Experiments were performed to test for a possible role of arginine vasopressin (AVP) in the renal vascular responses to the combination of hypoxia and varying levels of CO2 in the conscious rat. Animals were instrumented with pulsed Doppler flow probes on the left renal artery and with arterial and venous catheters. Renal blood flow (RBF) and mean arterial blood pressure (MABP) were determined in conscious, unrestrained rats under the following conditions: 1) hypocapnic hypoxia [arterial PO2 (PaO2) = 26 Torr; arterial PCO2 (PaCO2) = 21 Torr]; 2) isocapnic hypoxia (PaO2 = 34 Torr; PaCO2 = 36 Torr); 3) hypercapnic hypoxia (PaO2 = 42 Torr; PaCO2 = 57 Torr); and 4) room air control (PaO2 = 93 Torr; PaCO2 = 38 Torr). MABP fell from 104 +/- 2 to 83 +/- 5 mmHg during hypocapnic hypoxia but was unaffected by the other stimuli. RBF was significantly reduced by both hypocapnic and hypercapnic hypoxia and unchanged in the other protocols, whereas renal vascular resistance (RVR) was elevated only in the hypercapnic hypoxia group. Additional experiments were performed to test whether activation of V1-vasopressinergic receptors during hypoxia might mediate the observed changes in renal hemodynamics. Experiments were performed as before except that at the midpoint of hypoxic or room air exposure, 10 micrograms/kg of the specific V1 vasopressinergic antagonist d(CH2)5Tyr(Me)AVP was administered. However, administration of the V1 antagonist had no effect on the observed renal hemodynamic responses to hypoxia. Therefore, although intense chemoreceptor stimulation by hypercapnic hypoxia may increase RVR and decrease renal perfusion, these renal hemodynamic responses do not appear to be mediated by increased circulating levels of AVP.