scholarly journals Renal vascular reactivity in the young spontaneously hypertensive rat.

Hypertension ◽  
1980 ◽  
Vol 2 (1) ◽  
pp. 45-52 ◽  
Author(s):  
M G Collis ◽  
C DeMey ◽  
P M Vanhoutte
Keyword(s):  
Vascular Reactivity ◽  
Spontaneously Hypertensive Rat ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Renal Vascular

Glomerular response to verapamil by isolated spontaneously hypertensive rat kidney

1985 ◽  
Vol 248 (5) ◽  
pp. F668-F673
Author(s):  
T. H. Steele ◽  
L. Challoner-Hue
Keyword(s):  
Spontaneously Hypertensive Rat ◽  
Rat Kidney ◽  
Calcium Regulation ◽  
Spontaneously Hypertensive ◽  
Cell Calcium ◽  
A Value ◽  
Hypertensive Rat ◽  
Wistar Kyoto ◽  
Altered Cell ◽  
Renal Vascular

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.

NO dependency of RBF and autoregulation in the spontaneously hypertensive rat

2003 ◽  
Vol 285 (1) ◽  
pp. F105-F112 ◽  
Author(s):  
Simona Racasan ◽  
Jaap A. Joles ◽  
Peter Boer ◽  
Hein A. Koomans ◽  
Branko Braam
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Lower Limit ◽  
Vascular Resistance ◽  
Spontaneously Hypertensive Rat ◽  
Renal Vascular Resistance ◽  
Renal Vasculature ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Renal Vascular

In the spontaneously hypertensive rat (SHR), renal blood flow (RBF) has been reported to be very dependent on nitric oxide (NO); however, autoregulation is normal, albeit shifted to higher perfusion pressures. To test the hypothesis that in the SHR NO dependency of RBF autoregulation is diminished, we investigated RBF autoregulation in anesthetized young male SHR and normotensive Wistar-Kyoto (WKY) rats before and during acute intravenous NO synthase (NOS) inhibition with Nω-nitro-l-arginine (l-NNA) and urinary excretion of nitrate plus nitrite (UNOxV) at different renal perfusion pressures (RPP). Under baseline conditions, SHR had higher mean arterial pressure (147 ± 4 mmHg) and renal vascular resistance (16 ± 1 U) than WKY (105 ± 4 mmHg and 10 ± 0.5 U, respectively, P < 0.05). RBF was similar (9.4 ± 0.5 vs. 10.3 ± 0.1 ml · min-1 · g kidney wt-1). Acute NOS blockade increased mean arterial pressure similarly, but there was significantly more reduction in RBF and hence an enhanced increase in renal vascular resistance in SHR (to 36 ± 3 vs. 17 ± 1 U in WKY, P < 0.001). The renal vasculature of SHR is thus strongly dependent on NO in maintaining basal RBF. The lower limit of autoregulation was higher in SHR than WKY in the baseline situation (85 ± 3 vs. 71 ± 2 mmHg, P < 0.05). Acute l-NNA administration did not decrease the lower limit in the SHR (to 81 ± 3 mmHg, not significant) and decreased the lower limit to 63 ± 2 mmHg ( P < 0.05) in the WKY. The degree of compensation as a measure of autoregulatory efficiency attained at spontaneous perfusion pressures was comparable in SHR vs. WKY but with a shift of the curve toward higher perfusion pressures in SHR. Acute NOS blockade only increased the degree of compensation in WKY. Remarkably, UNOxV was significantly lower at spontaneous RPP in SHR. After reduction of RPP, the observed decrease in UNOxV was significantly more pronounced in WKY than in SHR. In conclusion, the renal circulation in SHR is dependent on high levels of NO; however, the capacity to modulate NO in response to RPP-induced changes in shear stress seems to be limited.

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