Postsynaptic αAl-Adrenoceptors in the Hypertensive Rat: Studies on Vascular ReactivityIn Vivoand Receptor BindingIn Vitro

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Abstract
An increase in vascular responsiveness (increase in diastolic blood pressure) to phenylephrine (PE), noradrenaline (NA) or angiotensin (AII) was seen in pithed SHR when compared with normotensive controls (WKY). This increase in vasoconstrictor effect was not seen with the postsynaptic α2-adrenoceptor agonists BHT 933 or TL 99. In SHR and DOCA-salt hypertensive rats prazosin was significantly more potent as an antagonist of α1-receptor mediated vasoconstriction (PE, or the endogenous release of NA by electrical stimulation of the spinal cord), and was also more potent against NA administered by i.v. injection, compared with normotensive controls. The potency of yohimbine against the postsynaptic α2-receptor mediated pressor responses to TL 99 was not significantly different in SHR or normotensive rats. Although these results indicate an apparent shift in the ratio of postsynaptic α1/α2-receptor mediated effects in hypertension in vivo, these effects were not correlated with any changes in α-receptor density (B max) nor affinity (KD) of the ligands 3H-prazosin or 3H-yohimbine in membranes prepared from SHR. The