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1 Department of Nephrology and Hypertension, University Medical Center Utrecht, Utrecht, The Netherlands
* To whom correspondence should be addressed. E-mail: g.b.braam{at}azu.nl.
In spontaneously hypertensive rat (SHR), renal blood flow (RBF) has been reported to be very dependent upon 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 N-
-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 units) than WKY (105±4 mmHg and 10±0.5 units, respectively, p<0.05). Renal blood flow was similar (9.4±0.5 vs. 10.3±0.1 ml/min/gkw). 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 units vs. 17±1 units 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, NS) and decreased the lower limit to 63±2 mmHg (p<0.05) in the WKY. The degree of compensation as measure of autoregulatory efficiency attained at spontaneous perfusion pressures was comparable in SHR versus WKY, but with a shift of the curve towards higher perfusion pressures in SHR. Acute NOS blockade only increased the degree of compensation in WKY. Remarkably, UNOxV was significantly lower at spontaneous renal perfusion pressure in SHR. Following 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 renal perfusion pressure-induced changes in shear stress seems to be limited.
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