Effect of potassium on adrenergic nerve endings in bovine mesenteric lymphatics

This work concerned the effect of KCl (60 mM) on noradrenaline efflux from aminergic nerve endings in bovine mesenteric lymphatics. In high potassium Krebs solution containing cocaine (10(-7) M), the lymphatics showed some phasic contractions followed by a tonic contraction with a high initial peak. The high KCl solution also caused a transient but statistically significant increase of tritiated noradrenaline efflux (P less than 0.01) which was not blocked by tetrodotoxin (10(-7) M). However, 5 X 10(-6) M 5-hydroxytryptamine or 10(-5) M prostaglandin F2 alpha produced a contraction of the lymphatic smooth muscle similar in magnitude to the contraction by 60 mM KCl. In this case, however, no increase was observed in 3H efflux. A Ca-antagonist, D-600 (10(-4) M) inhibited the potassium-induced rise in tritiated noradrenaline efflux and suppressed dose-dependently the contractile response to high potassium solution. These observations support the suggestion that the effect of KCl on 3H-release reflects an effect of kinetics of exchange across the nerve ending rather than an effect of contraction per se on isotope exchange through the complex extracellular matrix, and that the activation of Ca channels in the adrenergic nerve terminals may contribute to the release of noradrenaline in high KCl solution.