Biomedical subjects

R D Buńag

Publications and source records attributed to R D Buńag.

3 recordsLinked 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↗

PubMed1976

Exaggeration of experimental hypertension in rats by contraceptive steroids (Enovid).

The possibly additive pressor effects of contraceptive steroids were studied by treating hypertensive rats chronically with Enovid. Renal hypertensive rats were unaffected by drug treatment during the first 5 weeks, but, from the 6th to the 8th week, Enovid-treated rats had much higher systolic pressures than those given corn oil alone. However, these differences dwindled and became insignificant from the 9th to the 16th week despite continued treatment. Subsequently, other rats were pretreated with Enovid or corn oil for 5 weeks before hypertension was induced by implanting deoxycorticosterone acetate (Doca). In contrast to the equivocal results obtained previously, Doca hypertension was consistently more pronounced in rats treated with Enovid than in those given corn oil. This pressure difference was later verified by direct measurement of phasic aortic pressures from indwelling catheters and by the postmortem finding that Enovid-treated rats had larger hearts than corn oil-treated ones. The exact mechanism by which Enovid enhances Doca hypertension is still undetermined, but sympathetic hyperactivity was considered an unlikely explanation, since responses to posterior hypothalamic stimulation, norepinephrine, or ganglion blockade with pentolinium were unaltered.

Animals↗

PubMedDate not supplied

Insulin reverses hypertension and hypothalamic depression in streptozotocin diabetic rats.

Daily subcutaneous injections of lente insulin reduced the hypertension and bradycardia which developed consistently in streptozotocin diabetic rats. Insulin-treated rats also became less hyperglycemic, drank less water, and gained weight faster than untreated diabetic controls. Behavioral and tachycardiac effects elicited by electrical stimulation of the ventromedial hypothalamus while the rats were awake were similar, but attendant pressor responses were larger in those that had been treated with insulin. Under subsequent urethane anesthesia, pressor and sympathetic responses to hypothalamic stimulation, as well as pressor responses to tyramine and vasopressin, were augmented in insulin-treated rats. A generalized increase in cardiovascular reactivity caused by insulin seemed unlikely since pressor responses to norepinephrine were unaltered. Enhanced hypothalamic responsiveness was considered due to improvement of diabetic encephalopathy rather than to direct CNS stimulation by insulin because the injected insulin had mostly dissipated by the time pressor responses were recorded. By showing that insulin treatment produced changes opposite to those occurring during induction of diabetes our results suggest that insulin can alleviate cardiovascular and hypothalamic dysfunction in streptozotocin-induced diabetes.

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