Affiliation:
1. Departments of Pediatrics and Physiology and Biophysics, State University of New York at Stony Brook, Stony Brook, New York 11794-8661
Abstract
To characterize the effects on the rat renal preglomerular microvasculature of insulin-like growth factor I (IGF-I), experiments were performed using the in vitro blood-perfused juxtamedullary nephron preparation. IGF-I induced a reversible vasodilation of pre- but not postglomerular microvessels in a dose-dependent manner (10−9–10−7M). The IGF-I-induced vasodilation was similar in all preglomerular vascular segments: interlobular artery, 11.5 ± 1.2% of control ( n = 16); mid-afferent arterioles, 11.6 ± 1.7% ( n = 24); and juxtaglomerular afferent segments, 16.1 ± 2.8% ( n = 19). Renal autoregulatory capacity was not reduced by IGF-I. Pretreatment with the nitric oxide (NO) synthase inhibitor N G-nitro-l-arginine methyl ester (10−4 M) completely inhibited the vasodilatory response to IGF-I. IGF-I induced a rapid increase of NO concentration in intact renal microvessels, monitored by a NO-selective voltametric microelectrode. Pretreatment with the cyclooxygenase inhibitor indomethacin (10−5 M) not only abrogated the IGF-I-induced dilation, but, moreover, IGF-I elicited a small but significant (∼10%) vasoconstriction in all preglomerular vessels. These results indicate that the renal vascular effects of IGF-I involve activation of two endogenous vasodilators (NO and vasodilatory prostaglandins). In addition, IGF-I may also release an undefined vasoconstrictor.
Publisher
American Physiological Society
Cited by
21 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献