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P2 Purinoceptor Saturation by Adenosine Triphosphate Impairs Renal Autoregulation in Dogs

Department of Physiology, Tulane University School of Medicine, New Orleans, Louisiana.

Correspondence to Dr. Dewan S. A. Majid, Department of Physiology, SL39, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112. Phone: 504-584-2600; Fax: 504-584-2675; E-mail: majid{at}mailhost.tcs.tulane.edu

Abstract. Recent studies have suggested a role for P2 purinoceptors on vascular smooth muscle cells in the mechanism of renal autoregulation. Experiments were performed in anesthetized dogs (n = 9) to examine renal blood flow (RBF) auto-regulatory efficiency before and after saturation of P2 purinoceptors with acute intra-arterial administration of ATP (1 mg/kg per min). Dogs were pretreated with the nitric oxide synthase inhibitor nitro-L-arginine (NLA) (50 µg/kg per min), to avoid endothelial P2 receptor-mediated effects on nitric oxide release caused by the intra-arterial ATP infusions. NLA treatment decreased RBF (5.3 ± 0.3 to 3.6 ± 0.2 ml/min per g) and sodium excretion (3.6 ± 0.4 to 0.9 ± 0.2 ml/min per g) without producing significant changes in GFR (0.92 ± 0.04 to 0.90 ± 0.06 ml/min per g) or RBF autoregulatory efficiency. ATP administration to NLA-treated dogs resulted in further decreases in RBF (2.8 ± 0.2 ml/min per g), GFR (0.58 ± 0.05 ml/min per g), and sodium excretion (0.6 ± 0.2 µmol/min per g). In addition, there was marked impairment of RBF autoregulatory efficiency during ATP infusion. The slopes of the arterial pressure-blood flow relationships at renal arterial pressures of >75 mmHg were significantly altered, from 0.003 ± 0.001 to 0.2 ± 0.002 ml/min per g per mmHg. Discontinuation of ATP infusion restored RBF autoregulatory efficiency. Norepinephrine (5 µg/kg per min) administration in these NLA-treated dogs decreased RBF (2.5 ± 0.3 ml/min per g; n = 4) to a similar extent, compared with ATP, but did not impair RBF autoregulation. These results support the hypothesis that P2 purinoceptors may be involved in mediating autoregulatory adjustments in renal vascular resistance.

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