Studies that question the existence of alpha-2 adrenoceptors in tail arteries of normotensive Sprague-Dawley rats.

Many pharmacological studies have demonstrated two distinct types of alpha adrenoceptor in the vasculature; these receptors have been named alpha-1 and alpha-2. In the present study, using isolated perfused tail arteries from normotensive Sprague-Dawley rats, we have demonstrated two types of alpha adrenoceptor but neither of these could be classified as an alpha-2 adrenoceptor. Dose-dependent contraction of rat tail arteries was produced by the following alpha adrenoceptor agonists or agonist-antagonist combination: phenylephrine (PE alpha-1), clonidine (alpha-1 and alpha-2), clonidine in the presence of 10(-7) M prazosin (alpha-2) and BHT-920 (alpha-2). The ED50 values for PE and clonidine were four orders of magnitude lower than those for clonidine plus prazosin and BHT-920. In addition, the action of PE was faster in onset than that of BHT-920, reached a higher maximum (5-fold) and attenuated more rapidly than that of BHT-920. The specific alpha-2 adrenoceptor antagonist yohimbine, in concentrations as high as 10(-6) M, did not antagonize arterial responses to BHT-920. However, responses to BHT-920 were antagonized by the alpha-1 adrenoceptor antagonist prazosin, in concentrations as low as 10(-10) M, and by the serotonin/alpha-1 adrenoceptor antagonist ketanserin (10(-7) M). These results suggest that the two alpha-adrenoceptor types in isolated rat tail arteries are both of the alpha-1 type. We also found that whereas responses to PE were stable and reproducible between 2 and 5 hr of arterial perfusion, responses to BHT-920 increased progressively over 5 hr. The latter effect probably resulted from a gradual disappearance of the arterial endothelium.