We have examined the responsiveness of alpha- and beta-adrenoceptors in aortae from 1.5, 3, 6 and 24 month old rats. The isometric contraction to phenylephrine was antagonised competitively by prazosin with a pA2 value of 9.45, suggesting that the receptor is an alpha 1-adrenoceptor. The potency of phenylephrine was significantly reduced in 24 months old as compared with all younger rats combined. The maximum contraction to phenylephrine was unaltered in 24 month old rats. The maximum contraction to potassium chloride was significantly less than that to phenylephrine only in 1.5 months old rats. In tissues contracted by potassium chloride, isoprenaline produced a marked relaxation in 1.5 months old animals, but there was a progressive loss with increasing age of the beta-adrenoceptor-mediated relaxation which was markedly reduced by 6 months and abolished in 24 months old. It is concluded that, in the rat aorta, there is a decrease in alpha 1-adrenoceptor responsiveness in senescence, and a loss of beta-adrenoceptor-mediated responses in maturation.

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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.

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