Studies on the possible causal relationship between the Ca<sup>2+</sup> channel current density in the vascular muscle cell (VMC) and increases in blood pressure were extended by a comparison of stroke-prone spontaneously hypertensive rats (SP-SHR) with N/nih outbred normotensive rats. Maximal amplitudes of both L-type and T-type Ca<sup>2+</sup> channel currents were significantly increased in SP-SHR without a difference in cell capacitance. SP-SHR peak current amplitudes in 20 mM Ba<sup>2+</sup> averaged 446 ± 64 pA while N/nih averaged 156 ± 25 pA (clearly separated statistically). Both L-type and T-type Ba<sup>2+</sup> currents (I<sub>Ba</sub>) were significantly increased in SP-SHR, shown also by peak current frequency distributions. There was a significant shift to the left of both activation (7 mV) and inactivation (15 mV) current-voltage (I-V) plots. SP-SHR I<sub>Ba</sub> recovery from inactivation was significantly slower (103 versus 61 ms) than in N/nih VMC. The increases in SP-SHR I<sub>Ba</sub> amplitude under maximized conditions correlated with increases in blood pressure. Together with earlier observations of increased vascular muscle Ca<sup>2+</sup> current density coexistent with blood pressure elevation in Kyoto-Wistar SHR, these data provide evidence for altered function of Ca<sup>2+</sup> channels as a fundamental component of hypertension. Since the Ca<sup>2+</sup> channel alterations exist in venous VMCs of newborn SP-SHR rats (in a low pressure blood vessel and at a time when increased Ca<sup>2+</sup> current density could not be an effect of increased blood pressure), our results add to the growing evidence of Ca<sup>2+</sup> channel abnormalities as a cause of genetic hypertension.