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  • Title: Involvement of the vascular renin-angiotensin system in beta adrenergic receptor-mediated facilitation of vascular neurotransmission in spontaneously hypertensive rats.
    Author: Kawasaki H, Cline WH, Su C.
    Journal: J Pharmacol Exp Ther; 1984 Oct; 231(1):23-32. PubMed ID: 6149303.
    Abstract:
    This study was conducted to investigate the possible involvement of the vascular renin-angiotensin system in the isoproterenol (ISO)-induced facilitation of adrenergic neurotransmission in the mesenteric vasculature. The isolated, perfused mesenteric vascular beds from normotensive Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) were used for these studies. ISO at concentrations from 10(-9) to 10(-6) M caused significantly greater enhancement of the pressor response to periarterial nerve stimulation (PNS) in preparations from SHR than in those from WKY. The pressor responses to exogenous norepinephrine (NE) were, however, inhibited by ISO to a similar degree in preparations from both WKY and SHR. The enhancement of the PNS response produced by ISO was markedly attenuated by propranolol at 5 X 10(-7) M (nonselective beta receptor blocker) and by ICI 118,551 at 5 X 10(-7) M (selective beta-2 receptor blocker), whereas practolol at 5 X 10(-6) M (selective beta-1 receptor blocker) caused a potentiation of the ISO-induced enhancement of responses to PNS in preparations from both WKY and SHR. All three beta blockers generally abolished the ISO-induced inhibition of the pressor responses to exogenous NE. The selective beta-2 adrenergic receptor agonists, salbutamol (3 X 10(-8) to 3 X 10(-7) M) and terbutaline (10(-7) to 3 X 10(-7) M), caused significantly greater enhancement of the PNS response in preparations from SHR than in those from WKY, whereas the selective beta-1 agonist, dobutamine, caused only inhibition of the PNS responses in preparations from both WKY and SHR. These three agonists all tended to reduce the pressor responses to exogenous NE. The ISO-induced enhancement of the responses to PNS was also significantly reduced by either captopril (5 X 10(-6) M) or [Sar1-Ile8]angiotensin II (5 X 10(-7) M) in preparations from SHR. Neither captopril nor [Sar1-lle8] angiotensin II had an effect on the pressor response to NE infusion or on the ISO-induced inhibition of NE responses. Angiotensin I produced an enhancement of the pressor responses to PNS and to NE infusion with the effect being greater on the response to PNS than to NE in the preparations from SHR but not in those from WKY. This enhancement of the PNS response by angiotensin I was abolished by either captopril (5 X 10(-7) M) or [Sar1-Ile8]angiotensin II (5 X 10(-7) M) in preparations from both WKY and SHR.(ABSTRACT TRUNCATED AT 400 WORDS)
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