Hyperosmolarity: effects on nerves and smooth muscle of cutaneous veins

Helical strips from dogs' saphenous veins were mounted in an organ bath (Krebs-Ringer solution, 37 degrees C) for isometric tension recording. Additional strips were incubated with [7-3H]norepinephrine and mounted for superfusion and isometric tension recording. The perfusate was collected every 2 min for estimation of total radioactivity and for column chromatographic separation of [3H]norepinephrine and its metabolites. Increasing osmolarity by sucrose caused a slow contraction that was maximal at 500-550 mosM and was accompanied by a reduction in total 3H efflux. The contraction was unaffected by a Ca2+-free medium, alpha-adrenegic blockade, and beta-adrenergic stimulaton. It was depressed by cooling (29 degrees C) and by anoxia combined with a glucose-free medium. Contractions elicited by K+ and Ba2+ were augmented by hyperosmolarity, but those caused by sympathetic nerve stimulation, tyramine, and norepinephrine were depressed. The output of [3H]norepinephrine during nerve stimulation was reduced. Thus, the hyperosmolarity causes 1) contraction of vascular smooth muscle, 2) augmentation of the contractile response to K+ and Ba2+, 3) depression of the excitation caused by norepinephrine, and 4) inhibition of the neuronal release of norepinephrine.

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