We studied the effects of dietary Ca2+ on blood pressure, survival, and calcium channel function to investigate cardiovascular disease mechanisms in stroke-prone spontaneously hypertensive rats. Beginning at 3 weeks of age, rats were fed high sodium chloride diets (8.0%) in combination with either high (2.0%) or low (0.2%) Ca2+ diets for 8 weeks. At 12 weeks of age, survival was 90% in the high Ca2+ group and 30% in the low Ca2+ group. The higher blood pressure and lower survival in the low Ca2+ group suggest an intensification of altered vascular muscle cell mechanisms by a dietary Ca2+ deficit. Nimodipine (1-10 nM) effectively blocked L-type Ca2+ currents in isolated vascular muscle cells from both groups. Contraction of isolated cells that were not patch clamped to high potassium solutions were also blocked by 1 nM nimodipine. Disappearance of the L-type Ca2+ channel current was accelerated by holding at depolarizing potentials (positive to -50 mV) and by depolarizing steps to 0 mV. Nimodipine block of the L-type Ca2+ currents in vascular muscle is believed to contribute substantially to antihypertensive properties and stroke prevention, actions that may develop fully only in stroke-prone spontaneously hypertensive rats on a diet of at least normal Ca2+.