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Biomedical subjects

T Bennett

Publications and source records attributed to T Bennett.

At least 271 records · Page 15Linked to original sources
PubMed1987

Diabetes mellitus and thermoregulation.

Diabetes mellitus is accompanied by a variety of alterations in metabolic, cardiovascular, and neuronal function. This paper provides a comprehensive review of the ways in which these pathophysiological aspects of diabetes may impair thermoregulatory function. The influence of diabetic neuropathy and vasculopathy on the control of peripheral blood flow is reviewed and the additional effects of changing levels of blood glucose and insulin are discussed. Both hypoglycaemia and diabetic ketoacidosis are associated with hypothermia, but the reasons for this in ketoacidosis are not clear. Impairment of heat conservation may contribute to and could be a consequence of autonomic neuropathy. The final section of the paper describes a study of our own in which metabolic stability was maintained by infusing insulin intravenously before and during the determination of the thermoregulatory responses to acute cold stress. Under these conditions, there was impairment of reflex vasoconstriction in the limbs of diabetics with neuropathy. This failure to reduce heat loss resulted in half the diabetics with neuropathy shivering in response to moderate cooling, which in some subjects was accompanied by a fall in core temperature. Diabetics without neuropathy and nondiabetics neither shivered nor dropped core temperature.

Blood Glucose↗
PubMed1987

Abnormal blood pressure recovery during ganglion blockade in diabetic rats.

The aim of the present study was to determine the extent to which vasopressin or the renin-angiotensin system contributed to the recovery of blood pressure following acute hypotension induced by treatment with pentolinium and captopril, or pentolinium and the vasopressin antagonist d(CH2)5DAVP, respectively, in conscious, free-moving rats treated 21 days previously with saline or streptozotocin (STZ) (60 mg/kg ip). Half the animals given STZ were subsequently treated with insulin (about 4.5 U/day). The STZ-treated animals demonstrated a resting bradycardia and systolic hypotension. The vasopressin-mediated recovery in blood pressure seen following administration of pentolinium, in the presence of captopril, and the renin-angiotensin-mediated recovery seen following administration of pentolinium, in the presence of d(CH2)5DAVP, were both found to be significantly (P less than 0.05) attenuated in the STZ-treated animals. These abnormalities were absent in the animals injected with STZ and treated daily with insulin, but receiving their last dose 24 h before measurement. At that time the animals had elevated blood glucoses. These results indicate that the abnormalities observed were not due to toxic effects of STZ or to hyperglycemia per se.

Animals↗
PubMed1987

Rats with regenerating adrenals are more hypertensive in the morning than afternoon.

In rats following unilateral nephroadrenalectomy and contralateral adrenal enucleation, adrenocortical tissue regenerates and secretes some steroids in abnormal amounts but with a diurnal rhythmicity. This study investigated whether the level of blood pressure (BP) in these rats also varies with the time of day. Systolic BP was measured by the tail-cuff method twice daily [between 0700 and 1000 h (A.M.) and again between 1400 and 1700 h (P.M.)] in conscious Wistar rats before and after unilateral nephroadrenalectomy and either contralateral adrenal-enucleation (AE) or sham-operation (SO); all rats were given 1% NaCl to drink postoperatively. During the 4th wk after surgery, systolic BP in AE rats was higher than in SO rats at both times of day, but the difference was greater A.M. (SO = 142 +/- 2 mmHg, AE = 176 +/- 4 mmHg) than P.M. (SO = 138 +/- 2 mmHg, AE = 150 +/- 2 mmHg). The hypertension and the A.M.-P.M. changes in BP in AE rats were also seen with intra-arterial recording. These phenomena were not directly associated with changes in plasma volume, plasma Na+ concentration, or in the plasma levels of corticosterone or 18-hydroxydeoxycorticosterone.

18-Hydroxydesoxycorticosterone↗
PubMed1987

Pressor sensitivities to vasopressin, angiotensin II, or methoxamine in diabetic rats.

We investigated the pressor sensitivities to vasopressin, angiotensin II, and methoxamine of intact and ganglion-blocked rats that had been treated 21 days earlier with streptozotocin or saline. No differences in blood pressure or heart rate responses to vasopressin or angiotensin II were found between the intact groups when these peptides were administered intravenously in equimolar doses. After ganglion blockade a significant enhancement in pressor responsiveness to both vasopressin and angiotensin II was observed in the control groups, but in the streptozotocin-treated animals no enhancement in pressor sensitivity to vasopressin was found. Furthermore, although a significant augmentation of the responses to angiotensin II was observed, it was smaller than that seen in the ganglion-blocked control group. Neither group showed enhanced pressor responsiveness to methoxamine. These results indicate that the previously observed diminished contributions from endogenous vasopressin and the renin-angiotensin system to blood pressure recovery following ganglion blockade in streptozotocin-treated rats may have been due, at least in part, to diminished pressor responsiveness.

Angiotensin II↗
PubMed1987

Exogenous corticosterone acetate attenuates the hypotension induced by ganglion blockade in conscious Long Evans and Brattleboro rats.

The effects of acute administration of corticosterone acetate (7.5 mg/kg bolus; 5 mg.kg-1h-1 infusion) on plasma corticosterone levels and blood pressure (BP) responses to hypotension induced by ganglion blockade (with pentolinium) were studied in conscious Long Evans and Brattleboro (vasopressin-deficient) rats. Steroid infusion raised plasma corticosterone levels similarly in both strains of rat, but there was no effect on resting BP. However, the fall in BP after pentolinium administration was less in the steroid-treated groups of both strains than in their vehicle-injected counterparts. During infusion of pentolinium the ensuing recovery in BP was abolished by captopril administration. Steroid treatment did not affect this recovery but did attenuate the hypotensive effects of captopril. In Long Evans rats, only, there was a further vasopressin-mediated, recovery in BP during the infusion of pentolinium and captopril. This recovery was not accentuated by the presence of the steroid. In a further experiment, infusion of corticosterone acetate after the onset of hypotension (induced by pentolinium, captopril and d(CH2)5DAVP in Long Evans rats or by pentolinium and captopril in Brattleboro rats) caused a progressive increase in BP in both strains. These findings demonstrate a pressor action of corticosterone acetate which is apparent after hypotension induced by ganglionic blockade and which does not necessarily involve any interaction with the renin-angiotensin system or vasopressin.

Animals↗
PubMed1987

Effects of noradrenergic denervation on alpha-1 adrenoceptors and receptor-stimulated contraction of chick expansor secundariorum muscle.

Alpha-1 adrenoceptors were identified in the chick expansor secundariorum (ESM) smooth muscle by ligand binding (using [3H]prazosin) and organ bath techniques. We examined the effects of both reversible (6-hydroxydopamine-induced) and irreversible (surgical) noradrenergic denervation on alpha-1 adrenoceptors in the ESM. We also measured, in vitro, muscle contraction stimulated by the alpha-1 adrenoceptor agonist methoxamine and by 5-hydroxytryptamine. After both surgical and chemical denervation there were decreases in the number of [3H] prazosin binding sites in the ESM. After reversible denervation the decrease in receptor number persisted during a period in which there was extensive reinnervation of the muscle. At a time (7 days after injection) when the ESM was partially reinnervated the maximum methoxamine-stimulated response, but not that of 5-hydroxytryptamine, was reduced. After surgical (but not chemical) denervation there were increases in both protein content and wet weight of the muscle. However, at 7 days after denervation, these effects alone could not account for the observed decrease in receptor number. A small increase in sensitivity (1.4-fold) to methoxamine and a much larger increase in sensitivity (4.5-fold) to 5-hydroxytryptamine developed after surgical denervation but there appeared to be nonspecific decreases in maximum responses to the agonists. It is concluded that both surgical and chemical denervation produced a decrease in alpha-1 adrenoceptor number in the ESM; this may have contributed to the decrease in maximum contractile response. After surgical denervation a nonspecific supersensitivity developed in the ESM; it may be that a nonspecific contribution to methoxamine-stimulated responses was less apparent due to the loss of alpha-1 adrenoceptors.

Animals↗
PubMed1986

Neonatal treatment with capsaicin influences hormonal regulation of blood pressure in adult, water-deprived Long-Evans but not Brattleboro rats.

Conscious, adult, water-deprived Brattleboro rats treated neonatally with capsaicin or vehicle showed similar hypotensive responses to sequential inhibition of the renin-angiotensin system (with captopril) and antagonism of ganglionic transmission (with pentolinium). Following a comparable experimental protocol, Long-Evans rats treated neonatally with capsaicin showed a more marked hypotensive response to captopril administration than did vehicle-injected animals. Furthermore, following administration of captopril and pentolinium, the capsaicin-treated animals showed marked impairment of the vasopressin-dependent recovery of blood pressure. These results indicate that the greater hypotensive response to captopril in water-deprived. Long-Evans rats treated neonatally with capsaicin may be due to less effective compensation for inhibition of the renin-angiotensin system when vasopressin release is impaired.

Animals↗
PubMed1986

Endogenous vasopressin and baroreflex mechanisms.

This article reviews the anatomical and functional evidence for ascending pathways from specific brain regions to the PVN and SON which could influence AVP release. The majority of evidence favours the main projection being from a region in the caudal VLM which may coincide with the noradrenergic neurons of the A1 cell group. However, the transmitter(s) involved have yet to be identified, and whether the pathway is excitatory and/or inhibitory remains to be fully resolved. Anatomical and functional evidence is reviewed for descending projections from the SON and PVN to specific brain regions involved in cardiovascular control, and their possible involvement in baroreflex mechanisms is discussed. However, there is little unequivocal evidence that AVP is the main neurotransmitter utilized by descending projections from PVN to NTS and DMX. While, in some situations, circulating endogenous AVP exerts cardiovascular effects, details of its putative influences on baroreflex mechanisms are lacking.

Animals↗
PubMed1986

The influence of streptozotocin-induced diabetes mellitus on fluid and electrolyte handling in rats.

Intakes and urine outputs of fluid and electrolytes were measured daily in rats before, and for 3 weeks after, induction of diabetes by intraperitoneal injection of streptozotocin (STZ; 60 mg/kg); control animals received saline. Water intakes and urine outputs were increased on and after the first day after injection with STZ; after a transient period of negative water balance, fluid intakes and urine outputs increased in parallel. Food intake was reduced for the first 3 days after injection of STZ but thereafter there was a steady increase. On the final experimental day, the food intake of the diabetic group was 60% greater than that of the control group. Urinary electrolyte excretion was increased after injection of STZ; at the end of the experiment, the increase in urinary sodium excretion was similar to the increase in intake but the increase in urinary potassium excretion was less. On day 21 after injection of STZ plasma sodium concentration and packed cell volume were significantly reduced in the diabetic group but plasma potassium concentration was not. There was a difference between the measured osmolality and the calculated osmolarity of the plasma of the diabetic animals which was not seen in the controls. This difference was not due to pseudohyponatraemia, but was probably due to the presence of unidentified solutes, since there was a significant gap between the urinary osmolal and osmolar excretion in the diabetic animals that was not present in the control animals.

Animals↗
PubMed1986

The contribution of the autonomic nervous system, the renin-angiotensin system and vasopressin to the maintenance of arterial blood pressure in adrenalectomized Wistar rats.

Factors contributing to the maintenance of resting arterial blood pressure in sham-operated and adrenalectomized rats were assessed 14 weeks after operation; some animals were given 1% NaCl to drink throughout, and some animals were given sodium-free water instead of 1% NaCl for 2 days before the experiment. Inhibition of the renin-angiotensin (ANG) system (with captopril) and of the cardiovascular actions of vasopressin [with 1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid),8-D-arginine vasopressin (d(CH2)5DAVP)] had no hypotensive effects in sham-operated rats under any conditions, but antagonism of nicotinic ganglionic transmission (with pentolinium) caused a prompt fall in blood pressure. During combined administration of captopril, d(CH2)5DAVP and pentolinium to sham-operated rats, there was no significant recovery of blood pressure. Adrenalectomized rats drinking 1% NaCl showed a marked hypotension and tachycardia in response to captopril, but d(CH2)5DAVP had little effect, whether administered before or after captopril. Addition of pentolinium rendered these animals more hypotensive than the sham-operated rats. Adrenalectomized rats drinking sodium-free water for 2 days were hypotensive and blood pressures were lowered further by d(CH2)5DAVP or captopril under these conditions; there was no accompanying tachycardia. The results indicate that, in chronically adrenalectomized rats drinking 1% NaCl, blood pressure is maintained by autonomic nervous and renin-ANG systems with no discernible contribution from the peripheral cardiovascular actions of vasopressin. However, the latter contribute importantly to the support of blood pressure when the adrenalectomized rats are rendered hypovolaemic and hypotensive by substitution of sodium-free water to drink.

Adrenalectomy↗
PubMed1986

Withdrawal of salt supplementation from adrenalectomized Wistar rats distinguishes between those animals with, and those without, adrenocortical insufficiency.

The effects of replacing a 1% NaCl drinking solution with Na+-free water for 2 days on body weight and fluid and electrolyte balances were studied in adrenalectomized and sham-operated rats. Eight weeks after operation, after the animals had been drinking Na+-free water for 2 days, some adrenalectomized animals (about 75%; designated group experienced body weight losses which were outside the 99% confidence limits for the sham-operated rats (-9.2 to +5.3 g) whereas the remainder (designated group 2) were indistinguishable from the controls. The body weight loss in group 1 was associated with negative fluid, Na+ and K+ balances. In group 2 rats, fluid balance was maintained as well as in the sham-operated rats, but their handling of Na+ and K+ was different. In a separate experiment, plasma aldosterone, corticosterone, catecholamine and solute concentrations were measured in adrenalectomized rats from groups 1 and 2 (selected on the basis of body weight loss whilst drinking Na+-free water) and sham-operated rats, after drinking Na+-free water for 2 days. In group 1 animals, plasma aldosterone levels were unmeasurable and corticosterone was extremely low (less than 5% of controls). In group 2, aldosterone was measurable but low, and corticosterone was higher than in group 1 but lower than in sham-operated rats. In line with these findings, animals in group 1, but not those in group 2, were hyponatraemic and hyperkalaemic. These results are consistent with the activation of latent adrenocortical tissue in the group 2 animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Insufficiency↗
PubMed1986

Baroreflex sensitivity in conscious rats: the influence of recording site.

Arterial blood pressures were measured simultaneously in the thoracic and abdominal aortas in the same conscious rats. Intravenous administration of sodium nitroprusside caused a greater fall in systolic blood pressure in the abdominal aorta than in the thoracic aorta, whereas intravenous administration of methoxamine caused a greater rise in systolic blood pressure in the thoracic aorta. Hence baroreflex sensitivities derived from these data (by relating systolic blood pressure to the pulse interval of the succeeding beat) were appreciably different depending on the site of measurement. The changes in diastolic and mean arterial blood pressures induced by the drugs were similar at the two recording sites. It is suggested therefore that cardiac baroreflex sensitivity should be assessed in conscious rats by relating pulse interval to mean arterial blood pressure recorded at a site other than the thoracic aorta since cannulation at that site impairs baroreflex responsiveness.

Animals↗
PubMed1986

Vasopressin and the cardiovascular system: physiology or pharmacology?

Anesthetized rats of different strains show a hypotensive response to administration of an antagonist of the V1 receptors for vasopressin [d(CH2)5DAVP]. Such an effect is not seen in conscious, water-replete animals or in Long-Evans rats challenged with a subcutaneous injection of polyethylene glycol (PEG) to cause isosmotic hypovolemia. However, Long-Evans rats experiencing a similar volume reduction due to water deprivation show hyperosmolality and exhibit a small hypotensive response to d(CH2)5DAVP. Inhibition of the renin-angiotensin system following administration of d(CH2)5DAVP causes a greater hypotension in PEG-treated than in water-deprived Long-Evans rats. In both experimental conditions, the fall in blood pressure is greater than when captopril administration precedes that of d(CH2)5DAVP, indicating that prolonged administration of d(CH2)5DAVP may be interfering with mechanisms other than those mediated by peripheral V1 receptors. However, administration of d(CH2)5DAVP and captopril to water-deprived Long-Evans rats rarely causes the profound hypotension seen in water-deprived Brattleboro rats given captopril alone. In some adrenalectomized Wistar rats, following withdrawal of salt supplementation, the hypotensive response to d(CH2)5DAVP is the greatest seen in any experimental model. These results indicate that AVP is overtly involved in the support of blood pressure in various hypotensive states and, more importantly, may be responsible for the maintenance of a "normal" blood pressure in some conditions. However, the involvement of AVP in cardiovascular regulation in the majority of normotensive conditions is intriguingly subtle.

Adrenalectomy↗