Dopamine and norepinephrine increase venous return by stimulating alpha and beta adrenoceptors in the dog.

The cardiopulmonary bypass technique was used to compare the effects of dopamine and norepinephrine on venous return, and to identify the adrenoceptors involved in the responses. Intraarterial boluses of dopamine and norepinephrine produced similar increases in mean arterial pressure and similar increases in venous return, but dopamine required 10-30 x larger doses than norepinephrine to produce the same effect. Phenoxybenzamine virtually abolished the venous responses to the lowest doses of both agonists and diminished the venous responses to larger doses. Propranolol had little or no effect on venous responses to the low doses but substantially diminished the responses to larger doses. These results indicate that the increase in venous return produced by dopamine or norepinephrine involves both alpha and beta adrenoceptors. To determine whether the beta adrenoceptor belonged to subtype beta 1, the "selective" beta 2 agonist, salbutamol, was used. The reported affinity of salbutamol in dogs for arterial beta 2 receptors is fivefold greater than that for cardiac beta 1 receptors. However, the dose-response curves of salbutamol on the venous and arterial systems overlapped, indicating that the increase in venous return represents a combination of properties common to both beta 1 and beta 2 adrenoceptors.