In spontaneously hypertensive rats (SHR), oral antihypertensive doses of nifedipine exert potent inhibitory effects on pressor responses elicited by xylazine and angiotensin II, and by stimulation of the complete sympathetic outflow, suggesting that extracellular calcium is a prerequisite for responses to these stimuli. On the other hand, only those pressor responses to low doses of phenylephrine are affected by nifedipine, suggesting less dependence of phenylephrine on extracellular calcium. The results, therefore, indicate that postsynaptic alpha-adrenoceptors mediating pressor responses to neuronally released noradrenaline and phenylephrine may differ in their dependence on extracellular calcium, although they are both considered to be of the alpha 1-subtype. The evidence also suggests that this ability of nifedipine to inhibit pressor responses to neuronally released noradrenaline, as well as pressor responses to angiotensin II, contributes to the efficacy of this drug as an antihypertensive in SHR.