TY - JOUR
T1 - Effects of insulin-like growth factor I on the renal juxtamedullary microvasculature
AU - Tönshoff, Burkhard
AU - Kaskel, Frederick J.
AU - Moore, Leon C.
PY - 1998/1
Y1 - 1998/1
N2 - 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.
AB - 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.
KW - Nitric oxide
KW - Nitric oxide electrode
KW - Prostaglandins
KW - Renal autoregulation
KW - Renal microcirculation
UR - http://www.scopus.com/inward/record.url?scp=0031892556&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0031892556&partnerID=8YFLogxK
U2 - 10.1152/ajprenal.1998.274.1.f120
DO - 10.1152/ajprenal.1998.274.1.f120
M3 - Article
C2 - 9458831
AN - SCOPUS:0031892556
SN - 1931-857X
VL - 274
SP - F120-F128
JO - American Journal of Physiology - Renal Physiology
JF - American Journal of Physiology - Renal Physiology
IS - 1 43-1
ER -