Role of alpha-1 adrenoceptor subtypes mediating constriction of the rabbit ear thermoregulatory microvasculature

An acute in vivo preparation of the microvasculature of the rabbit ear was used to evaluate the functional role of alpha1 (α1)‐adrenoceptor subtypes in thermoregulatory microcirculation. The effect of α1‐adrenoceptor subtype blockade on phenylephrine‐induced vasoconstriction was assessed with the α1A, α1B, and α1D‐adrenoceptor‐selective antagonists 5‐methyl‐urapidil (10−8 M), chloroethylclonidine (10−5 M), and 8‐[2‐[4(2‐methoxyphenyl)‐1‐piperazinyl]ethyl]‐8‐azaspirol[4.5]decane‐7,9‐dionedihydrochloride (BMY7378) (10−6 M), respectively. The results demonstrated that pretreatment of the ear microvasculature with 5‐methylurapidil or BMY7378 shifted the phenylephrine concentration‐response curve rightward and significantly changed the log of the phenylephrine concentration, causing half‐maximum stimulation (EC50) in arterioles (p < 0.05). BMY7378 shifted the phenylephrine concentration‐response curve of the arteriovenous anastomoses about 100‐fold rightward (p < 0.05). All three α1‐adrenoceptor antagonists eliminated the vasoconstrictive effects of phenylephrine on venules. The results indicate that the ear microvasculature has a heterogenous distribution of α1‐adrenoceptor subtypes. The α1A and α1D‐adrenoceptor subtypes appear to have a greater influence on constrictive function in arterioles, whereas the α1D‐adrenoceptor is the dominant constrictor of arteriovenous anastomoses. In general, the α1‐adrenoceptor does not play a major vasoconstrictor role in venules. Chloroethylclonidine, an irreversible α1B‐adrenoceptor antagonist, induced contractile responses in the ear microvasculature, probably due to its α2‐adrenoceptor agonist effects. This study extended our understanding of the adrenergic receptor control mechanisms of a cutaneous thermoregulatory end organ characterized by two parallel perfusion circuits providing nutritional and thrmoregulatory functions.