An investigation of alpha-adrenoceptor responsiveness in the vas deferens of spontaneously hypertensive rats.

alpha-Adrenoceptor-mediated responses were investigated in isolated vasa deferentia from spontaneously hypertensive rats (SHR) and normotensive Wistar rats (NWR). There was no significant difference between NWR and SHR in the inhibition of the isometric contraction to single pulse field stimulation by alpha 2-selective agonists in prostatic portions, nor by alpha 2-selective agonists and the alpha 1-selective agonist, amidephrine in epididymal portions in the presence of nifedipine to prevent postjunctional actions of alpha-1-selective agonists. There was no significant difference between NWR and SHR in the potency of amidephrine in causing a postjunctionally mediated potentiation of the isometric contraction to single pulse field stimulation in prostatic portions but the maximum potentiation was significantly reduced in SHR. However, the maximum potentiation of the isometric contraction by the calcium entry facilitator, Bay K 8644, was not significantly different between NWR and SHR. The maximum direct contraction to amidephrine, but not to Bay K 8644, was also significantly reduced in SHR. The irreversible alpha 1-adrenoceptor antagonist, phenoxybenzamine was more potent in SHR than NWR in reducing the maximum potentiation by amidephrine of the stimulation-evoked isometric contraction and in reducing the maximum direct contraction to amidephrine. It is concluded that there is a reduced postjunctional alpha 1-mediated responsiveness in the vas deferens of SHR due probably to a reduction in receptor number.