Cyclic AMP in the rat jugular vein: Relationship to vascular relaxation

Abstract

Most blood vessels contract to norepinephrine whereas the rat jugular vein relaxes. In the present study, we sought to determine if differences in the adenylate cyclase system accounted for the differing beta adrenergic responses of blood vessels. Cyclic AMP levels in the rat jugular vein incubated in vitro were lower than levels in the femoral vein or mesenteric artery. In the jugular vein, papaverine, an inhibitor of phosphodiesterase, produced a small, but not significant increase in cyclic AMP levels although in the femoral vein and mesenteric artery, cyclic AMP levels were doubled and tripled, respectively. Norepinephrine increased cyclic AMP only in jugular veins contracted with serotonin or in the presence of papaverine, whereas a marked increase in cyclic AMP occurred in the other vessels in the absence of serotonin or papaverine. In the presence of papaverine, the increase in cyclic AMP by norepinephrine in the jugular vein was less than in the other tissues. Neither the β 1-receptor antagonist, practolol, nor the β 2-receptor antagonist, N-isopropylmethoxamine, blocked the increase in jugular vein cyclic AMP produced by norepinephrine in the presence of papaverine. However, practolol and N-isopropylmethoxamine added together, significantly attenuated the norepinephrine-induced increase in cyclic AMP. These data indicate that relaxation of the rat jugular vein to norepinephrine is not associated with higher resting cyclic AMP levels, or a more responsive β-adrenergic-sensitive adenylate cyclase system.