Evidence for an antihypertensive factor from the adrenal medulla of SHR modulating neurogenic vasoconstriction
Source: Acta Physiologica, Volume 167, Number 3, November 1999 , pp. 195-202(8)
Abstract:The aim of this study is to investigate some vasoactive properties of the blood of spontaneously hypertensive rats (SHR). Isolated segments of rat tail arteries obtained from normotensive rats (Wistar–Kyoto (WKY) and Wistar) were perfused with blood from conscious donor rats (WKY, Wistar or SHR). Alterations of the neurogenic constrictor responses (NCR) of the isolated segments evoked by electrical stimulation were studied. The amplitude of NCR of the isolated arteries was studied during perfusion with blood according to the perfusion scheme WKY1(1)–SHR1(2)–WKY1(3) and WKY1(1)–WKY2(2)–WKY1(3). The release of 3H-noradrenaline ([3H]-NA) from vascular sympathetic fibres was measured. The influence of adrenal demedullation on NCR was estimated. We have shown that NCR of isolated arteries decreased by 28.3 ± 7.9% (P < 0.05 vs. WKY1(1)) during perfusion with blood from SHR (scheme WKY1(1)–SHR1(2)–WKY1(3)). In these experiments, release of [3H]-NA from sympathetic fibres of the artery segments decreased by 39.9 ± 9.6% during the perfusion with blood from SHR vs. WKY1(1) (P < 0.05). Adrenal demedullation prevented the decrease of NCR during perfusion of the arteries with blood from SHR. In conclusion, the blood of SHR has some antihypertensive factor(s), which causes decrease of NCR in the tail artery from normotensive rats. This decline is accompanied by the decrease of release in [3H]-NA from the transmural sympathetic fibres and is abolished after adrenal demedullation of blood donor rats.
Document Type: Research Article
Affiliations: 1: Department of Human and Animal Physiology, Biological Faculty, Moscow State University, Russia 2: Department of Cardiovascular Pathology, Cardiology Research Center, Moscow, Russia 3: Department of Pharmacology, Faculty of Basic Medicine, Moscow State University, Russia
Publication date: November 1, 1999