AJP - Renal Physiology, Vol 248, Issue 5 668-F673, Copyright © 1985 by American Physiological Society
Glomerular response to verapamil by isolated spontaneously hypertensive rat kidney
T. H. Steele and L. Challoner-Hue
We investigated the possibility that altered cell calcium regulation may
affect function of isolated Kyoto spontaneously hypertensive rat (SHR)
kidneys as compared with kidneys from Wistar-Kyoto control (WKY) rats. The
kidneys were perfused at 120 and 160 mmHg. At 120 mmHg, SHR glomerular
filtration rate (GFR) was 0.24 +/- 0.04 compared with WKY GFR of 0.70 +/-
0.10 ml/min (P = 0.001). At 160 mmHg, SHR GFR was 0.48 +/- 0.05 compared
with WKY GFR of 1.09 +/- 0.05 ml/min (P less than 0.001). At 120 mmHg,
addition of norepinephrine increased renal vascular resistance (RVR) by 50%
and decreased SHR GFR by 27% and WKY GFR by 57% (P = 0.04). At 160 mmHg,
norepinephrine elicited similar changes. Addition of verapamil, 5-10
microM, in the presence of norepinephrine returned RVR to 100-110% of
control. With verapamil at 120 mmHg, SHR GFR increased to 0.84 +/- 0.23
ml/min, a value 3.5 times that of control (P = 0.03). In contrast, WKY GFR
in the presence of norepinephrine and verapamil was 0.97 +/- 0.07 ml/min,
unchanged from control (P = 0.07). At 160 mmHg, norepinephrine and
verapamil also failed to increase WKY GFR above control (P = 0.4) but
increased SHR GFR to 52% above control (P = 0.03). Isolated SHR kidneys
exhibited exaggerated GFR responses to verapamil but not to norepinephrine.
Abnormal cell calcium regulation may underlie the marked decrease in GFR
when SHR kidneys are perfused acutely at normotensive perfusion pressures.
