To investigate the role of decreased venous distensibility in the regulation of cardiac output, cardiopulmonary hemodynamic measurements were performed at rest and after a volume load (6% dextran in saline, 12 ml/kg iv) in 18 awake dogs with chronic one-kidney, one-wrapped hypertension and 9 normotensive control dogs. The distribution of blood volume between the peripheral and cardiopulmonary vascular beds and the increase in cardiac output after volume load in the two groups of dogs were the same. There was no echocardiographic evidence of left ventricular dysfunction (shortening fraction) in hypertensive dogs. The rise of heart rate after volume load in hypertensive dogs, 17 +/- 3 beats/min (mean +/- SE), was attenuated compared to that of control dogs, 38 +/- 4 (p less than 0.001). Compared to values in normotensive dogs, the in vitro left atrial pressure-volume curves of hypertensive dogs were shifted in the direction of the pressure axis (p less than 0.02). The findings do not provide a role for decreased venous distensibility in the regulation of cardiac output in chronic renal hypertension. Decreased distensibility of the left atrium may play a role in the pathogenesis of the attenuated Bainbridge effect in hypertensive dogs.