Endogenous vasopressin and postural control of blood pressure in man.
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Arginine Vasopressin↗
Biomedical subjects
T Bennett
Publications and source records attributed to T Bennett.
Effects of hyperinsulinaemia on the cardiovascular responses to graded hypovolaemia in normal and diabetic subjects.
1. Two experiments were carried out. The first with five normal male subjects was placebo controlled and single blind, each subject being studied on two occasions. Lower body subatmospheric pressure (LBSP) was used to assess the cardiovascular effects of graded hypovolaemia before and during either a hyperinsulinaemic, euglycaemic clamp or a placebo clamp using 0.9% (w/v) NaCl only. 2. During hyperinsulinaemia, resting systolic blood pressure rose and was accompanied by forearm vasodilatation. Forearm blood flow (FABF) and heart rate (HR) were higher at each level of LBSP during than before hyperinsulinaemia. In addition, hyperinsulinaemia was accompanied by a small increase in noradrenaline, but packed cell volume did not change. 3. In the second experiment, the effects of a hyperinsulinaemic euglycaemic clamp on the cardiovascular responses to LBSP were assessed in seven diabetic subjects with peripheral and autonomic neuropathy. 4. In contrast to the normal subjects, there was a slight fall in systolic blood pressure during the clamp but no effect was noted on HR or FABF. Mean arterial blood pressure was lower at each level of LBSP during hyperinsulinaemia compared with the pre-clamp period. Packed cell volume fell during the clamp and plasma noradrenaline rose. In one of the diabetic subjects, a precipitous fall in blood pressure occurred during hyperinsulinaemia when LBSP of 10 mmHg (1.3 kPa) was applied, this manoeuvre having been well tolerated before the clamp. 5. The mode of action of hyperinsulinaemia is not clear, but there was, however, no evidence that a fall in plasma volume had occurred.
Adult↗
Effect of intravenous infusion of adrenaline on the cardiovascular responses to distal body subatmospheric pressure in man.
1. On two separate occasions, at least 1 week apart, seven young healthy male subjects received intravenous infusions of either adrenaline [0.27 nmol (50 ng) min-1 kg-1] or saline (154 mmol/l NaCl), plus ascorbic acid (5.68 mmol/l), over 30 min. 2. On each occasion, the subjects were exposed to distal body subatmospheric pressure (DBSP), 0 to 50 mmHg (0 to 6.65 kPa) in 10 mmHg (1.33 kPa) steps, before infusion, during the final 15 min of the infusion, and at 15 min and 30 min after the cessation of the infusion. 3. Venous adrenaline concentrations of 2.85 +/- 0.22 nmol/l were achieved during the adrenaline infusion, compared with 0.49 +/- 0.07 nmol/l during the saline infusion (P less than 0.001). At 15 min and at 30 min after cessation of the adrenaline infusion, venous adrenaline concentrations had fallen to levels similar to those achieved after the cessation of the saline infusion. 4. Heart rate rose significantly from 58 +/- 4 beats/min to 67 +/- 4 beats/min during the adrenaline infusion (P less than 0.05), but there was no further significant change in response to 50 mmHg (6.65 kPa) DBSP. At 30 min after the cessation of the adrenaline infusion, heart rate rose from 60 +/- 4 beats/min to 78 +/- 7 beats/min in response to 50 mmHg DBSP. This increase was significantly greater than that observed before the adrenaline infusion [58 +/- 4 beats/min to 69 +/- 7 beats/min during 50 mmHg (6.65 kPa) DBSP; P less than 0.01].(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Involvement of beta 2-adrenoceptor-mediated mechanisms in the cardiovascular responses to alpha 1- and alpha 2-adrenoceptor antagonism in conscious, unrestrained, Long Evans and Brattleboro rats.
1. Intra-arterial blood pressures and heart rates were recorded in conscious, unrestrained, Long Evans and Brattleboro rats receiving sequential, continuous administrations of selective alpha 1- (prazosin) and alpha 2- (idazoxan) adrenoceptor antagonists. The same protocols were also run in the presence of ICI 118551 (a selective antagonist of beta 2-adrenoceptors). 2. Prazosin and idazoxan caused large, but transient, hypotensions in Long Evans and Brattleboro rats. In the continued presence of both drugs there were marked, intermittent, depressor episodes and tachycardias in both strains of rat. 3. In the presence of low or high doses of ICI 118551 the hypotensive responses to prazosin and idazoxan were markedly reduced in both strains of rat and blood pressures showed little variability, although intermittent tachycardias still occurred. 4. In adrenal-demedullated Long Evans rats, the hypotensive responses to prazosin and idazoxan were attenuated and in the presence of both drugs, blood pressure was relatively steady, although intermittent tachycardias still occurred. 5. In the presence of prazosin and idazoxan, when a depressor episode was not occurring, administration of captopril caused hypotension in Long Evans and Brattleboro rats. In the latter, the reduction in blood pressure was sustained, whereas there was a recovery in blood pressure in Long Evans rats. This recovery was punctuated by depressor episodes, and was abolished by a V1-receptor antagonist (d(CH2)5DAVP). 6. Long Evans rats given two primed doses of the non-selective alpha-adrenoceptor antagonist, phentolamine, exhibited variation in blood pressure similar to that seen in the presence of prazosin and idazoxan. As in the latter case, blood pressure variability was inhibited by the beta 2-adrenoceptor antagonist, ICI 118551. 7. Administration of idazoxan into a lateral ventricle in Long Evans rats receiving phenoxybenzamine intravenously did not cause blood pressure instability. However, intravenous administration of idazoxan in the same animals produced intermittent depressor episodes and tachycardias similar to those seen in the presence of prazosin and idazoxan. 8. The simplest explanation of the results is that beta 2-adrenoceptor-mediated depressor mechanisms contribute to the hypotensive responses to alpha 1- and alpha 2-adrenoceptor antagonism. Furthermore, in the presence of adequate peripheral alpha 1- and alpha 2-adrenoceptor antagonism, blood pressure may be maintained by the renin-angiotensin system and vasopressin (although it is only when the former system has been antagonized that a clear-cut pressor action of vasopressin is apparent). Under these conditions, blood pressure maintenance is interrupted by intermittent depressor episodes that are largely due to adrenal medullary activation.
Adrenal Medulla↗
Regional haemodynamic effects of depressor neuropeptides in conscious, unrestrained, Long Evans and Brattleboro rats.
1. The regional haemodynamic effects of i.v. bolus doses of atrial natriuretic peptide (ANP, 1 and 10 nmol), calcitonin gene-related peptide (CGRP, 0.05 and 0.5 nmol) and corticotropin-releasing factor (CRF, 1 and 5 nmol) were assessed in conscious Long Evans and Brattleboro rats chronically instrumented with miniaturized, pulsed Doppler probes. 2. The low dose of ANP was without effect on mean arterial pressure (MAP), but caused tachycardia and hindquarters vasodilatation with vasoconstriction in renal and mesenteric beds in Long Evans rats. With the high doses of ANP these effects were more pronounced and MAP fell. In Brattleboro rats there was a primary renal vasodilatation. 3. The low dose of CGRP caused a slight fall in MAP in Long Evans rats, tachycardia and a renal vasodilatation. The high dose of CGRP caused marked hypotension, tachycardia and renal, mesenteric and hindquarters vasodilatation in both strains of rat. However, only in Long Evans rats were there secondary renal and mesenteric vasoconstrictions. 4. The low dose of CRF caused falls in MAP in both strains of rat, accompanied by renal and, particularly, mesenteric vasodilatation. Administration of the high dose of CRF caused profound, prolonged hypotension, tachycardia and mesenteric vasodilatation. There was also (late onset) hindquarters vasodilatation accompanying renal vasoconstriction that followed the initial vasodilatation in this vascular bed. 5. These results indicate that appropriate doses of particular peptides may be capable of promoting flow through individual peripheral vascular beds.
Animals↗
Regional hemodynamic responses to adrenoceptor antagonism in conscious rats.
Changes in blood pressure and renal, mesenteric, and hindquarters vascular resistances were measured in conscious Long-Evans and Brattleboro (vasopressin-deficient) rats in response to sequential, continuous administrations of prazosin and idazoxan in the absence or presence of ICI 118551 (beta 2-adrenoceptor antagonist) or propranolol. The large transient hypotensions elicited by prazosin and, subsequently, by idazoxan were associated with renal and hindquarters vasodilatations in both strains of rat. In Brattleboro rats, prazosin also elicited mesenteric vasodilatation. Pretreatment with ICI 118551 reduced the initial hypotensive effects and hindquarters vasodilatations elicited by prazosin and idazoxan, but the hemodynamic effects of prazosin were not significantly affected by propranolol. These results are consistent with propranolol antagonizing beta 1-adrenoceptor-mediated effects on the heart and the renin-angiotensin system that act to offset a beta 2-adrenoceptor-mediated vasodilatation, which contributes to the effects elicited by alpha-adrenoceptor antagonism. Hemodynamic responses to captopril and d(CH2)5DAVP (in Long-Evans rats) in the presence of adrenoceptor antagonists were consistent with a major cardiovascular role of the renin-angiotensin system and a less overt role of vasopressin until the latter system was blocked.
Adrenergic alpha-Antagonists↗
Regional hemodynamic effects of atrial natriuretic peptide or captopril in Brattleboro rats.
The regional hemodynamic effects of rat atrial natriuretic peptide (ANP) (1 and 10 nmol) were measured in the same conscious Brattleboro rats in water-replete and in water-deprived states (14 h). In the latter condition, the effects of ANP were compared with those of captopril (3.2 mumol). In rats in the water-replete state, the low dose of ANP had no significant effects on mean arterial pressure (MAP) or renal, superior mesenteric, or hindquarter vascular resistances, although heart rate (HR) showed a transient increase. The high dose of ANP caused a fall in MAP and an increase in HR. Renal and hindquarter vascular beds showed dilatation followed by constriction; there was a mesenteric vasoconstriction only. In rats in the water-deprived state, the low dose of ANP caused a marked fall in MAP but only a transient increase in HR; there was marked hindquarters vasodilation. The high dose of ANP caused dramatic hypotension and bradyarrhythmia; an initial hindquarter vasodilation gave way to vasoconstriction; renal and mesenteric vasoconstrictions also occurred. The initial effects of captopril on MAP were similar to those of the high dose of ANP, but the regional hemodynamic effects of captopril indicated a potent inhibition of both primary and secondary vasoconstrictor mechanisms.
Animals↗
Abnormal thermoregulation in diabetic autonomic neuropathy.
Hypothermia has been reported to be more common in diabetic people than in nondiabetic people, and we have investigated the possibility that autonomic neuropathy may be associated with disordered thermoregulation. After an overnight fast and maintenance of normoglycemia, 12 insulin-treated diabetic patients with and 11 without neuropathy and 12 nondiabetic control subjects, all less than 55 yr, were subjected to external cooling by perfusing water at 16 degrees C through a liquid-conditioned coverall for less than or equal to 45 min. Patients with autonomic neuropathy had impaired vasoconstriction to cooling, particularly in the foot, calf, and forearm. Core temperature rose by 0.2 degrees C in control subjects and by 0.15 degrees C in patients with diabetes but no neuropathy. In contrast, group mean core temperature was unchanged in those with autonomic neuropathy and fell in 3 subjects (P less than .001). Cooling caused shivering in 6 patients with diabetic autonomic neuropathy, but not in those with neuropathy or control subjects (P less than .05). Baseline metabolic rates were similar in all three groups, but the increase after cooling was significantly greater among those who shivered (P less than .05-.02). Thus, young diabetic patients with autonomic neuropathy have impaired thermoregulation to a relatively short period of external cooling, even during metabolic stability, which may predispose to hypothermia.
Adult↗
Physiological aspects of the aging cardiovascular system.
Most putative studies on the physiology of the aging cardiovascular system in humans have been cross-sectional. The results are therefore bedeviled by selective mortality and probably influenced by subclinical disease processes. Even accepting these problems, critical reading of the published literature shows that there is very little substantive evidence for the "well-known" age-related changes in cardiovascular physiology such as baroreflex impairment, sympathetic hyperactivation, adrenoceptor dysfunction, or neurohumoral abnormalities.
Aged↗
The cardiovascular responses to sequential inhibition of alpha-adrenoceptors, the renin-angiotensin system and vasopressin in rats with adrenal regeneration hypertension.
The cardiovascular responses to selective alpha 1- and alpha 2-adrenoceptor antagonism (with prazosin and idazoxan, respectively) were assessed in rats 4 weeks after unilateral nephro-adrenalectomy, contralateral adrenal enucleation and the provision of a 1% NaCl solution as drinking fluid (AEN rats) and in sham-operated (SON) rats. Measurements were made between 0700 and 1000 h and between 1400 and 1700 h, since we have previously shown that resting blood pressures (BPs) in AEN rats are higher in the morning than in the afternoon. Following prazosin administration (morning or afternoon), BP fell to similar levels in both SON and AEN rats. Idazoxan, given 20 min after the start of prazosin infusion, caused similar transient falls in BP in all four groups of rats. Following the subsequent additional antagonism of angiotensin II (Ang II) production (with captopril) and vasopressin (V1) receptors [with d(CH2)5DAVP], BP in AEN rats studied in the morning was higher than in SON rats at that time of day, and higher than in AEN rats studied in the afternoon. These findings suggest than an additional underlying mechanism capable of increasing BP exists in AEN rats studied in the morning.
Adrenal Glands↗
Blood pressure recovery following haemorrhage in rats with streptozotocin-induced diabetes mellitus.
The effect of hypotensive haemorrhage on blood pressure recovery was compared in saline- and streptozotocin-injected rats. Absolute plasma volumes (and calculated blood volumes) were not different between the two groups. After haemorrhage of similar volumes at similar rates, there were no significant differences in the recoveries in blood pressures or heart rates between control and diabetic animals. In other control and diabetic groups, posthaemorrhage treatment with the converting enzyme inhibitor captopril (at 20 min) and the vasopressin (V1-receptor) antagonist d(CH2)5DAVP (at 40 min) did not have any deleterious effects on blood pressure recovery at these times. These results support the proposition that neither the renin-angiotensin system nor vasopressin are importantly involved in blood pressure recovery at these time points after hypotensive haemorrhage in conscious rats. They are also consistent with the lack of difference between untreated control and diabetic groups, despite previous findings showing impairments of renin-angiotensin- and vasopressin-mediated effects after acute hypotension induced by pentolinium in diabetic rats.
Animals↗
Pyridoxine in the treatment of premenstrual syndrome: a retrospective survey in 630 patients.
We present a survey summarising the retrospective reports of the therapeutic effect of pyridoxine (vitamin B6) in 630 women suffering from premenstrual syndrome (PMS) who attended a PMS clinic during the period 1976-1983. The daily doses of pyridoxine hydrochloride varied from 40 to 100 mg early in the study and from 120 to 200 mg in the later period of the investigations. The response to treatment was recorded as good (no significant residual complaints) in 40 per cent or more of patients taking 100-150 mg pyridoxine daily and in 60 per cent of patients treated with 160-200 mg daily. Together with partial response (useful benefit but still some significant complaints), the positive effect of the treatment increased to 65-68 per cent and 70-88 per cent respectively. No symptoms consistent with a diagnosis of peripheral neuropathy were reported.
Adolescent↗
Models of adrenal regeneration hypertension in the rat.
Blood pressure was measured indirectly (using the tail-cuff method) and intra-arterially in conscious rats following one of three experimental procedures carried out in order to determine which resulted in the most marked and reproducible form of adrenal regeneration hypertension (ARH). All rats were unilaterally adrenalectomized and given NaCl solution (1%). In some rats, the remaining adrenal gland was either enucleated (AE rats) or compressed (AC rats) but both kidneys were left intact. During the fourth week after surgery, indirectly measured systolic blood pressure was higher in AE and AC rats than in sham-operated (SO) rats but, when measured intra-arterially, the magnitude of the developed hypertension was small (AC rats) or was absent altogether (AE rats). However, when a kidney was removed at the time of enucleation (AEN rats), the levels of systolic blood pressure, measured indirectly or intra-arterially, were markedly and consistently higher than in the corresponding group of uninephrectomized SO rats. The magnitude of the developed hypertension was similar in mature male and immature female AEN rats. We conclude that mature male rats, unilaterally nephro-adrenalectomized and given NaCl solution (1%), provide a marked and reproducible model of ARH.
Adrenal Glands↗
Alterations in beta-adrenoceptor number and catecholamine content of chick atria after reversible sympathetic denervation with 6-hydroxydopamine.
1. The characteristics of [3H]-dihydroalprenolol (DHA) binding were determined in atria from untreated chicks. [3H]-DHA binding to atrium homogenates was rapid (k1 = 8.52 X 10(8) l mol-1 min-1), reversible (k-1 = 0.47 min-1), saturable, and of high affinity (KD = 0.6-1.0 nmol/l). Isoprenaline competed for specific [3H]-DHA binding in a stereoselective manner; IC50 values (mumol/l) were: (-)isoprenaline 0.12, (+)isoprenaline 4.7. 2. The number of [3H]-DHA binding sites and catecholamine content of left and right atria were examined after injection of chicks with a single dose of 6-hydroxydopamine hydrobromide (100 mg/kg). There were transient increases in the number of [3H]-DHA binding sites in both the left and the right atrium after 6-OHDA treatment. These increases were quicker in onset and in offset in the right atrium than in the left atrium. [3H]-DHA binding was significantly increased in the left atrium at 5 and 7 days, and in the right atrium at 3 and 5 days after 6-OHDA injection. 3. Saturation binding isotherms indicated that the increase in [3H]-DHA binding was due to an increase in beta-adrenoceptor number with no change in affinity for [3H]-DHA. 4. Twenty four hours after 6-OHDA treatment there was a significant (80%) decrease in noradrenaline content of left and of right atria. 5. The decrease in noradrenaline content was reversible, noradrenaline levels returning to 55% of control in left atrium and to 71% of control in right atrium by 21 days after 6-OHDA treatment. These changes are consistent with reversible sympathetic denervation of the atria.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
The effect of insulin-induced hypoglycaemia on gastrointestinal motility in man.
The effect of insulin-induced hypoglycaemia on gastro-jejunal motility was studied in five, healthy, male subjects using tethered, pressure sensitive, radiotelemetry capsules. Thirty minutes after the intravenous injection of soluble insulin (0.15 unit/kg body weight), a significant reduction in blood glucose concentration (control: 5.26 +/- 0.19 SEM mmol/l; insulin: 1.48 +/- 0.44 mmol/l; P less than 0.001) was associated with a rise in heart rate (mean peak rise 29 +/- 8 beats/min, P less than 0.05), systolic arterial blood pressure (mean peak rise 28 +/- 4 mmHg, P less than 0.01) and plasma pancreatic polypeptide concentration (control: 20 +/- 7 pmol/l; insulin: 287 +/- 66 pmol/l; P less than 0.01). These events coincided with a short period of jejunal motor activity, which was not associated with gastric motor activity nor with raised plasma motilin concentrations. During the control study, there were no changes in blood glucose concentration, heart rate, arterial blood pressure or plasma pancreatic polypeptide concentrations, and there was no jejunal motor activity. The interval between successive gastric migrating motor complexes (MMC) was not significantly different in the insulin and control studies (control: median interval 110 min, range 108-148 min; insulin: median interval 124 min, range 115-125 min), suggesting that the fasting gastrojejunal MMC and jejunal motor activity arose independently. Insulin-induced hypoglycaemia is accompanied by jejunal motor activity, which may underlie the abdominal symptoms associated with hypoglycaemia.
Adult↗
Adrenal regeneration hypertension in the rat.
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Adrenal Cortex Hormones↗
Post-exercise hypotension: the effects of epanolol or atenolol on some hormonal and cardiovascular variables in hypertensive men.
1 Eight men with primary hypertension were treated for 3 weeks with placebo, epanolol (200 mg or 400 mg), or atenolol 100 mg in a randomised cross-over study. Each active treatment period was preceded by a 3 week placebo treatment period and both investigators and subjects were blind to the active drug sequence. 2 At the end of each period, measurements were made of resting cardiovascular (heart rate, blood pressure, forearm blood flow) and biochemical variables (plasma renin, angiotensin II, aldosterone, adrenaline, noradrenaline, vasopressin, sodium and potassium concentrations and osmolality). Responses to exercise (including gas exchange, sweat rate, and ratings of perceived exertion) and the reflex cardiovascular adjustments to distal body subatmospheric pressure were also assessed. 3 The reduction of exercise-induced tachycardia by epanolol 400 mg was comparable to that of atenolol. There was very little difference in the effects of atenolol or epanolol 400 mg on resting blood pressure, but in both cases blood pressures were usually significantly lower than with epanolol 200 mg. 4 Although each active treatment influenced the renin-angiotensin system and circulating levels of catecholamines, the exercise-induced reduction in blood pressure was unaffected. Thus, the hypotensive effects of pharmacological and non-pharmacological interventions were additive.
Adrenergic alpha-Antagonists↗
Water deprivation: effects on fluid and electrolyte handling and plasma biochemistry in Long-Evans and Brattleboro rats.
1. Intakes and urine outputs of fluid and electrolytes were measured before, during and after water deprivation in normal rats (Long-Evans strain) and in vasopressin-deficient rats (Brattleboro strain). 2. In a parallel experiment it was confirmed that the water-deprivation schedule used (Long-Evans rats 53 h, Brattleboro rats 14 h), and previously shown to cause similar percentage reductions in plasma volumes in the two strains, did produce more marked hypernatraemia and hyperosmolality and a greater percentage reduction in body weight in Brattleboro than in Long-Evans rats. 3. In Long-Evans rats, water deprivation caused a gradual reduction in urine output, a reduction in food intake and, during the first 24 h, increases in Na+ and K+ output. In Brattleboro rats, the reduction in urine output was more pronounced, but despite this total water losses were greater than from Long-Evans rats. Brattleboro rats showed a greater reduction in food intake. Their urinary Na+ and K+ losses were elevated during the first 9 h of water deprivation; thereafter these variables fell but remained above the level of intake. 4. The cumulative Na+ losses during water deprivation were similar in the two strains but the cumulative K+ losses in the Brattleboro rats were greater than in the Long-Evans rats. Thus the relative hypernatraemia and hyperkalaemia in water-deprived Brattleboro rats compared to water-deprived Long-Evans rats cannot be explained simply on the basis of differences in renal fluid and electrolyte handling. 5. There were significant increases in plasma angiotensin II and aldosterone levels at the end of the water deprivation periods in both strains of rat, and after the drinking water was returned there was a marked anti-natriuresis consistent with an expression of one of the renal actions of aldosterone.
Aldosterone↗