1P241 Modulation of angiotensin II on sympathetic transmission in canine isolated, perfused splenic artery

• Published in: Journal of Pharmacological Sciences Vol. 91; no. suppl.1; p. 148
• Main Authors: Yan Xiao-Pin, Chiba Shigetoshi
• Format: Journal Article
• Language: Japanese
• Published: The Japanese Pharmacological Society 2003
• ISSN: 1347-8613

Angiotensin II (Ang II) has been known to facilitate the sympathetic adrenergic vasoconstriction by enhencement of noradrenaline (NA) release. Previous experiments in our laboratory demonstrated that periarterial electrical nerve stimulation induced a double-peaked vasoconstriction consisting of an initial transient, predominantly P2X-purinoceptor-mediated, constriction followed by a prolonged, mainly α1-adrenoceptor-mediated, response in the canine splenic artery. The purpose of this study was to determine the modulatory effects of exogenous and endogenous Ang II on the purinergic and adrenergic transmissions of double-peaked vasoconstrictions in the canine splenic artery. Ang II (0. 1 nmol) and Ang I (1 nmol) significantly potentiated the double-peaked vasoconstrictions, but did not affect the basal vascular tone and vasoconstrictor responses to exogenous NA and ATP. The potentiating effects of those were inhibited by KRH-594 (10 nM), a selective Ang II type I (AT1) receptor antagonist, but were not influenced by PD123319 (0. 1 p M), a selective Ang II type 2 (AT2) receptor antagonist. The treatment with enalapril (0. 1μM), an angiotensin converting enzyme inhibitor, abolished the effects of Ang I. The results indicate that the release of NA and ATP from sympathetically innervated canine splenic artery is enhanced by Ang II via activation of the prejunctional AT1 receptor subtype.