MORIMOTO Satoshi
   Department   School of Medicine(Tokyo Women's Medical University Hospital), School of Medicine
   Position   Associate Professor
Article types Original article
Language English
Peer review Peer reviewed
Title Modulation of endothelin-1 coronary vasoconstriction in spontaneously hypertensive rats by the nitric oxide system.
Journal Formal name：American journal of hypertension
Abbreviation：Am J Hypertens
ISSN code：08957061/08957061
Domestic / ForeginForegin
Volume, Issue, Page 13(1 Pt 1),pp.83-7
Author and coauthor Miki S, Takeda K, Kiyama M, Hatta T, Moriguchi J, Kawa T, Morimoto S, Nakamura K, Itoh H, Nakata T, Sasaki S, Nakagawa M
Publication date 2000/01
Summary To determine whether nitric oxide contributes to the augmented vasoconstrictive response to endothelin-1 (ET-1) in coronary vessels of hypertensive hearts, and also whether L-arginine administration can inhibit the augmented response to ET-1, we designed experiments to measure coronary perfusion resistance in isolated hearts of spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) with or without L-arginine administration (0.5 g/L) for 2 weeks. The hearts were paced at a constant rate and perfused by the Langendorff technique at constant pressure (75 mm Hg). Perfusion flow and pressure were monitored, and coronary vascular resistance (CVR) was calculated. ET-1 infusion elicited dose-dependent increases in CVR in both WKY and SHR. At an ET-1 concentration of 1.5 x 10(-9) mol/L, the response was significantly greater in SHR. In L-NAME-treated WKY and SHR, responses to ET-1 were augmented, compared with those of nontreated rats, and this augmentation was greater in WKY. L-arginine administration reduced the CVR response to ET-1 in SHR, whereas it did not change responses to ET-1 in WKY. These findings suggest that the augmented vasoconstriction of the coronary artery induced by ET-1 in hypertensive hearts was due to a reduction in nitric oxide release in coronary vessels and that L-arginine can partially inhibit the vasoconstrictive response of the coronary artery.
DOI 10.1016/s0895-7061(99)00100-4
PMID 10678275