Inhibitory action on alpha-human atrial natriuretic polypeptide on vascular adrenergic neurotransmission is attenuated in spontaneously hypertensive rats.

Publisher Website
Google Scholar
Abstract
The purpose of the present study is twofold, firstly to investigate the effects of alpha-human atrial natriuretic polypeptide (.alpha.-hANP) on norepinephrine overflow from sympathetic nerve endings, and secondly to compare vascular responsiveness in perfused mesenteric preparations in spontaneously hypertensive rats (SHR, Okamoto and Aoki, 7-9 weeks old) and a cohort of Wistar Kyoto rats (WKY). In preliminary studies using normotensive Wistar rats, the pressor responses to electrical nerve stimulation or exogenous norepinephrine application were inhibited by .alpha.-hANP. Norepinephrine overflow was also suppressed by .alpha.-hANP, during nerve stimulation. The pressor responses and norepinephrine overflow during nerve stimulation were significantly greater in SHR than in WKY rats. The inhibitory effect of .alpha.-hANP on these responses was reduced in SHR. These results indicate that .alpha.-hANP could affect both pre- and post-synaptic sites of the resistance vessels. Further, the reduced inhibition of pressor responses and norepinephrine overflow by .alpha.-hANP in SHR suggests an insufficient regulation of adrenergic transmission by .alpha.-hANP in hypertension.