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Biomedical subjects

T Bennett

Publications and source records attributed to T Bennett.

At least 235 records · Page 13Linked to original sources
PubMed1989

Regional haemodynamic effect of vasopressin infusion in conscious, unrestrained, Brattleboro rats.

1. Incremental rates of infusion (0.027-4.0 pmol min-1) of exogenous vasopressin were given for 10 min periods to conscious, Brattleboro (i.e. vasopressin-deficient) rats, which had been chronically instrumented with pulsed Doppler probes and intravascular catheters (to permit assessment of regional haemodynamic changes). 2. There were no significant effects of the two lowest rates of infusion (0.027 and 0.105 pmol min-1) but, after 10 min of vasopressin infusion at 0.313 pmol min-1, superior mesenteric vasoconstriction had occurred unaccompanied by any other changes. Infusion of vasopressin at 0.687 pmol min-1 produced increases in blood pressure and in both mesenteric and hindquarters vascular resistance, but not change in renal vascular resistance or heart rate. These results do not indicate specific interactions between exogenous vasopressin and baroreflex mechanisms to offset the pressor effect of the neuropeptide. 3. The marked bradycardia, hypertension and renal, mesenteric and hindquarters vasoconstriction seen after 10 min infusion of vasopressin at 4.0 pmol min-1 were all abolished 10 min after administration of an antagonist of V1-receptors [+)-(CH2)5Tyr(Et)DAVP); additional antagonism of V2-receptors (with the non-selective antagonist (+)-(CH2)5Tyr(Et)VAVP) had no effects on any measured variable. Hence, the present experiments provide no evidence for important vasodilator effect of vasopressin in conscious, Brattleboro rats.

Animals↗
PubMed1989

The effects of infusions of arginine vasopressin or 1-deamino-8-D-arginine vasopressin on common carotid vascular resistance in conscious, Long Evans rats.

1. Intravenous infusions of arginine vasopressin or 1-deamino-8-D-arginine vasopressin (DDAVP) were given to conscious, Long Evans rats chronically instrumented with bilateral, common carotid, pulsed Doppler probes and intravascular catheters. 2. During infusion of vasopressin at 0.3 nmol min-1 there was an increase in common carotid vascular resistance with no change in mean blood pressure or heart rate. Following infusion there was a common carotid vasodilatation. 3. During infusion of vasopressin at 3.0 nmol min-1 there were increases in mean arterial blood pressure and in common carotid vascular resistances, accompanied by bilateral reductions in flow and in heart rate. Administration of (+)-(CH2)5Tyr(Et)DAVP (a V1-receptor antagonist), during the continued infusion of vasopressin, reversed the effects of the latter on mean blood pressure and heart rate; under these conditions there were increases in common carotid blood flows above baseline, in company with bilateral vasodilatations. The latter effects persisted after cessation of vasopressin infusion. 4. Infusions of DDAVP were without significant effects on any measured cardiovascular variable. 5. The results do not provide straightforward support for the claim that vasopressin acts to promote cerebral perfusion, at least when V1-receptor effects are unopposed. Furthermore, it seems likely tha the vasodilator influence of vasopressin on the common carotid vascular bed is not due to stimulation of V2-receptors.

Animals↗
PubMed1989

Regional haemodynamic effects of human alpha- and beta-calcitonin gene-related peptide in conscious Wistar rats.

1. A comparative study was carried out to assess the regional haemodynamic effects of intravenous infusion of human alpha- and beta-calcitonin gene-related peptide (CGRP; 0.006, 0.06 and 0.6 nmol h-1) in conscious, unrestrained Wistar rats. 2. With human alpha-CGRP, tachycardia was always accompanied by a fall in mean arterial blood pressure (MBP), but human beta-CGRP at the middle dose caused tachycardia with no significant hypotension. 3. Human alpha- and beta-CGRP both caused dose-dependent falls in MBP accompanied by common carotid and hindquarters vasodilatations and increased flows. The highest dose of alpha- and beta-CGRP caused mesenteric vasoconstriction and renal vasodilatation, but the latter was not associated with an increase in flow. 4. With the intermediate dose, human alpha-CGRP caused more significant haemodynamic changes than did human beta-CGRP. In addition, comparison with previous experiments involving infusion of rat alpha-CGRP indicated that human alpha-CGRP had more potent haemodynamic effects than the former.

Animals↗
PubMed1989

Regional hemodynamic effects of calcitonin gene-related peptide.

Cardiovascular responses to infusions of rat alpha-calcitonin gene-related peptide (CGRP; 0.06, 0.6, 6.0 nmol/h) or rat alpha-atrial natriuretic peptide (ANP; 3.7 nmol/h) were measured in conscious rats. During infusion of the low dose of CGRP, when mean arterial pressure (MAP) was little affected, there were reductions in common carotid, renal, mesenteric, and hindquarter vascular resistances (the magnitude of the responses in the same descending order). However, only flow in the common carotid vessels was increased above base line. After infusion, there was a hindquarter vasoconstriction. During infusion of the higher doses of CGRP, there were dose-related decreases in MAP and increases in heart rate associated with (hyperemic) hindquarter vasodilatations and mesenteric vasoconstrictions. The common carotid vasodilatation peaked with the intermediate dose of CGRP; the changes in renal vascular resistance were not dose related. After infusion of the high dose of CGRP there were persistent (at least 60 min) common carotid and hindquarter vasodilatations and mesenteric vasoconstriction, with a transient overshoot in renal vascular resistance. Infusions of CGRP and ANP matched for their effects on MAP had similar influences on mesenteric hemodynamics, but all other variables were affected differently.

Animals↗
PubMed1989

Regional hemodynamic changes following hypovolemia in conscious rats.

Regional hemodynamic responses to subcutaneous injection of hyperoncotic polyethylene glycol (PEG) were assessed in Long-Evans (i.e., normal) and Brattleboro [i.e., arginine vasopressin (AVP)-deficient] rats with chronically implanted, pulsed Doppler probes. The results were compared with saline-injected time controls. PEG injection elicited an early (30 min) selective mesenteric vasoconstriction in Long-Evans rats; 4-5 h after PEG the mesenteric vasoconstriction was greater in Long-Evans than in Brattleboro rats, but the renal and hindquarters vasoconstrictions were similar in both strains. There was a transient mesenteric vasodilatation [with no change in blood pressure (BP)] in Long-Evans rats given an antagonist of the V1-receptor actions of AVP 5 h after PEG. In the presence of the AVP antagonist, Long-Evans rats showed a marked dependence on the vasoconstrictor actions of the renin-angiotensin system for the maintenance of BP, similar to Brattleboro rats. Both strains also showed marked hypotensive responses to inhibition of sympathoadrenal activity (with pentolinium). Hence, AVP has clear-cut hemodynamic effects after PEG administration, but its role is not indispensable.

Animals↗
PubMed1989

Diabetes mellitus in Brattleboro rats: cardiovascular, fluid, and electrolyte status.

Because plasma arginine vasopressin (AVP) levels are raised during streptozotocin (STZ)-induced diabetes mellitus (DM), it is possible that AVP contributes to the pattern of change in fluid and electrolyte handling and cardiovascular status after STZ treatment. Therefore we have made daily measurements of cardiovascular and metabolic variables in normal (Long-Evans) and AVP-deficient (Brattleboro) rats treated with saline or STZ. Twenty-four days after STZ, both strains had similar weight loss and increases in fluid intake, but the increase in food intake was greater in Long-Evans than in Brattleboro rats. After STZ, bradycardia developed in both strains, but only Brattleboro rats had reduced blood pressure. Plasma variables were measured 25 days after STZ. Packed cell volume and plasma sodium concentration were reduced in STZ-treated Long-Evans rats compared with saline-treated controls but were unchanged in STZ-treated Brattleboro rats. The results indicate that although AVP deficiency does not seriously affect the ability to maintain fluid and electrolyte balance after STZ treatment, there may be consequences for cardiovascular control.

Animals↗
PubMed1989

Synthetic capsaicin reversibly impairs vasopressin-mediated blood pressure recovery.

The vasopressin-mediated recovery of arterial pressure observed in adult rats following pharmacological blockade of the sympathetic nervous and renin-angiotensin systems is reduced by neonatal capsaicin treatment. We now demonstrate a similar but reversible effect following treatment of adult Wistar or Sprague-Dawley rats with N-vanillylnonanamide (50 mg/kg sc). One day after treatment, Wistar, but typically not Sprague-Dawley, rats had lost weight and exhibited increased sensitivity to the anesthetic effects of methohexital sodium. In both strains, captopril treatment caused hypotension. After captopril and ganglionic blockade, vasopressin-mediated recovery of arterial pressure was significantly inhibited. Furthermore, treated Wistar rats had reduced sensitivity to the ocular irritancy of N-vanillylnonanamide when examined 2 days postdose. All deficits reversed within 2 wk of dosing. These data suggest that capsaicin-sensitive systems participate in homeostatic mechanisms engaged during acute hypotension. Because the dose of N-vanillylnonanamide employed in the present study has previously been shown to destroy unmyelinated afferent fibers when administered to adult rats, recovery of the functional deficits may reflect regeneration of damaged processes or assumption of their function by undamaged neurons innervating adjacent sites. By extrapolation from other studies of capsaicin, damage to some central neurons may also be involved.

Animals↗
PubMed1989

Differential cardiovascular effects of centrally administered vasopressin in conscious Long Evans and Brattleboro rats.

The cardiovascular effects of arginine vasopressin (AVP) administered into a lateral cerebral ventricle or into the cisterna magna were investigated in conscious Long Evans (control) rats and AVP-deficient Brattleboro rats. The effects of subpressor intracerebroventricular and intracisternal doses of AVP on cardiac baroreflex sensitivities were also determined. Intracerebroventricular and intracisternal AVP increased blood pressure of both strains of rat in a dose-dependent manner. The maximum pressor response produced by intracerebroventricular AVP in Long Evans rats was 13 +/- 2/13 +/- 1 mm Hg (systolic/diastolic, n = 6) after 100 ng AVP. The pressor response to the highest intracerebroventricular dose of AVP tested in Brattleboro rats (30 ng) was 46 +/- 13/21 +/- 6 mm Hg (n = 6). Intracerebroventricular AVP caused a tachycardia in Brattleboro rats but had no effect on heart rate of Long Evans rats. At doses greater than 1 ng, the increases in blood pressure produced by intracisternal AVP in both groups of rats were significantly greater than the increases produced by the same doses given intracerebroventricularly. Heart rate fell in a dose-dependent manner after intracisternal AVP in Long Evans rats but not in Brattleboro rats. Cardiac baroreflex sensitivities of Brattleboro rats were not significantly different from those of Long Evans rats and were not modified by intracerebroventricular (0.3 ng) or intracisternal (0.1 ng) AVP. In Long Evans rats, intracisternal AVP (0.3 ng) increased cardiac baroreflex responses to both increases and decreases in pressure. Intracerebroventricular AVP (0.3 ng) increased the sensitivity of the reflex in response to an elevation but not to a reduction in blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Renal vasodilatation after central administration of galanin.

Galanin, a recently described brain-gut neuropeptide, exists in central nervous pathways subserving cardiovascular regulation in the rat. To investigate the possibility that this peptide is involved in the central control of cardiovascular function we administered galanin (1 or 5 nmol) into a lateral cerebral ventricle in conscious, Long-Evans and Brattleboro rats, chronically instrumented with pulsed Doppler probes for monitoring regional haemodynamics. In both strains galanin caused renal vasodilatation at a dose that had no significant effects on blood pressure or heart rate. These results highlight the need to monitor regional haemodynamics when assessing putative physiological roles of peptides in central cardiovascular regulation.

Animals↗
PubMed1988

Cardiovascular and dipsogenic effects of angiotensin II administered i.c.v. in Long-Evans and Brattleboro rats.

The concurrent cardiovascular and dipsogenic effects produced by i.c.v. administration of angiotensin II (AII) have been investigated in vasopressin-deficient (Brattleboro) and control (Long-Evans) rats. When animals were allowed to drink during testing, the pressor effect of i.c.v. AII (500 ng) in Long-Evans rats (26 +/- 3/26 +/- 3 mm Hg) was significantly greater than that produced when drinking water was not available (19 +/- 2/18 +/- 2 mm Hg). There was a significant decrease in heart rate only when water was available. There was no pressor response to i.c.v. AII in Brattleboro rats not allowed to drink, whereas blood pressure increased by 17 +/- 3/14 +/- 1 mm Hg in response to i.c.v. AII when drinking water was present. There were no significant changes in heart rate following i.c.v. AII in Brattleboro rats. When baseline drinking was taken into account, Brattleboro rats still drank significantly more water than Long-Evans rats in response to i.c.v. AII. Pretreatment of Long-Evans rats with the V1 vasopressin antagonist, D(CH2)5Tyr(Et)DAVP, decreased the pressor effect of i.c.v. AII to a level not significantly different from that of Brattleboro rats allowed to drink. Under these conditions the amount drunk by Long-Evans rats was not significantly less than that drunk by Brattleboro rats. These results confirm that the central pressor actions of AII are mediated, in part, by release of vasopressin and suggest that the greater dipsogenic effect of i.c.v. AII in Brattleboro compared with Long-Evans rats may be due, partly, to its lesser pressor activity in these animals.

Angiotensin II↗
PubMed1988

Regional haemodynamic responses to intracerebroventricular administration of rat calcitonin gene-related peptide in conscious, Long-Evans and Brattleboro rats.

Rat calcitonin gene-related peptide (CGRP) was administered intracerebroventricularly (0.25 nmol in 5 microliter) to conscious, Long-Evans and Brattleboro rats, chronically instrumented with pulsed Doppler probes around the left renal and superior mesenteric arteries and the distal abdominal aorta. Tachycardias occurred in both strains, but only in Long-Evans rats was there a (modest) pressor effect of CGRP. However, both strains of rat showed renal vasodilatation and mesenteric vasoconstriction. These results indicate that the central pressor effect of CGRP in Long-Evans rats may not be due to generalized sympathetic activation, and make it unlikely that circulating vasopressin contributes to the mesenteric vasoconstriction.

Animals↗
PubMed1988

Cardiovascular actions of neuropeptide Y in the hypothalamic paraventricular nucleus of conscious Long Evans and Brattleboro rats.

The central cardiovascular effects of neuropeptide Y (NPY) have been investigated by microinjection of the peptide into the hypothalamic paraventricular nucleus (PVN) of conscious rats. NPY (100 ng) elicited a significant bradycardia in both Long Evans (control) rats (-27 +/- beats/min) and vasopressin-deficient Brattleboro rats (-19 +/- 6 beats/min). There was a slight fall in systolic blood pressure in both strains which was significant only in Long Evans rats. A higher dose of NPY (1000 ng) had no significant effect on blood pressure or heart rate, but produced a marked behavioural response characterized by initiation of foraging behaviour. These results provide further support for a role for NPY in central cardiovascular regulation, but provide no evidence of an indispensable involvement of vasopressin-containing pathways in the observed responses.

Animals↗
PubMed1988

Diversity of fast myosin heavy chain expression during development of gastrocnemius, bicep brachii, and posterior latissimus dorsi muscles in normal and dystrophic chickens.

The expression of fast myosin heavy chain (MHC) isoforms was examined in developing bicep brachii, lateral gastrocnemius, and posterior latissimus dorsi (PLD) muscles of inbred normal White Leghorn chickens (Line 03) and genetically related inbred dystrophic White Leghorn chickens (Line 433). Utilizing a highly characterized monoclonal antibody library we employed ELISA, Western blot, immunocytochemical, and MHC epitope mapping techniques to determine which MHCs were present in the fibers of these muscles at different stages of development. The developmental pattern of MHC expression in the normal bicep brachii was uniform with all fibers initially accumulating embryonic MHC similar to that of the pectoralis muscle. At hatching the neonatal isoform was expressed in all fibers; however, unlike in the pectoralis muscle the embryonic MHC isoform did not disappear. With increasing age the neonatal MHC was repressed leaving the embryonic MHC as the only detectable isoform present in the adult bicep brachii muscle. While initially expressing embryonic MHC in ovo, the post-hatch normal gastrocnemius expressed both embryonic and neonatal MHCs. However, unlike the bicep brachii muscle, this pattern of expression continued in the adult muscle. The adult normal gastrocnemius stained heterogeneously with anti-embryonic and anti-neonatal antibodies indicating that mature fibers could contain either isoform or both. Neither the bicep brachii muscle nor the lateral gastrocnemius muscle reacted with the adult specific antibody at any stage of development. In the developing posterior latissimus dorsi muscle (PLD), embryonic, neonatal, and adult isoforms sequentially appeared; however, expression of the embryonic isoform continued throughout development. In the adult PLD, both embryonic and adult MHCs were expressed, with most fibers expressing both isoforms. In dystrophic neonates and adults virtually all fibers of the bicep brachii, gastrocnemius, and PLD muscles were identical and contained embryonic and neonatal MHCs. These results corroborate previous observations that there are alternative programs of fast MHC expression to that found in the pectoralis muscle of the chicken (M.T. Crow and F.E. Stockdale, 1986, Dev. Biol. 118, 333-342), and that diversification into fibers containing specific MHCs fails to occur in the fast muscle fibers of the dystrophic chicken. These results are consistent with the hypothesis that avian muscular dystrophy is a developmental disorder that is associated with alterations in isoform switching during muscle maturation.

Age Factors↗
PubMed1988

Cardiac baroreflex sensitivities in conscious, unrestrained, Long Evans and Brattleboro rats.

Cardiac baroreflex sensitivity (BRS; i.e. the slope of the line relating change in pulse interval to change in systemic arterial pressure) was assessed in response to an increase in mean blood pressure (MBP) evoked by methoxamine or a decrease evoked by sodium nitroprusside. Measurements were made in Long Evans (i.e. control) and in Brattleboro (i.e. vasopressin (AVP)-deficient) rats, following acute and chronic intravascular catheterization, and in water-replete and water-deprived states (the latter designed to reduce plasma volume and activate AVP-dependent mechanisms (in Long Evans rats]. There were no differences between the corresponding values for cardiac BRS in Long Evans and Brattleboro rats. Furthermore, water deprivation caused no significant changes in cardiac BRS in either strain. These results do not support the claim that absence of endogenous AVP in Brattleboro rats is associated with marked impairment of cardiac BRS, and indicate that chronic changes in circulating AVP do not cause systematic changes in cardiac BRS.

Animals↗
PubMed1988

Adrenoceptors and cardiovascular regulation in conscious, unrestrained, Long Evans and Brattleboro rats.

In conscious rats, in the presence of prazosin and idazoxan (alpha 1- and alpha 2-adrenoceptor antagonists, respectively), blood pressure (BP) and heart rate (HR) become unstable, due to the occurrence of 'spontaneous' depressor and tachycardic episodes. These events could be triggered also by auditory stimuli, and were blocked by antagonism of beta 2-adrenoceptors. In adrenal-demedullated animals treated with prazosin and idazoxan, BP was less variable than in sham-operated animals, but bolus injections of adrenaline or salbutamol could simulate the 'spontaneous' depressor events seen in the latter. The marked swings in HR were not explained by sensitization of the cardiac baroreflex in the presence of idazoxan, but were probably due to blockade of prejunctional autoinhibitory alpha 2-adrenoceptors, amplifying the effects of intermittent sympatho-adrenal activation.

Acoustic Stimulation↗
PubMed1988

Cardiovascular consequences of water deprivation in female Long Evans and Brattleboro rats.

Female Long Evans and Brattleboro rats were studied while water-replete and after water deprivation sufficient to cause hypovolaemia of similar degree in the two strains. A comparison was made of the blood chemistry and cardiovascular status in the two conditions, and the ability of the renin-angiotensin system, sympathoadrenal activity and (in Long Evans rats) vasopressin to influence blood pressure were assessed by pharmacological blockade of these systems. Under water-replete conditions there were significant differences between plasma variables in the two strains (Long Evans: vol., 3.67 +/- 0.07 ml/100 g b. wt., sodium, 142 +/- 0.3 mmol/l; osmolality, 290 +/- 1 mosmol/kg; Brattleboro: vol., 3.89 +/- 0.07 ml/100 g b. wt.; sodium 148 +/- 0.4 mmol/l; osmolality 304 +/- 2 mosmol/kg). Inhibition of the renin-angiotensin system (with captopril) had a slightly greater hypotensive effect in Brattleboro than in Long Evans rats. In both strains the hypotensive effects of captopril were enhanced markedly in the presence of pentolinium, and, under those conditions there was a vasopressin-dependent recovery of blood pressure in Long Evans rats that was absent in Brattleboro rats. Water deprivation caused a greater proportional reduction in body weight, and increase in plasma sodium and osmolality in Brattleboro than in Long Evans rats, although resting cardiovascular statuses were not markedly different. Despite Brattleboro rats having substantial hypernatraemia (156 +/- 1.0 mmol/l), that should have acted to inhibit renin release, they showed a profound hypotensive response to captopril that was not apparent in Long Evans rats. Thus, the absence of vasopressin in female Brattleboro rats severely affects cardiovascular adaptation to water deprivation. Comparison of the present results with published data obtained from male Long Evans and Brattleboro rats shows marked sex differences in the response to the same water deprivation protocol, and indicates that data obtained from males and females should not be cumulated.

Animals↗
PubMed1988

Regional haemodynamic effects of neuropeptide Y, vasopressin and angiotensin II in conscious, unrestrained, Long Evans and Brattleboro rats.

The regional haemodynamic responses to equipressor doses of neuropeptide Y (NPY), vasopressin (AVP) and angiotensin II (AII) were assessed in conscious Long Evans and Brattleboro rats, chronically instrumented with miniaturized, pulsed Doppler probes. NPY caused particularly potent renal vasoconstrictions in intact rats of both strains. However, there were differential changes in regional vascular sensitivity of NPY following administration of pentolinium and captopril, indicating that 'buffer' mechanisms were an important determinant of responses to NPY. A marked mesenteric and low renal sensitivity to AVP was seen in both strains in all conditions. AVP was the most potent of the 3 pressor agents, and no evidence was found for it interacting uniquely with buffer mechanisms. The pressor action of AII was offset by a tendency towards hindquarters vasodilatation that was converted to a marked vasoconstriction when pentolinium and captopril were administered. It is feasible that, in the intact rat, AII stimulated adrenal medullary adrenal release which caused beta-adrenoceptor-mediated vasodilatation that acted to offset the direct vasoconstrictor effects of AII.

Angiotensin II↗