We present evidence showing that renal blood flow (RBF) in the anesthetized nondiuretic rat can be measured reliably and accurately using a noncannulating flow transducer and an electromagnetic flowmeter. In vitro calibration yielded a linear relationship (r=0.998) between flowmeter output voltage and blood flow rates from 0.2 to 10.3 ml/min. Excellent agreement was observed between simultaneous determinations of RBF by the flowmeter and the PAH clearance technique. Glomerular filtration rate and RBF for a kidney with a flow transducer around its renal artery did not differ significantly from corresponding values for the undisturbed contralateral kidney. The relationship of mean RBF with steady-state variations in perfusion pressure was evaluated in 13 nondiuretic rats. RBF averaged 6 ml/min.g kidney wt at arterial pressures (AP) above 100 mmHg. A high degree of autoregulatory efficiency was observed when mean AP varied between 105 and 145 mmHg. Over this pressure range RBF changed only 3% as changes in intrarenal vascular resistance and AP were directly related (r=0.994). Below 95-105 mmHg RBF decreased in a curvilinear fashion with the concavity toward the pressure axis.
Using a small-diameter electromagnetic flow transducer, the effect on the autoregulation of renal blood flow (RBF) of two structurally different prostaglandin synthetase inhibitors, indomethacin, 4 mg/kg BW, and meclofenamate, 5 mg/kg BW, was studied in nondiuretic rats anesthetized with either the oxybarbiturate, sodium pentobarbital, or the thiobarbiturate, Inactin. Regardless of the anesthetic agent, RBF remained relatively constant above a perfusion pressure of 105 mmHg. Treatment with either indomethacin or meclofenamate had no measurable effect on the autoregulatory response. Each agent, however, resulted in an increase in the renal vascular response to exogenous angiotensin II, an effect consistent with prostaglandin synthetase inhibition. Base-line RBF was significantly reduced by indomethacin or meclofenamate only in those animals that had previously received angiotensin. These results support the hypothesis that, in th rat, autoregulation of RBF occurs independently of prostaglandin activity, but that a relationship does exist between the renal vascular actions of angiotensin II and prostaglandins.
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