Effects of captopril on neurosecretion and vascular responsiveness in hypertension.
The purpose of the present study was to investigate the mechanisms of hypotensive action of an angiotensin converting enzyme inhibitor (captopril) in hypertension. In perfused mesenteric vasculatures from spontaneously hypertensive rats (SHR) and normotensive Wistar kyoto rats (WKY), the effects of captopril on the vascular responsiveness and norepinephrine overflow from the adrenergic nerve endings were examined. The vasoconstrictor responses and norepinephrine overflow during the electrical nerve stimulation was significantly enhanced in SHR compared with WKY. Captopril reduced not only vasoconstrictor responses but also norepinephrine overflow during the nerve stimulation in a dose-dependent fashion. The suppressions of these responses by captopril were significantly greater in SHR than in WKY. These results demonstrate that captopril could affect the presynaptic site of the resistance vessels and cause a decrease in electrically-stimulated norepinephrine overflow from the adrenergic nerve endings. The marked reduction of the pressor responses and norepinephrine overflow to nerve stimulation by captopril in the SHR suggests that the renin-angiotensin system in the vascular beds in enhanced in this model of hypertension.
D000818:Animals; D002216:Captopril / Q000494:pharmacology*; D004558:Electric Stimulation; D006439:Hemodynamics / Q000187:drug effects*; D006973:Hypertension / Q000503:physiopathology*; D009489:Neurosecretion / Q000187:drug effects*; D009638:Norepinephrine / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D013152:Splanchnic Circulation / Q000187:drug effects; D013564:Sympathetic Nervous System / Q000187:drug effects; D009435:Synaptic Transmission / Q000187:drug effects
D002216:Captopril; D009638:Norepinephrine