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Am J Physiol Renal Physiol 274: F120-F128, 1998;
0363-6127/98 $5.00
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Vol. 274, Issue 1, F120-F128, January 1998

Effects of insulin-like growth factor I on the renal juxtamedullary microvasculature

Burkhard Tönshoff, Frederick J. Kaskel, and Leon C. Moore

Departments of Pediatrics and Physiology and Biophysics, State University of New York at Stony Brook, Stony Brook, New York 11794-8661

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 (10-9-10-7 M). 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.

renal microcirculation; nitric oxide; nitric oxide electrode; prostaglandins; renal autoregulation


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