Y. Inishi et al., MODULATION OF RENAL HEMODYNAMICS BY IGF-1 IS ABSENT IN SPONTANEOUSLY HYPERTENSIVE RATS, Kidney international, 52(1), 1997, pp. 165-170
We recently reported that attenuation of vasoactive agent-induced calc
ium signal and cell contraction of mesangial cell by insulin-like grow
th factor 1 (IGF-1), observed in normal mesangial cells, is totally ab
olished in spontaneously hypertensive rat (SHR) mesangial cells. This
phenomenon might be related to the well-known aberrant regulation of S
HR glomerular hemodynamics. Since it has been reported that in vivo IG
F-1 infusion increases renal plasma flow (RPF) and glomerular filtrati
on rate (GFR), we examined whether the modulation of renal function by
IGF-1 is altered in SHR. We performed in vivo renal clearance studies
using eight-week-old SHR and control Wistar Kyoto rats (WKY) before a
nd after IGF-1 (5 mu g/kg) infusion into the left renal artery for 20
minutes. Mean arterial pressure was not affected by IGF-1 in both WKY
and SHR. In WKY, IGF-1 increased GFR and RPF, and decreased renal vasc
ular resistance (RVR). However, GFR, RPF, and RVR were not altered by
IGF-1 in SHR, while systemic infusion of angiotensin II antagonist, CV
-11974, increased GFR and RPF. The present data shaw that the modulati
on of renal hemodynamics by IGF-1 is absent in SHR. This might be rela
ted the pathophysiology of the development of hypertension.