Deleterious effects of purinergic P2X1 and P2X7 receptors (P2XR) in angiotensin II (AngII)-dependent hypertension include increased renal vascular resistance, and impaired autoregulation and pressure natriuresis. However, their specific effects on the determinants of glomerular hemodynamics remain incompletely delineated. To investigate the P2XR contributions to altered glomerular hemodynamics in hypertension, the effects of acute blockade of P2X1R, P2X7R and P2X4R with NF449, A438079 and PSB12054 respectively, were evaluated in AngII-infused rats (435 ng/kg/min). P2X1R or P2X7R blockade reduced afferent (6.85 ± 1.05 vs. 2.37 ± 0.20 Dyn.s.cm-5) and efferent (2.85 ± 0.38 vs. 0.99 0.07 Dyn.s.cm-5) arteriolar resistances, leading to increases in glomerular plasma flow (75.82 ± 5.58 vs. 206.7 ± 16.38 nl/min), ultrafiltration coefficient (0.0198 ± 0.0024 vs. 0.0512 ± 0.0046 nl/min/mmHg) and single nephron glomerular filtration rate (22.73 ± 2.02 vs. 51.56 ± 3.87 nl/min) to near normal values. Blockade of P2X4R did not elicit effects in hypertensive rats. In normotensive Sham rats, only the P2X1R antagonist increased plasma flow and single nephron glomerular filtration rate, whereas the P2X4R antagonist induced glomerular vasoconstriction consistent with evidence that P2X4R stimulation increases release of nitric oxide, from endothelial cells. Mean arterial pressure remained unchanged in both hypertensive and normotensive groups. Western Blot analysis showed overexpression of P2X1R, P2X7R and P2X4R protein in the hypertensive rats. While it has generally assumed that the altered glomerular vascular resistances in AngII hypertension are due to AT1 receptor-mediated vasoconstriction these data indicate a predominant P2X1R and P2X7R control of glomerular hemodynamics in AngII hypertension.