Effects of a voltage dependent calcium channel antagonist, nifedipine, on the responses of blood pressure, and secretion of atrial natriuretic peptide (ANP) and aldosterone to angiotensin II (Ang II) were compared in male Wistar and spontaneously hypertensive rats (SHR). A low, control or high sodium diet (2, 10 or 25 mmol Na/100 g diet) was fed for 6 weeks from the age of 6 weeks. On the morning of the experiment catheters were inserted under ether anesthesia in the femoral artery for pressure recording and blood sampling, and in the femoral vein for drug infusion. Ang II was infused at a rate of 250 ng/kg/min for 20 min. Nifedipine mixed with Ang II was infused at a rate of 16μg/kg/min for 20 min. Arterial blood samples were collected before and after infusion of Ang II with or without nifedipine. The control plasma level of aldosterone was inversely related to the amount of salt intake, whereas the plasma ANP level was not different between the salt groups. SHR showed a higher basal plasma ANP but a lower aldosterone concentration than Wistar rats. Infusion of Ang II produced a significant increase in blood pressure and plasma levels of aldosterone and ANP: The % increase was not significantly different either between the salt groups or between SHR and Wistar rats. SHR showed a greater pressor response to Ang II but a remarkably smaller decrease in heart rate after Ang II infusion than Wistar rats, With increasing sodium intake, the effect of Ang II on aldosterone secretion was decreased, whereas that on ANP secretion or blood pressure was not changed. Nifedipine decreased the responses of blood pressure and heart rate to Ang II in all groups. Nifedipine caused almost a complete inhibition of Ang II induced ANP secretion, but only a partial inhibition of Ang II induced aldosterone secretion or vasoconstriction. These results indicate that calcium dependent processes were involved in Ang II induced vasoconstriction, and secretions of aldosterone and ANP. However, the calcium dependent process far ANP secretion was considerably different from that for aldosterone secretion or vasoconstriction evoked by ang II. The ang II induced increase in ANP secretion appeared to be caused primarily by activating voltage-dependent calcium channels, whereas Ang II induced aldosterone secretion and vasoconstriction was not.