1. We investigated the role of vascular smooth muscle α-adrenoceptor subtypes in the vasoconstrictor response of femoral arteries and veins to dopamine and whether the vasoconstriction is modified by endothelium-dependent relaxation mediated via tile activation of α2-adrenoceptors in ring preparations of femoral arteries and veins from mongrel dogs. 2. Dopamine contracted both arteries and veins in a dose-dependent manner and this contraction was inhibited by pretreatment with phentolamine or prazosin. Pretreatment with yohimbine shifted the dose-response curve for dopamine to the right in femoral veins, but not in arteries. 3. Phenylephrine contracted femoral arteries and veins in a dose dependent manner and this contraction was inhibited by pretreatment with prazosin. 4. Clonidine produced a bell-shaped dose-response curve in femoral veins and this curve was shifted upwards by pretreatment with N(G)-nitro-L-arginine (L-NNA). In contrast, femoral arteries were not affected by clonidine. N(G)-Nitro-L-arginine potentiated contractile responses to dopamine in both veins and arteries. This potentiation was inhibited by yohimbine or by the removal of the endothelium in both arteries and veins. 5. These results suggest that dopamine contracts femoral arteries via stimulation of α1-adrenoceptors and contracts femoral veins via stimulation of both α1- and α2-adrenoceptors and that these contractions are attenuated by the vasodilator action of dopamine via α2-adrenoceptor-mediated release of endothelium derived relaxing factor.
|Number of pages||7|
|Journal||Clinical and Experimental Pharmacology and Physiology|
|Publication status||Published - 1998|
All Science Journal Classification (ASJC) codes
- Physiology (medical)