An investigation of α‐adrenoceptor responsiveness in the vas deferens of spontaneously hypertensive rats

Abstract

1ax-Adrenoceptor-mediated responses were investigated in isolated vasa deferentia from spontaneously hypertensive rats (SHR) and normotensive Wistar rats (NWR). 2 There was no significant difference between NWR and SHR in the inhibition of the isometric contraction to single pulse field stimulation by M2-selective agonists in prostatic portions, nor by 2-selective agonists and the al-selective agonist, amidephrine in epididymal portions in the presence of nifedipine to prevent postjunctional actions of a-1-selective agonists.3 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 reducd in SHR. 4 The irreversible a,-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. 5 It is concluded that there is a reduced postjunctional a,-mediated responsiveness in the vas deferens of SHR due probably to a reduction in receptor number.

No evidence for differences between pre‐ and postjunctional α2‐adrenoceptors in the periphery

“…However, there were methodological differences between the present results and those of Hieble et al (1988): single pulse versus 0.1 Hz stimulation; prostatic portion versus whole vas; xylazine versus UK 14,304 as agonist. The isometric contraction of the prostatic portion of the rat vas deferens is nonadrenergic and unaffected by postjunctional a-adrenoceptor antagonism but can be augmented by postjunctional al-adrenoceptor agonism (see Docherty & Warnock, 1985). A similar prejunctional potency to the present result for SK&F 104078 in the rat vas deferens was obtained by Bertie et al, (1988).…”