Reduced alpha 1-adrenoreceptor mediated responsiveness in vas deferens from spontaneously hypertensive rats.

alpha-adrenoreceptor-mediated responses were investigated in isolated vasa deferentia from spontaneously hypertensive rats (SHR), Wistar Kyoto rats (WKY) and normotensive rats (NWR). There was no significant difference between NWR, WKY and SHR in the inhibition of the isometric contraction to single pulse field stimulation by the alpha 2-selective agonist xylazine in prostatic portions, nor by xylazine 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, WKY 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 contraction by the calcium entry facilitator, Bay K 8644, was not significantly different between NWR, WKY and SHR. The maximum direct contraction to amidephrine, but not to Bay K 8644, was also significantly reduced in SHR. It is concluded that the altered alpha 1-adrenoreceptor-mediated responsiveness in SHR is due not to genetic strain, but is presumably linked to development of hypertension.