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Biomedical subjects

T Bennett

Publications and source records attributed to T Bennett.

At least 289 records · Page 16Linked to original sources
PubMed1986

Fluid and electrolyte handling in Long Evans and Brattleboro rats following injection of polyethylene glycol.

1. Intake and output of water, Na+ and K+ were measured in Long Evans and Brattleboro rats (deficient in hypothalamic and pituitary vasopressin) before and after subcutaneous injection of polyethylene glycol (PEG) sufficient to cause a substantial hypovolaemia. 2. In the Long Evans rats an initial fluid retention (due to oliguria and polydipsia) was accompanied by Na+ retention and K+ loss. On the second day there was a diuresis but Na+ retention persisted until days 3 and 4 when there was a natriuresis. 3. Brattleboro rats initially also showed fluid retention but this was achieved by hypodipsia with a greater oliguria; there was an accompanying retention of Na+ and K+. On the second day, a reduced fluid balance was still accompanied by Na+ retention but associated with kaliuresis. Diuresis and natriuresis occurred on the third day after PEG injection. 4. Thus, rats deficient in vasopressin respond to hypovolaemia by retaining fluid. The renal actions of aldosterone do not explain fully the changes in renal electrolyte handling.

Animals↗
PubMed1986

Pressor contributions from angiotensin and vasopressin after polyethylene glycol.

Isosmotic volume depletion was induced by subcutaneous injection of 5 ml of polyethylene glycol (PEG; 20 M; 30%) in Long-Evans rats and in rats deficient in hypothalamic vasopressin (Brattleboro rats). In the PEG-treated Long-Evans rats, captopril caused a hypotension that was greater than that seen in saline-injected controls. Pretreatment with the vasopressin (V1 receptor) antagonist d(CH2)5DAVP did not, itself, cause a fall in blood pressure, but it enhanced the hypotensive effect of captopril in the PEG-treated Long-Evans rats. The PEG-treated Brattleboro rats had similar resting blood pressures to the PEG-treated Long-Evans rats, but in the former group, captopril caused a more profound and progressive hypotension than was seen in any of the present experimental regimes used in the Long-Evans rats. This suggests that, during hypovolemia induced by PEG, Brattleboro rats were either more dependent on the renin-angiotensin system for the maintenance of arterial blood pressure than were Long-Evans rats treated acutely with a vasopressin (V1) receptor antagonist or less able to recruit sympathoadrenal mechanisms to compensate for the sudden loss of the renin-angiotensin system.

Angiotensin II↗
PubMed1986

Factors contributing to the maintenance of arterial blood pressure in adult rats treated neonatally with guanethidine.

Adult rats treated neonatally with guanethidine had normal arterial blood pressures, but these were more dependent on the renin-angiotensin system than in control animals. Antagonism of V1-receptors (with d(CH2)5DAVP) enhanced the depressor effects of captopril in guanethidine-treated animals, but blood pressure was unaffected by this manoeuvre in control animals. Although there is evidence that sympathetic efferent vasomotor function is abolished following the schedule of neonatal guanethidine treatment used, pentolinium had a hypotensive effect in the presence of d(CH2)5DAVP and captopril, indicating that the adrenal medulla could have been contributing to the maintenance of blood pressure. This is consistent with the finding of marked supersensitivity to exogenous adrenaline in guanethidine-treated rats.

Animals↗
PubMed1985

Interactions between neural mechanisms, the renin-angiotensin system and vasopressin in the maintenance of blood pressure during water deprivation: studies in Long Evans and Brattleboro rats.

1. Plasma volumes and cardiovascular status were assessed in rats with a congenital deficiency in hypothalamic vasopressin (Brattleboro strain) and in the parent strain (Long Evans), in water-replete and water-deprived states. 2. Water-replete Brattleboro rats were not hypovolaemic; water deprivation (14 h in Brattleboro rats, 53 h in Long Evans rats) produced similar percentage reductions in plasma volumes in the two groups. 3. In the water-replete state, cardiovascular variables were similar in Long Evans and Brattleboro rats. Inhibition of ganglionic transmission (with pentolinium) or of the renin-angiotensin system (with captopril), separately, did not have a greater effect on blood pressure in Brattleboro rats than in Long Evans rats. Recovery from hypotension caused by pentolinium was characterized by large swings in blood pressure in both groups of rats. These pressor episodes were abolished by administration of captopril to Brattleboro rats. After administration of pentolinium and captopril to Long Evans rats there was a substantial, although intermittent, recovery in blood pressure that was abolished by an antagonist of the cardiovascular actions of vasopressin. 4. In the water-deprived state, blood pressures were similar in Long Evans and Brattleboro rats; both groups showed an elevation in diastolic blood pressure relative to the water-replete state. After administration of pentolinium, there was a more marked recovery in blood pressure than was seen in the water-replete state. Administration of captopril alone had a slightly greater effect on blood pressure in Long Evans rats in the water-deprived, compared with the water-replete, state. However, in the former condition, Brattleboro rats showed a profound and progressive hypotension in response to captopril, indicating an indispensable role for the renin-angiotensin system in the maintenance of blood pressure in these animals during water deprivation. 5. Only when the renin-angiotensin system and neural activity were inhibited did vasopressin express its full, independent, pressor potential in Long Evans rats. However, evidence was obtained that vasopressin may exert important effects on cardiovascular regulation via neural mechanisms and through interactions with the renin-angiotensin system.

Animals↗
PubMed1985

The effect of adrenaline upon cardiovascular and metabolic functions in man.

On three separate occasions, at least 1 week apart, seven young healthy male subjects received intravenous infusions of either adrenaline, 50 ng min-1 kg-1 (high A), adrenaline, 10 ng min-1 kg-1 (low A) or sodium chloride solution (saline: 154 mmol of NaCl/l) plus ascorbic acid, 1 mg/ml (control), over 30 min. Venous adrenaline concentrations of 2.19 +/- 0.15 nmol/l, 0.73 +/- 0.08 nmol/l and 0.15 +/- 0.03 nmol/l were achieved during the high A, low A and control infusions respectively. Heart rate rose significantly by 19 +/- 3 beats/min (high A) and by 6 +/- 1 beats/min (low A). Heart rate remained significantly elevated 30 min after cessation of the high A infusion, despite venous plasma adrenaline concentration having fallen to control levels. The diastolic blood pressure fell during the high A and low A infusions, but the systolic blood pressure rose only during the high A infusion. Vasodilatation occurred in the calf vascular bed during both high A and low A infusions. The changes in hand blood flow and hand vascular resistance were not statistically significant, although there was a tendency to vasoconstriction during the infusion of adrenaline. Metabolic rate rose significantly by 23.5 +/- 1.8% (high A) and by 11.8 +/- 1.6% (low A). Metabolic rate remained elevated between 15 and 30 min after termination of the high A infusion. There was an initial transient increase in respiratory exchange ratio (RER) during the adrenaline infusions. During the later stages of the adrenaline infusions and after their cessation, RER fell, probably reflecting increased fat oxidation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

The effect of undernutrition on thermoregulation in the elderly.

With use of a liquid-conditioned coverall, the thermoregulatory responses to a lowering of environmental temperature from 35 degrees C to 23 degrees C were assessed in eight normally nourished and six undernourished elderly female patients, during their convalescence after surgical repair of a fracture of the femoral neck. There was no difference in the peripheral vasoconstriction of the two groups in response to a cold environment. On lowering the environmental temperature, the increase in metabolic rate was significantly impaired in the undernourished group compared with the normally nourished group (P less than 0.05). There was a small decrease in core temperature in the undernourished group (median change -0.1 degree C) during the period of exposure to the lowest environmental temperature (23 degrees C). This was significantly different from the lack of change (median change 0 degrees C) in core temperature observed in the normally nourished group (P less than 0.05). This defect of thermogenesis may underlie the propensity of undernourished elderly patients to suffer hypothermia and fracture of the femoral neck in the winter months.

Aged↗
PubMed1985

Redevelopment of elevated blood pressure following adrenalectomy in rats with isolation-induced hypertension.

We have previously shown that rats housed in individual metabolism cages develop arterial hypertension and that this can be prevented by adrenalectomy. In the present work the influence of adrenalectomy on blood pressure, heart rate and on fluid and electrolyte balance was investigated in rats with established isolation-induced hypertension. Seven days after adrenalectomy, systolic blood pressure was reduced to levels similar to those seen before the induction of hypertension; the fall in blood pressure was accompanied by tachycardia. It is likely that the reduction in blood pressure was partly due to volume depletion, since adrenalectomized rats showed reductions in fluid, sodium and potassium balance during the first week after operation. Over the following 3 weeks, blood pressure and heart rate returned to pre-operative hypertensive levels, associated with increasingly positive balances for fluid and sodium. Maintenance of elevated blood pressure in isolated rats following adrenalectomy is likely to have been aided by activation of the renin-angiotensin system, since infusion of saralasin caused profound hypotension in these circumstances, whereas it had a slight pressor effect in intact rats with isolation-induced hypertension.

Adrenalectomy↗
PubMed1985

Pressor sensitivity to exogenous vasopressin in conscious, adult rats treated neonatally with capsaicin.

Pressor responses to exogenous arginine vasopressin were assessed in adult rats that had been treated neonatally with capsaicin or its vehicle. Measurements were made under control conditions, after inhibition of baroreflexes (with pentolinium), and after inhibition of baroreflexes (with pentolinium) and the production of angiotensin II (with captopril). Resting arterial blood pressures and pressor sensitivities to exogenous arginine vasopressin were similar in capsaicin-treated and vehicle-injected rats. Sixty minutes after the administration of pentolinium, systolic and diastolic blood pressures were reduced in both groups of rats and the pressor responses to arginine vasopressin were similarly and significantly enhanced. In both groups of rats 60 min after administration of pentolinium and captopril, systolic and diastolic blood pressures were lower than in the presence of pentolinium alone, but pressor responses were not different from those seen in control conditions. The possibility that the present results are explicable in terms of baroreflexes, the renin-angiotensin system and endogenous vasopressin interacting to influence the pressor sensitivity to exogenous vasopressin is discussed. From the present findings, it seems that our previous observation of impaired, vasopressin-mediated blood pressure recovery following acute hypotension in capsaicin-treated rats cannot be attributed to a reduced pressor sensitivity to the hormone.

Animals↗
PubMed1985

The influence of neonatal treatment with capsaicin on the control of blood pressure in adult rats in water-replete and water-deprived states.

Arterial blood pressures and heart rates were measured in water-replete and in water-deprived (48 h) conscious, adult rats that had received capsaicin (50 mg kg-1) or its vehicle neonatally. Resting arterial blood pressures and heart rates in capsaicin-treated rats were not different from the controls in either the water-replete or the water-deprived state. Inhibition of the vascular actions of vasopressin (with 1-beta-mercapto,-beta, beta-cyclopentamethylenepropionic acid, 8-D-arginine vasopressin, (d(CH2)5DAVP] had no significant effect on blood pressures in the water-replete animals but caused a significant hypotension in water-deprived rats; the magnitude of the hypotension was the same irrespective of whether the animals had received capsaicin or its vehicle. During angiotensin converting enzyme inhibition (with captopril) and ganglion blockade (with pentolinium), the vasopressin-mediated blood pressure recovery was more gradual in the capsaicin-treated animals than in the controls, but after 60 min blood pressures were similar in all groups. Collectively the results indicate that although the full development of vasopressin-dependent mechanisms following acute hypotension takes longer when a large proportion of unmyelinated afferent fibres have been destroyed by neonatal treatment with capsaicin, 48 h of water deprivation results in a normal involvement of vasopressin-dependent mechanisms in the maintenance of blood pressure.

Animals↗
PubMed1985

Functional involvement of vasopressin in the maintenance of systemic arterial blood pressures after phenoxybenzamine or phentolamine administration: studies in Long-Evans and Brattleboro rats.

The alpha adrenoceptor antagonists phenoxybenzamine and phentolamine are reported to have opposite effects on vasopressin release, the former inhibiting and the latter enhancing it. In this study we have assessed the functional involvement of vasopressin in the maintenance of blood pressure in conscious rats after administration of either phenoxybenzamine or phentolamine. In normal (Long-Evans) rats, phenoxybenzamine caused a small fall in arterial blood pressure, whereas phentolamine initially caused a profound hypotension which was followed by a fluctuating recovery back to normotensive levels. Similar effects were seen in rats deficient in hypothalamic vasopressin (Brattleboro strain). Administration of an antagonist of the cardiovascular actions of vasopressin [1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid)-8-D-arginine vasopressin] in the presence of either alpha adrenoceptor antagonist alone was without effect in Long-Evans or Brattleboro rats, but, under these conditions, subsequent administration of captopril caused a profound and sustained hypotension in both strains. Administration of captopril in the presence of either alpha adrenoceptor antagonist alone caused a prompt fall in blood pressure which was sustained for the duration of the experiment in the Brattleboro rats. However, under these conditions, the blood pressure of the Long-Evans rats showed some recovery over the subsequent 45 min; this recovery was antagonized by [1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid)-8-D-argine vasopressin]. It is concluded that after alpha adrenoceptor antagonism with either phenoxybenzamine or phentolamine, the renin-angiotensin system exerts a major pressor influence. However, after captopril administration in the presence of phenoxybenzamine or phentolamine, vasopressin contributes to the maintenance of arterial blood pressure in Long-Evans rats; the magnitude of this contribution is similar irrespective of the alpha adrenoceptor antagonist used.

Adrenergic alpha-Agonists↗
PubMed1984

The antihypertensive effect of dietary potassium chloride loading in rats with adrenal regeneration hypertension.

Adrenal regeneration hypertension was induced in male Wistar rats by unilateral adrenal enucleation, contralateral adrenalectomy and the provision of a 1% (w/v) NaCl solution for drinking. A fivefold increase in dietary KCl content caused a significant reduction in the systolic blood pressure of hypertensive rats but not of control rats. During the increase in potassium intake there was a marked polydipsia. When 1% NaCl solution was the drinking fluid, the resultant increase in sodium intake was associated with an abolition of the antihypertensive effect of potassium loading, but when the sodium intake was held constant, the antihypertensive effect was maintained. In rats with adrenal regeneration hypertension, plasma volume was significantly higher, and packed cell volume and plasma protein concentrations were significantly lower than in control rats. These differences were abolished after 4 days of dietary KCl supplementation. Increased dietary potassium intake was associated with significantly lower serum aldosterone concentrations and significantly higher plasma potassium concentrations in adrenal enucleated rats compared with controls. The possibility that a reduction in extracellular fluid volume (due to a natriuresis) and/or a peripheral vasodilatation contributed to the antihypertensive effect of KCl loading is discussed.

Adrenal Glands↗
PubMed1984

The influence of acute starvation on the cardiovascular responses to lower body subatmospheric pressure or to standing in man.

The cardiovascular responses to lower body subatmospheric pressure or to standing were measured in the same nine normal male subjects after a 12 h and after a 48 h fast. After the 48 h fast there was a significant reduction in diastolic blood pressure and forearm vascular resistance (relative to the values after a 12 h fast) when subjects were supine. During exposure to lower body subatmospheric pressure, subjects who had fasted for 48 h showed an inability to maintain systolic blood pressure, accompanied by an impairment of forearm vasoconstriction and an exaggerated tachycardia (relative to their responses after a 12 h fast). Similar disorders of cardiovascular homoeostasis were seen on standing. The results are consistent with an inhibition of sympathetic nervous activity after a 48 h fast, but other possibilities are discussed.

Adult↗
PubMed1984

The influence of environmental temperature upon the thermoregulatory responses to ethanol in man.

Ten healthy male subjects ingested ethanol (BP; 0.5 g/kg body weight) after an overnight fast, on two separate occasions, at environmental temperatures of either 21 degrees C or 30 degrees C. The mean maximal fall in deep body temperature was not significantly different on the two occasions, being 0.18 degrees C and 0.17 degrees C respectively. Metabolic rates throughout the experiments at the two temperatures were not significantly different. The vasodilatation of the hand and forearm vascular beds after ethanol ingestion was markedly reduced at the lower environmental temperature. In three subjects who ingested a higher dose of ethanol (BP; 1.0 g/kg body weight) after an overnight fast, at an environmental temperature of 21 degrees C, the mean maximum fall in core temperature was 0.15 degrees C, which was not significantly different from the change seen after consumption of the lower dose of ethanol. It is likely that the failure of ethanol ingestion to provoke hypothermia at the lower environmental temperature was due to the attenuated vasodilatation observed under these conditions.

Adult↗