The current study was undertaken to determine whether receptors in the left ventricle are capable, when stimulated, of inhibiting plasma arginine vasopressin (AVP) in the conscious dog. Dogs were instrumented to measure aortic pressure and heart rate. In addition, a catheter was implanted in the left circumflex coronary artery. Left ventricular receptors were stimulated by the intracoronary infusion of veratrine, which evoked a hypotension and bradycardia. Control experiments consisted of intravenous infusion of veratrine. Plasma AVP, osmolality, and sodium and potassium concentrations were measured at intervals following the infusion. Similar experiments were done during the intravenous infusion of sodium nitroprusside (NP) to lower aortic pressure to the same extent as that seen with intracoronary infusion of veratrine. Experiments were also performed in chronic sinoaortic-denervated dogs. Intracoronary infusion of veratrine resulted in a significant decrease in aortic pressure from 93.9 +/- 2.8 to 70.5 +/- 4.5 mmHg. Control plasma AVP averaged 2.13 +/- 0.25 pg/ml and did not change significantly during this time. NP infusion lowered aortic pressure to a similar degree, and plasma AVP rose to 21.17 +/- 3.79 pg/ml after 5 min. There were no significant changes in any other plasma constituents. The results were similar in sinoaortic-denervated dogs. We conclude from the results of this study that receptors in the left ventricle are not capable of decreasing plasma AVP from low basal levels or from augmented levels.