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Biomedical subjects

T Bennett

Publications and source records attributed to T Bennett.

At least 307 records · Page 17Linked to original sources
PubMed1984

Post-exercise reduction of blood pressure in hypertensive men is not due to acute impairment of baroreflex function.

Two experiments were carried out in male subjects. In the first experiment heart rate and blood pressures were measured before, during and for 90 min after a 50 min period of intermittent exercise in seven hypertensive subjects. After exercise there was a marked reduction in systolic and diastolic blood pressures; this effect lasted throughout the 90 min observation period and was unaccompanied by tachycardia. In the second experiment heart rate and blood pressures were measured before and during the rest periods in a 50 min session of intermittent exercise in nine hypertensive and nine normotensive subjects. Following the first 10 min bout of exercise, resting blood pressures were significantly reduced in the hypertensive subjects; the reduction in blood pressure progressively increased following successive exercise periods. The normotensive subjects did not show a significant reduction in resting blood pressures until the fifth bout of exercise had been completed. In the second experiment also, the competence of baroreflexes was assessed by measuring cardiovascular responses to lower body subatmospheric pressure ( LBSP ) 30 min before and 30 and 60 min after exercise. The post-exercise reduction in blood pressure was not due to exercise-induced impairment of baroreflex mechanisms since the reduced blood pressure after exercise was well maintained during lower body subatmospheric pressure. Furthermore, after exercise, exposure to lower body subatmospheric pressure elicited greater increases in heart rate and forearm vascular resistance than were seen before exercise.

Adult↗
PubMed1984

The effect of a 48 h fast on the thermoregulatory responses to graded cooling in man.

The thermoregulatory responses to graded cooling were measured in 11 healthy male subjects after a 12 h fast and after a 48 h fast. The cooling stimulus was produced by changing the temperature of the skin of the trunk and legs with a water-perfused suit. Five levels of skin temperature from 35.5 to 24 degrees C were applied on each occasion. After a 12 h fast, core temperature was maintained during cooling. This maintenance of core temperature was associated with an increase in metabolic rate and a reduction in blood flow to the hand and to the forearm. After 48 h of fasting, the subjects could not maintain core temperature during cooling, and a decrease of 0.36 +/- 0.05 degrees C occurred as the suit temperature was reduced from 35.9 to 24 degrees C. Metabolic rate was slightly higher after the 48 h fast than after the 12 h fast, but similar increases in metabolic rate were observed during cooling. Vasoconstriction in the hand was initially less after a 48 h fast than after a 12 h fast, but at the lowest suit temperature, hand blood flow was similar, and low, on both occasions. After 48 h of fasting, forearm blood flow was elevated at all suit temperatures, being approximately twice the level recorded after the 12 h fast. Venous plasma noradrenaline levels did not change during cooling after the 12 h fast, whilst after 48 h of fasting a significant increase in noradrenaline level was observed at the lowest suit temperature. The results of this study provide further evidence that fasting induces an impairment of autonomic reflex mechanisms, but it is not clear whether this is due to a suppression of sympathetic nervous activity.

Adult↗
PubMed1984

The effects of acute or chronic ingestion of propranolol or metoprolol on the physiological responses to prolonged, submaximal exercise in hypertensive men.

We have studied the physiological responses to 50 min of intermittent, moderate exercise in hypertensive men after the ingestion of a single dose of placebo, propranolol or metoprolol, and also after 28 days treatment. In addition, subjective assessments of mood were made during the last 7 days of each period of chronic treatment. Heart rate and blood pressure, both at rest and during exercise, were significantly reduced by a single dose of propranolol or metoprolol; more marked effects were observed after chronic treatment. Ventilation and gas exchange during exercise were only slightly disturbed by single doses of propranolol or metoprolol, whereas chronic treatment had no effect. Perceived exertion scores were increased after a single dose of either drug, compared to placebo, and the effect of propranolol was greater than that of metoprolol. With chronic treatment there were fewer differences between the perceived exertion scores during exercise, although 'leg' fatigue remained greater after propranolol than after placebo. Sweating from the forehead during exercise was enhanced by a single dose of either beta-adrenoceptor antagonist, with propranolol having the greater effect. After chronic treatment the effect of propranolol was diminished, whereas the effect of metoprolol was maintained. Very few disturbances of mood were found after chronic ingestion of the beta-adrenoceptor antagonists.

Adult↗
PubMed1984

The effects of acute or chronic ingestion of propranolol or metoprolol on the metabolic and hormonal responses to prolonged, submaximal exercise in hypertensive men.

We have studied the effects of single oral doses of, and of 28 days treatment with, placebo, propranolol or metoprolol, on the metabolic and hormonal responses to prolonged exercise in hypertensive men. Blood glucose levels fell during exercise on all occasions. No additional effects of the beta-adrenoceptor antagonists, compared to placebo, were observed. The exercise-induced increase in plasma potassium was enhanced after a single dose of propranolol or metoprolol, and also after chronic treatment with propranolol. Chronic treatment with either drug led to an increase in plasma potassium levels at rest. The growth hormone response to exercise was potentiated by a single dose of metoprolol or propranolol, and after chronic treatment with the drugs. A single dose of propranolol (but not metoprolol) was associated with a marked increase in plasma cortisol and adrenaline levels during exercise. After chronic treatment no such increase occurred. In both the acute and chronic phases of the study, blood lactate levels were higher during exercise in the presence of either propranolol or metoprolol compared to placebo, whereas non-esterified fatty acid levels were lower. A single dose of metoprolol produced a significantly greater reduction in blood glycerol levels during exercise than a single dose of propranolol. After chronic treatment, both propranolol and metoprolol produced similar reductions in blood glycerol levels during exercise. After a single dose, both drugs significantly augmented the increase in plasma noradrenaline levels during exercise. A similar effect was seen after chronic treatment.

Blood Glucose↗
PubMed1984

Neonatal capsaicin treatment impairs vasopressin-mediated blood pressure recovery following acute hypotension.

Rats were treated with a single injection of either capsaicin (50 mg kg-1 s.c.) or vehicle on day 2 after birth. When the animals were adult, they were challenged with osmotic (water deprivation) and haemodynamic (acute hypotension) stimuli that normally evoke vasopressin release. Capsaicin-treated and vehicle-injected rats showed similar body weight losses and plasma osmolalities following 48 h of water deprivation. Thus it appears that neonatal treatment with capsaicin does not impair the antidiuretic response to plasma hyperosmolality. Following acute ganglion blockade in the presence of angiotensin converting enzyme inhibition, there was some recovery of blood pressure in the vehicle-injected rats, but recovery was significantly (P less than 0.001) less in the capsaicin-treated animals. The recovery may be attributed to vasopressin since it was abolished by an antagonist selective for the pressor action of the peptide (d(CH2)5DAVP). These results suggest that neonatal treatment with capsaicin impairs vasopressin-mediated recovery of blood pressure following acute hypotension. The possible involvement of baro- or chemoreceptor afferents is discussed.

Acute Disease↗
PubMed1983

Post-adrenalectomy hypotension in rats; absence of baroreflex resetting or effect of naloxone.

1. Male Wistar rats were either bilaterally adrenalectomized or sham-operated, and given 1% sodium chloride solution instead of tap water to drink. Seven days later, arterial blood pressures were recorded directly from conscious freely moving rats. 2. Systolic and diastolic blood pressures were significantly lower in the adrenalectomized rats, whereas heart rates were significantly higher than in sham-operated animals. The tachycardia was due to a combination of sympathetic hyperactivity and reduced vagal tone, which may have been reflex responses to a reduction in effective blood volume. 3. Baroreflex control of the sinus node was assessed from the pulse interval responses to rises (induced by methoxamine) or falls (induced by glyceryl trinitrate or sodium nitroprusside) in systemic arterial blood pressure. The relation between pulse interval and systolic blood pressure was described by the same curve in sham-operated and adrenalectomized rats, indicating that, in the latter, there was no change in baroreflex setting or sensitivity. 4. Intravenous administration of naloxone (2 mg/kg) had no effect on systemic arterial blood pressure in adrenalectomized rats, suggesting that endogenous opiates were not contributing to the hypotension.

Adrenalectomy↗
PubMed1983

The cardiovascular and renal responses to short-term isolation in Brattleboro rats.

1. The effects of isolation on systolic blood pressure, heart rate and fluid and electrolyte balances were studied in rats with a congenital inability to synthesize vasopressin (Brattleboro strain) and in the normal parent strain (Long Evans). 2. There was no significant difference between the systolic blood pressures of Brattleboro rats and Long Evans rats while the animals were housed in groups, although the heart rates of the Brattleboro rats were significantly higher. 3. After 5 days of isolation in metabolism cages, systolic blood pressure was significantly increased in the Long Evans rats, but not in the Brattleboro rats. 4. Since there were no significant differences between the fluid and electrolyte balances of the two groups after 5 days of isolation, it is unlikely that the hypertension in the Long Evans rats was attributable to a renal action of vasopressin. 5. It is possible that vasopressin was involved in the development of isolation-induced hypertension by virtue of its pressor effects. Alternatively, the failure of Brattleboro rats to develop hypertension may have been due to some abnormality in these animals other than the lack of vasopressin.

Animals↗
PubMed1983

Effects of haemorrhage in rats lacking vasopressin (Brattleboro strain): influence of naloxone.

1. The effects of naloxone on blood pressure recovery after either rapid arterial haemorrhage or prolonged venous haemorrhage were studied in rats lacking vasopressin (Brattleboro strain) and in control (Long Evans) rats. 2. To produce similar reductions in blood pressure, less blood had to be taken from the Brattleboro rats than from the Long Evans rats. 3. After rapid arterial haemorrhage in the absence of naloxone, blood pressure recovery was slower in Brattleboro rats than in Long Evans rats. Naloxone did not affect the response to rapid arterial haemorrhage in Long Evans rats, but improved blood pressure recovery in Brattleboro rats; despite this improvement, the Brattleboro rats remained hypotensive at a time when the Long Evans rats were normotensive. These findings suggest that both the absence of vasopressin and a depressor action of beta-endorphins may contribute to the poor ability of Brattleboro rats to cope with rapid haemorrhage. 4. After prolonged venous haemorrhage in the absence of naloxone, there was no difference between the recovery of blood pressure in Brattleboro rats and Long Evans rats. Naloxone improved blood pressure recovery to a similar extent in both strains of rat. These findings suggest that the absence of vasopressin does not impair blood pressure recovery after prolonged haemorrhage.

Animals↗
PubMed1983

The physiological effects of insulin-induced hypoglycaemia in man: responses at differing levels of blood glucose.

The aim of this study was to describe hormonal, cardiovascular and thermoregulatory responses to insulin-induced hypoglycaemia of differing levels of severity. Five normal male volunteers were rendered hypoglycaemic at intervals of 1 week by intravenous infusions of 3, 4 or 6 units of insulin/h, or by intravenous injection of 0.15 unit/kg body weight. Plasma glucose reached nadir values of 2.08 +/- 0.10, 1.82 +/- 0.21, 1.24 +/- 0.08 and 0.92 +/- 0.06 mmol/l (means +/- SEM) in the four experiments. Non-esterified fatty acid levels fell equally in all experiments but recovery was more rapid with severe hypoglycaemia. In contrast the rate of recovery of plasma glucose was slower with deeper hypoglycaemia and this appeared unrelated to the counter-regulatory response. Plasma glucagon, adrenaline and prolactin levels increased in proportion to the severity of hypoglycaemia, but peak concentrations of cortisol, growth hormone (somatotropin) and noradrenaline did not vary, suggesting that moderate hypoglycaemia had elicited maximal responses. When the areas under the curves were calculated, the cortisol responses were greater for the 6 units infusion and bolus injection than for the other infusions, and the growth hormone responses were similar for all three infusions but significantly greater with the bolus injection. Increases in heart rate and systolic blood pressure were related to the severity of hypoglycaemia, but changes in diastolic blood pressure and peripheral vascular resistance (assessed from calf and from hand blood flow) were not. Central temperature fell by 0.13 +/- 0.06 degrees C, 0.30 +/- 0.10 degrees C, 0.65 +/- 0.14 degrees C and 1.15 +/- 0.30 degrees C (means +/- SEM) in the four experiments, and the fall in skin temperature had a similar gradation. Many physiological responses to hypoglycaemia are not 'all-or-none', but vary according to the intensity of stimulus; some are already maximal at mild degrees of hypoglycaemia. Other changes are more complex, reflecting an interplay between opposing endocrine and neural responses.

Adult↗
PubMed1983

The influence of neonatal treatment with guanethidine on the development of isolation-induced hypertension in adult rats.

Rats housed individually in glass metabolism cages develop hypertension. Since previous experiments have provided some evidence for the involvement of the sympathetic nervous system in the maintenance of the hypertension, the present work was designed to explore the possible involvement of the sympathetic nervous system in the genesis of isolation-induced hypertension. Male and female Wistar rats were treated neonatally with guanethidine, with a protocol designed to produce an extensive peripheral sympathectomy; control rats received saline. The effects of isolation on systolic blood pressure and fluid and electrolyte balances were studied when the rats were mature. Guanethidine-treated rats did not develop hypertension in response to isolation whereas control rats did. There were no significant differences between the fluid and electrolyte balances of the guanethidine-treated rats compared with controls throughout the period of isolation. It is concluded that a fully functional sympathetic nervous system is required for the development of isolation-induced hypertension, but its involvement is not through a modulation of renal function.

Animals↗
PubMed1983

The effects of captopril on blood pressure, urinary water and electrolyte excretion and drinking behaviour in Brattleboro rats.

The effects of the orally active converting enzyme inhibitor, captopril (SQ 14225), on blood pressures and intakes and urine outputs of water and electrolytes were studied in rats with hereditary hypothalamic diabetes insipidus (Brattleboro strain) and in Long Evans rats (parent strain). Captopril given in the drinking water (30 mg day-1 kg-1) caused an increase in fluid intake and urine output in both strains of rat; the difference between intake and measured output did not change. Captopril caused a significant natriuresis when given to animals in the non-steady state but did not significantly affect the urinary electrolyte excretion of animals in a steady state; in the latter group, however, captopril caused a significant reduction in food intake. Hence, under both conditions, captopril caused a reduction in sodium balance. Systolic blood pressures were reduced by captopril (given in the drinking water) in Long Evans rats and in Brattleboro rats; there was no accompanying change in heart rate. Bolus administration of captopril (30 mg day-1 kg-1) either intragastrically or subcutaneously did not change the fluid intakes or outputs in either strain of rat. In a separate experiment, rats were given the choice to drink water or a captopril solution. The results showed that the increased fluid intake in response to captopril was not due to a liking for the taste of the solution. The dipsogenic response to captopril may have been due to the fall in blood pressure which occurred, leading to renin release and a peripheral build-up of angiotensin I, which was converted into angiotensin II in the central nervous system. The possibility that the same dose given as a bolus may have inhibited central, as well as peripheral, converting enzyme activity is discussed.

Animals↗
PubMed1982

Is exercise good for high blood pressure?

Ten men with uncomplicated essential hypertension (mean standing blood pressure 165/109 mm Hg) and 10 normal controls matched for age and weight were studied for the hypotensive potential of moderate exercise. Tests were conducted on a treadmill set to induce a steady heart rate of 120 beats/min and performed over five 10-minute periods separated by three minutes' rest and finishing with 30 minutes' sitting quietly in a chair.During exercise the mean systolic pressures were identical in the hypertensive patients and controls (175+/-SEM 5 mm Hg), the controls therefore sustaining an appreciably greater increase in pressure. During the 30-minute rest period after the tests both the control and hypertensive groups showed a significant and sustained fall in absolute systolic pressures as compared with pre-exercise values (p <0.001), the mean percentage reductions being 22% and 25% respectively.If a fall in blood pressure after exercise is maintained for four to 10 hours, then a "good walk" twice a day might be reasonable treatment for mild hypertension. Studies are continuing to determine the amount of exercise needed and the duration for which the reduction in blood pressure is maintained.

Adult↗
PubMed1982

Cardiovascular responses to lateral semicircular canal stimulation in man.

The cardiovascular effects of aural irrigation with water at 37 degrees C (control subjects, n = 6) or 44 degrees C (experimental subjects n = 11) were assessed from measurements of heart rate, brachial arterial blood pressure and forearm blood flow. The occurrence and intensity of vestibular stimulation was assessed from the electronystagmogram. The procedure had no significant effect on cardiovascular variables in control subjects or in subjects who were exposed to vestibular stimulation but who were not nauseated by it (n = 6). Those subjects who felt nauseous (n = 5) showed a tachycardia and forearm vasodilatation. These results provide no evidence that vestibular stimulation contributes to orthostatic reflexes in man.

Adolescent↗
PubMed1982

The effects of noradrenergic denervation on muscarinic receptors of smooth muscle.

1 Changes in the response to acetylcholine of expansor secundariorum muscles from chicks have been analyzed by pharmacological techniques and by [3-3H)-quinuclidinyl benzilate ([3-3H]-QNB) binding to quantify the muscarinic receptor population. 2 The expansor secundariorum muscle responded to acetylcholine up to the age of 30 days; the response declined thereafter. This developmental decrease in response to acetylcholine was prevented by surgical denervation. 3 In chicks aged less than 25 days, denervation did not affect the sensitivity of the expansor muscle to acetylcholine. In order chicks (above 40 days) denervation gradually restored the sensitivity of the expansor muscle to acetylcholine. Responses of the expansor muscle were always abolished by atropine (1 microM) indicating they were mediated by muscarinic receptors. 4 Binding studies with [3-3H]-QNB showed that changes in response of expansor muscle to acetylcholine were primarily due to changes in the muscarinic receptor population. 5 It is suggested that the noradrenergic innervation of the expansor muscle influences the number of muscarinic receptors expressed in the tissue.

Acetylcholine↗