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At least 289 records · Page 16Linked to original sources
PubMed1979

Sympathetic hyperresponsiveness to hypothalamic stimulation in young hypertensive rats.

The possible occurrence of central sympathetic dysfunction during development of spontaneous hypertension was studied by recording aortic pressure and sympathetic nerve activity concurrently during electrical stimulation of the posterior hypothalamus in 9-wk-old Kyoto-Wistar rats. Even at this early age, basal levels for both measurements were already elevated significantly in those with spontaneous hypertension. Increases in sympathetic neural firing induced by graded hypothalamic stimulation were always followed by corresponding increases in blood pressure; magnitude of both effects was appreciably larger in spontaneously hypertensive than in normotensive rats, as was the vasodepression caused by blocking autonomic ganglia with pentolinium. By contrast, pressor responses to injected norepinephrine were almost equal thereby suggesting that cardiovascular reactivity was unaltered and that enhanced responsiveness to hypothalamic stimulation was directly due to the concomitant increase in sympathetic nerve activity. Although the exact site from which sympathetic hyperactivity originates was unidentified, our results support the interpretation that sympathetic mechanisms involving the posterior hypothalamus participate in elevating blood pressure during development of spontaneous hypertension in rats.

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↗
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

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↗
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

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↗
PubMed1990

Atrial natriuretic peptide infusion causes vasoconstriction after autonomic blockade in conscious dogs.

Many studies have shown that atrial natriuretic peptide (ANP) reduces mean arterial pressure (MAP) in conscious animals by lowering cardiac output (CO) with no change or even increased total peripheral resistance (TPR). Because ANP is thought to be a vasodilator, the lack of fall in TPR in conscious animals is generally considered to be due to autonomic reflex increases in vascular resistance. In the present study in conscious, trained, chronically instrumented dogs (n = 7), we measured hemodynamic and renal excretory responses to 30-min infusions of alpha-human ANP (alpha hANP; 25, 50, and 100 ng.kg-1.min-1) in the presence and absence of autonomic nervous system blockade using the ganglion blocking agent pentolinium. In the absence of blockade, MAP and CO fell, whereas TPR rose with alpha hANP infusions, but these changes did not reach significance. There were significant increases in renal vascular resistance (RVR; 16-25%) and mesenteric vascular resistance (MVR; 14-40%). During autonomic nervous system blockade, alpha hANP caused dose-related reductions in MAP (7-12%), due to falls in CO (13-34%). Remarkably, the absence of autonomic reflex responses exposed substantial dose-related increases in TPR (5-33%). Autonomic blockade did not alter the ANP-induced increases in MVR but did abolish the rises in RVR. In summary, ANP caused vasoconstriction in mesenteric vasculature and substantial vasoconstriction in other nonrenal areas, independent of autonomic reflexes.

Animals↗