Deleterious effects of purinergic P2X₁and P2X₇receptors (P2XRs) in ANG II-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 ANG II-infused rats (435 ng·kg⁻¹·min⁻¹). P2X₁R or P2X₇R blockade reduced afferent (6.85 ± 1.05 vs. 2.37 ± 0.20 dyn·s⁻¹·cm⁻⁵) and efferent (2.85 ± 0.38 vs. 0.99 ± 0.07 dyn·s⁻¹·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⁻¹·mmHg⁻¹), 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-operated rats, only the P2X₁R antagonist caused an increase plasma flow and single-nephron glomerular filtration rate, whereas the P2X₄R antagonist induced glomerular vasoconstriction that was 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 proteins in hypertensive rats. Whereas it has been generally assumed that the altered glomerular vascular resistances in ANG II hypertension are due to AT₁receptor-mediated vasoconstriction, these data indicate a predominant P2X₁R and P2X₇R control of glomerular hemodynamics in ANG II hypertension.