Abstract
In spontaneously hypertensive rats (SHR), oral antihypertensive doses of nifedipine exert potent inhibitory effects on pressor responses elicited by xylazine and angiotensin II by stimulation of the complete sympathetic outflow, suggesting that extracellular Ca is a prerequisite for responses to these stimuli. Only those pressor responses to low doses of phenylephrine are affected by nifedipine, suggesting less dependence of phenylephrine on extracellular Ca. Postsynaptic .alpha.-adrenoceptors mediating pressor responses to neuronally released noradrenaline [norepinephrine]and phenylephrine may differ in their dependence on extracellular Ca, although they are both considered to be of the .alpha.1-subtype. This ability of nifedipine to inhibit pressor responses to neuronally released noradrenaline, as well as pressor responses to angiotensin II, apparently contributes to the efficacy of this drug as an antihypertnesive in SHR.