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.
D000818:Animals; D004558:Electric Stimulation; D005730:Ganglionic Blockers; D006973:Hypertension / Q000503:physiopathology*; D007034:Hypothalamus, Posterior; D009638:Norepinephrine / Q000494:pharmacology; D010425:Pentolinium Tartrate / Q000494:pharmacology; D051381:Rats; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D014661:Vasoconstriction / Q000187:drug effects
D005730:Ganglionic Blockers; D010425:Pentolinium Tartrate; D009638:Norepinephrine