secretion produced by a high NaCl concentration at the macula densa. To test this hypothesis, we studied the effects of the adenosine1 (A1)-receptor blocker 8-cyclopentyl-1,3-dipropylxanthine (CPX) on renin release from single isolated rabbit JGAs with macula densa perfused. The A1-receptor agonist, N6-cyclohexyladenosine (CHA), applied in the bathing solution at 10(-7) M, was found to inhibit renin secretion, an effect that was completely blocked by adding CPX (10(-5) M) to the bath. Applied to the lumen, 10(-5) M CPX produced a modest stimulation of renin secretion rates suppressed by a high NaCl concentration at the macula densa (P less than 0.05). The effect of changing luminal NaCl concentration on renin secretion rate was examined in the presence of CPX (10(-7) and 10(-5) M) in the bathing solution and in vehicle control experiments. The control response to increasing luminal NaCl concentration was a marked suppression of renin secretion, that was maintained as long as luminal NaCl concentration was high and was promptly reversible when concentration was lowered. CPX did not alter renin release when luminal NaCl was low, but diminished the reduction caused by high NaCl (P less than 0.01). It is concluded that A1-receptors are located within the JGA, and that A1-receptor activation inhibits renin release. A high NaCl concentration at the macula densa appears to influence A1-receptor activation, but a low NaCl concentration does not. The findings support participation of adenosine in macula densa control of renin secretion.

Adenosine↗

PubMed1990

Effect of angiotensin and other pressor agents on tubuloglomerular feedback responses.

Experiments were performed in anesthetized rats to examine the effect of an intravenous infusion of norepinephrine or vasopressin on the tubuloglomerular feedback (TGF) response of stop flow pressure (PSF). During infusion of norepinephrine at an average rate of 107.5 ng/kg min, mean femoral arterial pressure (MAP) increased from 102.1 +/- 3.55 to 113.7 +/- 3.44 mm Hg and PSF-max increased from 7.45 +/- 1.13 to 9.95 +/- 1.19 mm Hg. When MAP was returned to control by a suprarenal aortic clamp PSF-max was 5.64 +/- 1.09 mm Hg (NS vs. control). Similarly, at an infusion rate of 226.5 ng/kg min PSF-max was not significantly different from control (6.79 +/- 1.61 mm Hg). V1/2, the half-maximum flow rate, was not altered by norepinephrine whether MAP increased or was kept constant. Infusion of vasopressin at the pressor dose of 13.0 mU/kg min increased MAP by about 25 mm Hg and raised PSF-max from 6.56 +/- 0.84 to 14.45 +/- 1.54 mm Hg. However, when MAP was returned to normal PSF-max was 5.41 +/- 0.75 mm Hg (NS). Our data show that in contrast to angiotensin II, norepinephrine and vasopressin do not augment TGF responses when a rise in MAP is prevented. Angiotensin II appears to play a specific role in altering the sensitivity of the TGF mechanism.

Angiotensin II↗

PubMed1989

Interaction between loop of Henle flow and arterial pressure as determinants of glomerular pressure.

Experiments were performed in anesthetized rats to study the relationship between loop of Henle perfusion rate, arterial pressure, and stop-flow pressure (SFP) as an index of glomerular capillary pressure. In one set of experiments we measured the SFP feedback response to changes in loop perfusion at three levels of arterial pressure. The maximum SFP response fell significantly from 13.1 +/- 1.44 to 8.14 +/- 1.72 and 3.13 +/- 0.76 mmHg when arterial pressure was reduced from 118.1 +/- 1.27 to 98.8 +/- 0.51 and 78.8 +/- 1.72 mmHg. In other experiments arterial pressure was altered while loop perfusion rate was fixed at one of three levels. Without loop perfusion SFP changed with a slope of 0.27 +/- 0.04 mmHg/mmHg in the arterial pressure range between 80 and 130 mmHg. During perfusion at the flow rate at which response is half maximum, the slope was significantly reduced to 0.12 +/- 0.04. During perfusion at 45 nl/min, it was 0.03 +/- 0.05, a value not significantly different from zero. During dopamine administration (70 micrograms/kg min) SFP was pressure-dependent even during loop perfusion at 45 nl/min. These results show that arterial pressure determines TGF responsiveness and that the TGF signal determines the range of a regulatory input that is directly dependent on arterial pressure.

Animals↗

PubMed1989

Single nephron comparison of the effect of loop of Henle flow on filtration rate and pressure in control and angiotensin II-infused rats.

Experiments were performed in control and angiotensin II-infused rats to test whether the tubuloglomerular feedback responses of early proximal flow rate (VEP) and stop flow pressure (PSF) are elicited by the same flow rate changes. Paired measurements in the same nephron revealed that VEP responses were shifted to the left compared to those of PSF. The flow rate at which the response was half maximum, V1/2, was 14.7 +/- 1.25 nl/min for VEP and 18.9 +/- 0.97 nl/min for PSF (p less than 0.05). This difference in flow dependency was abolished by angiotensin II infusion (V1/2 was 14.6 +/- 0.87 nl/min for VEP and 15.4 +/- 1.09 nl/min for PSF). Furthermore, angiotensin infusion markedly augmented the feedback response magnitude.

Angiotensin II↗

PubMed1988

Renal disease and the development of hypertension in salt-sensitive Dahl rats.

To elucidate the role of the kidneys in the development of hypertension in Dahl salt-sensitive (S), as compared to resistant (R) rats of the JR strain, we analyzed functional and morphological changes before and after the administration of an 8% NaCl diet and the onset of hypertension. The diet was begun at six weeks of age and was continued until 12 weeks of age. At six weeks, blood pressure was not different between S and R rats. Hypertension occurred in S rats receiving the 8% NaCl diet at week 8, and in S rats receiving 0.9% NaCl at week 10. Albuminuria and proteinuria were found in S rats prior to the 8% NaCl diet and progressed regardless of diet. Electron microscopy of glomeruli revealed segmental loss of epithelial foot processes in S rats at six weeks prior to the 8% NaCl diet. Mesangial widening, arteriolar myo-intimal cell hyperplasia and interstitial fibrosis occurred in all S rats. Inulin and PAH clearances in S rats decreased with time, the changes being accelerated by the 8% NaCl diet. Micropuncture of S and R rats prior to the 8% NaCl diet revealed no glomerular hypertension in S rats. The number of glomeruli in S and R rats were not different. We conclude that prehypertensive S rats of the JR strain already have albuminuric glomerular disease not associated with reduced number of glomeruli or glomerular hypertension. The renal pathology is accelerated once hypertension develops. A lower NaCl intake delays, but does not prevent renal disease in S rats.

Albuminuria↗

PubMed1988

Effect of dopamine antagonists on the urine flow of rats infused with hypotonic saline.

1. The probable involvement of dopamine in the regulation of water excretion was investigated by administering dopamine antagonists intravenously to barbiturate--anaesthetized rats undergoing a water diuresis induced by the infusion of 0.83% glucose with 0.3% NaCl at the rate of 9 ml h-1. 2. Administration of 100 micrograms of the D1-/D2-dopamine antagonist, haloperidol, reduced the enhanced urine flow of rats infused with the hypotonic solution by 69% (from 75.4 +/- 13.0 to 23.6 +/- 6.0 microliter min-1, P less than 0.01). Similarly, the D1-receptor antagonist, SCH 23390, reduced urine flow by 58% (from 77.5 +/- 9.2 to 32.7 +/- 7.2 microliters min-1, P less than 0.01) and the D2-receptor antagonist, sulpiride, by 47% (from 66.2 +/- 8.6 to 35.1 +/- 6.8 microliter min-1, P less than 0.05). 3. The injection of SCH 23390 increased the urine osmolality from 189.6 +/- 27.5 to 479.8 +/- 45.8 mosm kg-1 (P less than 0.05). There was no significant change in sodium and potassium excretion in any of the experiments. Blood pressure (BP) decreased after haloperidol and SCH 23390 injection from control values of 121.7 +/- 1.7 and 116.5 +/- 7.4 to 113.3 +/- 3.3 and 106.0 +/- 8.8 mmHg respectively (P less than 0.05). 4. To study whether the influence of dopamine antagonists on urine flow during water diuresis depends on antidiuretic hormone (ADH), we administered 0.6 micrograms d(CH2)5-D-Phe-Ile-AVP (an ADH antagonist) shortly after the injection of 100 micrograms SCH 23390. The preferential V2 ADH-antagonist abolished the antidiuretic effect of SCH 23390 but did not affect its blood pressure reducing effect (from 118.6 +/- 5.6 to 103.2 +/- 4.6 mmHg, P <0.01). 5. These results suggest that dopamine antagonists blunted the hypotonic saline-induced diuresis by favouring ADH release through an interference with an inhibitory dopaminergic pathway.

Animals↗

PubMed1988

Renal response of anesthetized rats to low-dose infusion of atrial natriuretic peptide.

Studies were performed in rats to determine the minimum infusion rate of atrial natriuretic peptide (ANP) associated with detectable changes in renal function and to determine the change in plasma levels of the peptide produced by these infusion rates. Synthetic ANP-(4-28) was administered to anesthetized euvolemic rats at rates ranging between 10 and 230 ng.kg-1.min-1 for 30 min. Significant natriuresis and diuresis were seen with an infusion of 20 ng.kg-1.min-1. At this rate of infusion, plasma ANP averaged 279 +/- 19.9 pmol/l (vs. 158 +/- 11.8 pmol/l in control rats). A transient increase in K excretion was seen with infusions higher than 100 ng.kg-1.min-1. There was no measurable change in glomerular filtration rate up to an infusion of 160 ng.kg-1.min-1. A significant decrease in mean arterial pressure was only seen with an infusion of 230 ng.kg-1.min-1. In volume-expanded rats, infusion of ANP at 10 ng.kg-1.min-1 induced a significant natriuresis. Our results indicate that natriuresis and diuresis are caused by an infusion of ANP which produces changes in plasma ANP concentration that may well result from stimulation of endogenous ANP release. In contrast, changes in K excretion, glomerular filtration rate, and arterial blood pressure may require changes in plasma ANP that are not easily achievable by physiological interventions.

Animals↗

PubMed1988

Effect of adenosine analogues on tubuloglomerular feedback responses.

Adenosine has been invoked as a possible mediator of the vasoconstrictor response elicited through the tubuloglomerular feedback mechanism. These experiments were undertaken to study the effect of adenosine analogues on the magnitude of the stop-flow pressure (SFP) feedback response. With a control solution, maximum change of SFP during orthograde perfusion was 6.3 +/- 0.34 mmHg. When the adenosine1 (A1) receptor agonists CHA, CPA, or R-PIA were present in the perfusate in a concentration of 10(-5) M, SFP responses were significantly augmented and averaged 12.6 +/- 1.9 (P less than 0.001), 12.6 +/- 0.8 (P less than 0.001), and 10.3 +/- 1.1 mmHg (P less than 0.02), respectively. Diminished responses were seen at higher concentrations of A1 analogues. The A2-receptor agonist NECA did not significantly modify the control response at 10(-5) M, but reduced its magnitude at higher concentrations. During graded increases in loop flow rate essentially all of the response in the presence of CPA or R-PIA occurred in the 0-10 nl/min flow interval, whereas the most sensitive flow rate range in the control tubules was between 10 and 20 nl/min. In the presence of 10(-4) M furosemide SFP responses were abolished during perfusion with the control and NECA-containing solutions. In contrast, SFP fell by 11.8 +/- 1.26 mmHg and 8.7 +/- 1.25 mmHg with CHA or CPA solutions despite the presence of furosemide. Perfusion with 10(-6) M CPA in an isotonic mannitol solution was associated with a decrease of SFP by 16.3 +/- 1.42 mmHg, whereas the mannitol solution alone decreased SFP by only 0.6 +/- 0.18 mmHg. Our results show that luminal administration of A1-receptor analogues increases SFP feedback response magnitude, an effect that does not require the presence of a luminal NaCl signal.

Adenosine↗

PubMed1987

The tubuloglomerular feedback mechanism: functional and biochemical aspects.

Tubuloglomerular feedback is an intrarenal control mechanism designed to regulate the amount of salt entering the distal nephron. Its regulatory efficiency depends upon the magnitude of the vascular response to changes in the luminal signal (the feedback relationship) and on the adjustments in proximal absorption, which determine the macula densa signal (the feedforward relationship). Studies of the feedback relationship have established that the vascular response is related to macula densa solute concentration in a sigmoidal fashion, with the normal operating point located somewhere in the steep portion of the curve. Thus, tubuloglomerular feedback tonically suppresses glomerular filtration rate, an effect that may be even more pronounced in juxtamedullary nephrons. An alteration in the feedforward function and thus in the macula densa signal is likely to participate in the vascular resistance changes initiated by changes in arterial pressure, elevated protein intake, or ADH administration. Our understanding of the intra- and intercellular mechanisms underlying information transfer across the JGA is currently incomplete, but there is some information about the biochemical characteristics of the cellular components. The enzymatic and surface properties establish the distinct nature of the macula densa cells and indicate a distinct function.

Animals↗

PubMed1987

In situ studies of distal convoluted tubule in rat. II. K secretion.

Microperfusion and free-flow micropuncture studies were performed in anesthetized rats to compare the rates of K flux in early and late segments of the distal tubule. Early distal segments were located within the initial 40% of distal tubule length, and late distal segments were located within the terminal 35% of the distal tubule. In early distal segments of control rats, significant K secretion was observed at perfusion rates of 6 and 14 nl/min. In high-K rats significant K secretion was only observed at the lower perfusion rate. Late segments of control rats secreted 70.5 +/- 8.2 at the low flow rate and 139 +/- 18.9 pmol X min-1 X mm-1 at the high flow rate. In K-adapted rats, values were 134.4 +/- 30.2 and 178 +/- 29.3 pmol X min-1 X mm-1. During free flow, we observed a K flux in control rats of 11.0 +/- 9.4 pmol X min-1 X mm-1 (NS) in early segments and a K flux of 55 +/- 6.5 pmol X min-1 X mm-1 in late segments. In K-adapted rats, values were 18.3 +/- 6.7 (P less than 0.05) in early and 123 +/- 17.2 pmol X min-1 X mm-1 in late segments. The majority of our data suggests that the distal convoluted tubule secretes K at a low rate that is not influenced by flow rate or a high-K diet.

Animals↗

PubMed1987

Renal effects of atrial natriuretic peptides.

Administration of atrial natriuretic peptides (ANP) is followed by an immediate increase in the urinary excretion of NaCl and water. ANP modulates intrarenal segmental resistances without affecting renal blood flow to a marked extent. At higher concentrations ANP is capable of raising glomerular filtration rate which may contribute to the massive elevation of NaCl excretion seen under these circumstances. At lower concentrations of ANP NaCl excretion increases without measurable increases of GFR suggesting inhibition of transport by the peptides. Transport of fluid across proximal convoluted tubules does not appear to be inhibited by ANP to a marked extent. Atrial peptides produce a modest inhibition of loop of Henle chloride and water absorption in in situ perfused nephrons. Cl absorption along the accessible portion of the inner medullary collecting duct is not inhibited, but delivery of chloride to the earliest portions of the papillary collecting duct rises. This increase could result from a reduction in transport along the inaccessible portions of the inner medullary collecting duct, from secretion of NaCl along the outer or inner medullary collecting duct or from a change in deep nephron function.

Animals↗

PubMed1987

Evidence for an involvement of dopamine receptors in the natriuretic response to atrial natriuretic peptide.

Intravenous injection of atrial natriuretic peptides (ANP) induces a preferential vasodilatation of the renal resistance vessels. A similar effect is exerted by dopamine. Exogenous administration of this catecholamine induces, like the atrial peptides, diuresis and natriuresis, an effect prevented by dopamine receptor antagonists. In view of these parallels, the influence of dopamine antagonists on the diuretic response of anaesthetized rats to ANP was tested. The unselective dopamine antagonists haloperidol (50 micrograms, i.v.) and chlorpromazine (50 micrograms, i.v.) prevented the diuretic and natriuretic effect of a partially purified atrial extract, and significantly blunted that of alpha-hANP (1 microgram). Dopamine receptors are classified as DA-1 and DA-2. The DA-2 receptor antagonists metoclopramide (50 micrograms, i.v.) and sulpiride (50 micrograms, i.v.) did not affect ANP induced natriuresis. The DA-1 receptor antagonists SCH 23390 and SK&F 83566 dose-dependently counteracted the renal response to the intravenous administration of ANP. The administration of haloperidol (25, 50 and 100 micrograms, i.v.) to rats undergoing a putative ANP dependent natriuresis (isotonic saline loading) dose-dependently reduced both urine volume and sodium excretion. Atriopeptin II (10(-9)-10(-10) M) displaced tritiated spiperone, a dopamine antagonist, from specific binding sites in homogenates of renal medulla, papilla and cortex. These results suggest that dopamine receptors, most probably of the DA-1 subclass, are involved in the natriuretic response to ANP. The present experiments do not allow the conclusion as to whether ANP directly interacts with the dopamine receptors or whether it affects these receptors by releasing dopamine.

Animals↗

PubMed1986

ATPase activity in macula densa cells of the rabbit kidney.

Na-K- and Mg-activated ATPase activities were determined in maculae densae and glomeruli dissected from both superficial and juxtamedullary nephrons of normal rabbits, using an ultramicro method including a cycling reaction. Activities were expressed as Pi generated per macula densa or per glomerulus and normalized for tissue volume. Results indicate that the mean volume of superficial and juxtamedullary macula densa samples was not statistically different, while glomeruli from deep nephrons had sample volumes that were 29% larger than those from superficial nephrons (P less than 0.001). Correcting for volume both superficial and juxtamedullary macula densa samples had an Na-K-ATPase activity of 0.37 +/- 0.21 fmol X h-1 X (micron3)-1 X Mg-ATPase activity in both pools was also similar [0.41 +/- 0.07 and 0.52 +/- 0.1 fmol X h-1 X (micron3)-1]. Na-K-ATPase activity in macula densa cells is estimated to be about 1/40th the activity of surrounding cortical thick ascending limb cells. Total glomerular ATPase per unit volume was significantly higher in glomeruli from superficial than from deep nephrons [0.41 +/- 0.04 vs. 0.28 +/- 0.04 fmol X h-1 X (micron3)-1, P less than 0.05]. There was no statistically significant activity of Na-K-ATPase in either superficial or deep glomeruli. These results suggest that in contrast to previous reports, the macula densa contains Na-K-ATPase, but at a low level relative to surrounding tubular cells. Further, in normal rabbits, this activity is invariant in superficial and juxtamedullary samples.

Animals↗

PubMed1986

Filtration pressure response to infusion of atrial natriuretic peptides.

The present experiments were undertaken to assess the effect of an atrial extract (ANF) and of the synthetic atriopeptin II (APII) on filtration pressure of rat kidneys. Continuous recordings of stop flow pressure (SFP) were made to obtain an index of the change of glomerular capillary pressure produced by atrial peptides and its time course. Short-term infusion of ANF or APII increased SFP from 40.6 +/- 0.99 to 50.7 +/- 1.42 mm Hg (p less than 0.001) and from 44.0 +/- 1.28 to 52.7 +/- 1.75 mm Hg (p less than 0.001) respectively. The maximum response was achieved promptly. Return of SFP to control was slow: 20 minutes after termination of the infusion SFP was still elevated by 4.9 +/- 1.27 mm Hg (p less than 0.01). Tubule and stellate vessel pressures increased less than 2mm Hg, changes that were not significant. Arterial pressure fell 6 mm Hg (p less than 0.05). When arterial pressure was reduced by an aortic clamp to 85-90 mmHg prior to administration of APII the response of SFP was markedly blunted (from a mean increase of 9.0 +/- 1.07 mm Hg to 4.5 +/- 0.53 mm Hg). The increase of SFP probably reflects an increase of glomerular capillary pressure. The finding suggests that atrial peptides increase glomerular filtration rate at least in part by increasing filtration pressure.

Animals↗