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Biomedical subjects

F C Luft

Publications and source records attributed to F C Luft.

At least 451 records · Page 25Linked to original sources
PubMed1987

Dissociation between heart rate and sympathetic nerve responses to baroreceptor activation in spontaneously hypertensive rats.

We tested the baroreflex in conscious, stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto controls (WKY) with incremental bolus injections of nitroprusside and methoxamine. The change in heart rate (HR) per change in mean blood pressure (MAP) was greater in WKY than in SHRSP. In contrast, the change in splanchnic nerve activity (SpNA) per change in MAP was greater in SHRSP than in WKY. The sympathetic outflow in SHRSP seems more reactive to blood pressure changes than in WKY. The discordance in HR and SpNA changes suggests that the integration of autonomic function in SHRSP is impaired.

Animals↗
PubMed1987

Effects of atrial natriuretic factor in rats with renal insufficiency.

To test the effect of exogenous atrial natriuretic factor (ANF) on the kidney function of rats with chronic renal insufficiency, we examined the responses to bolus infusions of atriopeptin III in two models of renal insufficiency, namely, nephrosclerosis and glomerulonephritis. Hypertensive Dahl S rats receiving a high (8%) NaCl diet for 12 weeks, and rats with anti-glomerular basement membrane nephritis, both of which had glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) less than half those of respective control rats, exhibited similar relative increases In GFR and ERPF in response to atriopeptin III as did controls. Natriuresis, diuresis, and decreased blood pressure were as prominent in rats with either form of renal disease as in control rats. Rats receiving high NaCl intake, irrespective of renal function, had relatively exaggerated responses compared with rats receiving a normal NaCl diet. We conclude that rats with chronic renal insufficiency of diverse causes respond briskly to ANF despite presumed hyperperfused and hyperfiltering nephrons. Thus, diseased kidneys exhibit substantial renal functional "reserve." The renal response to ANF appears to be influenced by NaCl intake in both normal animals and those with renal insufficiency.

Animals↗
PubMed1987

Kinetics and pharmacodynamics of atrial natriuretic peptide and lithium clearance in the isolated perfused rat kidney.

We used the kinetics of atrial natriuretic peptide (ANP) and fractional lithium excretion to test the hypothesis that ANP-induced natriuresis is related directly to the ANP perfusate concentration and is mediated by a decrease in proximal tubular sodium reabsorption. Wistar rat kidneys were perfused for 90 min after administration of 1 microgram of human ANP. Comparisons were made to control perfusions. ANP had a short half-life (12.4 min) and a renal clearance 6-fold greater than the creatinine clearance. ANP treatment resulted in a significant peak increase in sodium (5.6-fold), lithium (2.1-fold), potassium (2.3-fold) and water (5.1-fold) excretion. The natriuretic response to ANP was delayed 25 min. Exogenous creatinine clearance, perfusion pressure, perfusion flow and renal vascular resistance were not affected. We conclude that the kidney eliminates ANP rapidly by mechanisms that appear to be located primarily in the peritubular circulation. The initial renal response to ANP did not follow perfusate concentrations. Rather, natriuresis increased as ANP concentrations decreased. The relationship was defined by a counterclockwise hysteresis loop. Natriuresis was not mediated by an increased delivery of sodium to the tubule, but may have been due to either a direct or an indirect action of ANP on the kidney.

Absorption↗
PubMed1986

Baroreceptor reflex effect on sympathetic nerve activity in stroke-prone spontaneously hypertensive rats.

To elucidate the relationship between responses in sympathetic outflow to incremental changes in blood pressure, we performed baroreflex activation experiments in conscious, stroke-prone, spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto (WKY) rats. We gave incremental bolus injections of nitroprusside and methoxamine and measured mean blood pressure (MAP), heart rate, and splanchnic nerve activity (SpNA). Change in heart rate per change in blood pressure was greater in WKY rats than in SHRSP indicating the decrease in baroreceptor sensitivity displayed in the latter strain. In contrast, change in SpNA per change in blood pressure was greater in SHRSP than in WKY rats. These findings suggest that sympathetic outflow in SHRSP is more reactive to blood pressure changes than in WKY rats. The discordance in heart rate and SpNA changes supports the notion that central neural integration of autonomic function in SHRSP is impaired.

Animals↗
PubMed1986

Intra- and interindividual variability in sodium intake in normal subjects and in patients with renal insufficiency.

To elucidate patterns of dietary sodium ingestion in free-living subjects, we collected 26 consecutive 24-hour urine specimens in 18 subjects who had not received instructions to limit the sodium content of their diets, and who were not aware that sodium intake would be estimated from the collections. Nine subjects with plasma creatinine values less than 2 mg/dL had a mean 24-hour UNaV of 156 mEq/d, with an interindividual variability of SD +/- 38 mEq. Their intraindividual variability was 61 mEq. Nine subjects with creatinine values greater than 2 mg/dL had a mean 24-hour UNaV of 108 mEq/d (P less than 0.05). The intraindividual variability of these subjects was 39 mEq/d. Subjects with normal renal function ingested more sodium than subjects with renal insufficiency, although the variability in both groups was extensive. These data confirm and extend earlier observations and illustrate the difficulty in identifying biologic correlations in the presence of considerable intraindividual variability. They underscore the futility of estimating mean dietary sodium intake with a single or occasional 24-hour urine collection in both normal subjects and patients with renal insufficiency.

Adolescent↗
PubMed1986

Short-term augmented calcium intake has no effect on sodium homeostasis.

To test the hypothesis that the supplementation of dietary calcium intake influences sodium homeostasis, the renin-angiotensin system, and sympathetic nervous system in a manner that might evoke a decrease in arterial blood pressure, we gave 16 participants (eight normal and eight with hypertension) placebo for 8 days, followed by 500 mg elemental calcium as the carbonate salt twice a day for 8 days. The same diet was prepared for each meal for the entire study. Sodium intake was fixed for each participant and averaged 150 mEq/day. All urine was collected every day. Blood was drawn at the end of the placebo and calcium periods for determinations of plasma renin, aldosterone, and norepinephrine values. Calcium supplementation increased urinary calcium excretion significantly in both groups. However, calcium supplementation failed to influence sodium or potassium excretion, serum electrolytes, total serum calcium, renin, aldosterone, or norepinephrine levels, or heart rate. Systolic and diastolic blood pressure were not influenced in normal subjects, but in patients with hypertension the supine systolic blood pressure decreased significantly. We conclude that blood pressure lowering effects of calcium, should they occur, are not likely the result of augmented urinary sodium excretion or of straight-forward influences on the renin-angiotensin system or sympathetic nervous system.

Administration, Oral↗
PubMed1986

Atrial natriuretic factor determinations and chronic sodium homeostasis.

To examine the physiological role of atrial natriuretic factor (ANF) in the maintenance of sodium homeostasis under various conditions, we performed experiments in rats across a wide range of sodium intake, in rats with chronic renal insufficiency at extremes of sodium intake, and in rats given desoxycorticosterone acetate. After three weeks of a very low sodium diet, regular diet, or regular diet plus 1% saline as drinking water, no difference in plasma values of immunoreactive atrial natriuretic factor (IR-ANF) were identified, while rats at the lowest level of sodium intake had elevated atrial values. Normal rats, and rats with 5/6 nephrectomy has plasma values of IR-ANF which were no different irrespective of their sodium intake, nor were atrial values in these rats different. Although mineralocorticoid "escape" could be documented by changes in urine sodium excretion, neither plasma nor atrial IR-ANF values showed differences either at 24 or 72 hr after "escape". The data are consistent with previous observations that ANF serves the purpose of affecting rapid adjustments to large alterations in circulating fluid volume. Chronic high sodium intake, adaptation to renal insufficiency, and adjustment to the effect of mineralocorticoid do not appear to be associated with increased circulating plasma concentrations of IR-ANF.

Animals↗
PubMed1986

Effects of volume expansion and contraction on potassium homeostasis in normal and hypertensive humans.

To investigate the role of potassium on blood pressure we measured serum potassium, urinary excretion of potassium and sodium, fractional excretion of potassium, urinary sodium:potassium ratio, plasma renin activity, aldosterone, and norepinephrine during dynamic maneuvers in normotensive and hypertensive subjects. After baseline measurements, we expanded intravascular volume with infusion of intravenous saline and then induced sodium and volume depletion by diuretic administration during a low sodium salt diet. These studies were performed in 431 normotensive and 478 hypertensive subjects enabling evaluation of the effects of age, race, and sex, as well as blood pressure, on the results. Among normotensives, we found that white subjects had significantly P less than 0.05) higher levels of serum and urine potassium, fractional potassium excretion and lower urinary sodium:potassium ratios than black subjects and that males had the same patterns of differences compared to females. Similar, but less consistent racial differences were seen among the hypertensive subjects. We also observed significant (P less than .05) correlations between urinary potassium excretion and body weight in both normal and hypertensive groups. In normal subjects, a significant correlation was observed between the urinary sodium:potassium ratio and blood pressure that was not seen in the hypertensives. The latter, however, displayed a significant (P less than .05) inverse relationship between serum potassium and blood pressure. Multiple regression analysis revealed that urinary potassium excretion was influenced by age, race, sex, body weight, blood pressure, creatinine clearance, renin, and aldosterone. These observations reveal important relationships between potassium homeostasis and blood pressure control that deserve further study.

Adult↗
PubMed1986

Differential actions of neuronal and hormonal vasopressin on blood pressure and baroreceptor reflex sensitivity in rats.

The central cardiovascular actions of arginine vasopressin (AVP) and the role of this peptide in the modulation of baroreceptor reflex (BRR) sensitivity were investigated in conscious, chronically instrumented rats. Intracerebroventricular (i.c.v.) injections of AVP (1-100 ng) produced dose-dependent pressor effects together with increases in heart rate, splanchnic, and renal sympathetic nerve activity and a reduction of mesenteric blood flow. These responses were prevented by i.c.v. pretreatment with a V1-AVP receptor antagonist. Furthermore, the central pressor effects of AVP were abolished by peripheral alpha-adrenoceptor blockade with phentolamine. In contrast to the i.c.v. injections, intravenous (i.v.) or intracarotid injections of AVP produced pressor responses accompanied by bradycardia and a decrease in sympathetic nerve activity. Intracerebroventricular pretreatment with a V1-AVP receptor antagonist shifted the slope of the BRR curve (increases in pulse interval plotted against increases in systolic blood pressure in response to i.v. methoxamine) toward higher sensitivity, whereas i.v. pretreatment with a V2-AVP receptor antagonist shifted the slope of the BRR curve toward lower sensitivity of the reflex. These findings suggest that central (neuronal) AVP, by acting on V1-AVP receptors in the brain, participates in central pressor mechanisms, activates the sympathetic nervous system, and desensitizes the BRR. Conversely, circulating (hormonal) AVP can sensitize the BRR by acting on V2-AVP receptors accessible from the blood. Our data provide evidence pointing to a direct interaction between the neuronal and the hormonal axis of the AVP system within cardiovascular control.

Animals↗
PubMed1986

Percutaneous transluminal angioplasty in complicated renal vascular hypertension.

Fourteen patients with renovascular hypertension complicated by renal impairment and/or a nonfunctioning kidney underwent percutaneous transluminal angioplasty of the remaining kidney(s) for the purpose of improving blood pressure control and/or renal function. The outcome of percutaneous transluminal angioplasty in these individuals was evaluated over periods ranging from 1 to 72 months. All patients had atherosclerotic renovascular hypertension as judged by the X-ray appearance of the stenotic lesions of the renal artery as well as evidence of aortic atherosclerosis. Four of the 14 subjects demonstrated a decrease in serum creatinine greater than or equal to 20% following the procedure, and an equal number showed a similar increase in serum creatinine. In the 1st month following the procedure, 5 patients required dialysis because of deterioration of renal function, 4 of whom subsequently died. Over the entire population, only 4 subjects showed improvement in blood pressure and renal function which persisted for 18 to 72 months. One of these subjects had a recurrence of renovascular hypertension and underwent successful repeat dilatation for bilateral disease after 2 years following the initial angioplasty. This patient remains improved. These observations confirm that when renovascular hypertension occurs in an older population with cardiac and renal disease or occurs in a solitary functioning kidney, the remote prognosis is not good. The improvement rate of 29% with dilatation alone in this population appears to be less than that observed following surgical intervention in a similar population. Thus, transluminal angioplasty should be reserved for those subjects who are not surgical candidates or who refuse surgical intervention.

Aged↗
PubMed1986

Effect of urapidil, clonidine, and prazosin on sympathetic tone in conscious rats.

To test the hypothesis that the hypotensive action of urapidil is in part related to a direct action on the brain, the central (intracerebroventricular) and peripheral (intravenous) effects of urapidil were studied and compared with those obtained with clonidine and prazosin. All studies were conducted in conscious, chronically instrumented stroke-prone spontaneously hypertensive rats (SHRSP). Efferent sympathetic nervous system activity was estimated by means of a bipolar electrode implanted on the splanchnic nerve. Only clonidine, administered intracerebroventricularly and intravenously, decreased sympathetic nerve activity. Urapidil and prazosin either did not affect sympathetic nerve activity after central administration or increased it after peripheral administration at low and high doses, respectively. Centrally administered urapidil and prazosin lowered blood pressure but also blocked the response to intravenously administered phenylephrine; this result suggests a peripheral effect. Centrally administered urapidil decreased heart rate. Urapidil given either intracerebroventricularly or into the cisterna magna had no influence on baroreceptor responses. Intravenous infusions of urapidil and prazosin in sufficient doses to lower blood pressure in spontaneously hypertensive rats by 50 mm Hg completely blocked the actions of phenylephrine. These data suggest that in conscious SHRSP urapidil lowers blood pressure through peripheral blockade of alpha 1-adrenergic receptors rather than by means of central sympathetic suppression. In this regard urapidil resembles prazosin rather than clonidine; however, the effect of urapidil on heart rate is consistent with a central mode of action.

Animals↗
PubMed1986

Definitions and characteristics of sodium sensitivity and blood pressure resistance.

Sensitivity and resistance to the effects of sodium were evaluated in normotensive and hypertensive humans by two approaches. Blood pressure was measured after an intravenous infusion of 2 L of normal (0.9%) saline and after sodium and volume depletion induced by a low sodium diet and furosemide administration in 378 normal volunteers and 198 subjects with essential hypertension. Those in whom mean arterial blood pressure decreased by at least 10 mm Hg after sodium and volume depletion were considered sodium-sensitive, and those with a decrease of 5 mm Hg or less (including an increase in pressure) were considered sodium-resistant. The second study utilized the blood pressure response to modest dietary sodium restriction in 74 normotensive subjects to identify sodium sensitivity and resistance. In both studies the responses were heterogeneous. In the first study significantly more hypertensive subjects were sodium-sensitive, as compared with those in the normotensive group (p less than 0.001). Plasma renin activity (low, normal, or high) did not predict sodium responses. In both groups sodium-sensitive individuals were significantly older (p less than 0.001) and had lower baseline renin values than sodium-resistant subjects. Factors related to the change in mean arterial blood pressure after sodium and volume depletion included baseline pressure (r = -0.54, p less than 0.001) and age (r = -0.16, p = 0.002 in the normotensive group; r = -0.28, p less than 0.001 in the hypertensive group). The response to dietary sodium restriction was also correlated with baseline pressure (r = 0.61, p less than 0.001) and the initial urinary sodium excretion (r = 0.27, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Differential modulation of the baroreceptor reflex by brain and plasma vasopressin.

Plasma vasopressin sensitizes the baroreceptor reflex, whereas vasopressin given into the cerebral ventricle overrides the baroreceptor reflex by means of sympathetic stimulation. To test the hypothesis that arginine vasopressin stimulates two different receptor subtypes (V1 and V2) in the central nervous system, we measured the baroreceptor reflex (change in pulse interval vs change in blood pressure) after administering methoxamine (10-300 micrograms/kg i.v.) in conscious rats. Animals were pretreated either with a V1 vasopressin receptor antagonist administered intravenously or intracerebroventricularly, or with a V2 receptor antagonist administered intravenously. The central V1 antagonist caused sensitization of the baroreceptor reflex, whereas the intravenous V2 antagonist attenuated it. The intravenous V1 vasopressin antagonist had no effect on baroreceptor reflex sensitivity. When the experiments were repeated in rats with hereditary diabetes insipidus, neither antagonist influenced the baroreceptor reflex. Volume expansion lowered circulating vasopressin levels and also attenuated the baroreceptor reflex--effects similar to those observed with the intravenous V2 antagonist. We conclude that vasopressin sensitizes the baroreceptor reflex through V2 receptors accessible from the blood and inhibits the reflex through V1 receptors in the brain that cannot be reached from the blood. These observations suggest a direct interaction between hormonal and neuronal vasopressin in cardiovascular control.

Animals↗
PubMed1986

Atriopeptin III kinetics and pharmacodynamics in normal and anephric rats.

To elucidate the disposition of atriopeptin III in plasma we performed experiments in normal and anephric rats. Bolus, i.v. atriopeptin III (250 ng) was given after which the rats were decapitated at 30-sec intervals. The half-life of atriopeptin III in normal rats was 26.5 sec, the volume of distribution was 352 ml and the plasma clearance was 500 ml/min. In anephric rats the half-life was 56.8 sec, the volume of distribution was 345 ml and the plasma clearance was 206 ml/min. In other rats atriopeptin III was given and urine was collected simultaneously. No atriopeptin III could be measured in the urine. We gave 0.0, 0.067, 0.125, 0.25, 0.5 and 1.0 ng/kg of bolus atriopeptin III to normal rats and measured effects on blood pressure, heart rate and plasma concentration at 30 sec, the time at which maximum effect on blood pressure occurred. Dose, change in blood pressure and plasma concentration were correlated. Heart rate increased, but not in a dose-dependent fashion. We conclude that atriopeptin III is cleared from rat plasma rapidly and that the kidneys account for 59% of its elimination by degradation rather than excretion. Because the effect of atriopeptin III on blood pressure is concentration-dependent, the transient changes exerted by atriopeptin III may be related to its rapid disappearance from plasma.

Animals↗
PubMed1986

Natriuresis and the renin axis in sodium-sensitive man.

We analysed the blood pressure, natriuretic and hormonal responses of 378 normal volunteers and 198 essential hypertensives after an intravenous infusion of 2 litres of isotonic saline and after a low-sodium diet and furosemide. Those in whom mean arterial blood pressure decreased by greater than 10 mmHg after sodium and volume depletion were considered sodium-sensitive, and those in whom a decrease of less than 5 mmHg was observed were considered sodium-resistant. Sodium-sensitive individuals had lower renin values than those who were resistant to sodium. Both normal and hypertensive sodium-sensitive individuals exhibited an 'exaggerated' natriuresis compared with resistant subjects. Sodium-sensitive subjects exhibited greater aldosterone responses to renin stimulation after volume depletion than resistant subjects. Sodium sensitivity is associated with exaggerated natriuresis as well as tighter coupling between renin and aldosterone. Relative volume expansion could account for the differences observed between sensitive and resistant individuals.

Aldosterone↗