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The beta-action of catecholamines on lymphatic smooth muscle was studied by observing the effect of isoprenaline on electrical and mechanical activity in the double sucrose-gap. Action potentials and phasic contractions evoked by depolarizing pulses were abolished within 2 min of drug addition. Isoprenaline hyperpolarized the membrane and increased membrane conductance. Tetraethylammonium (10 mM) did not itself affect membrane resistance but reduced the hyperpolarization and the increase in conductance caused by isoprenaline. Removal of K+ from the external solution reduced membrane conductance and increased the hyperpolarization due to isoprenaline. When the NaCl content of Krebs solution was replaced with LiCl or choline chloride, isoprenaline no longer blocked action potential firing and its effects on phasic contractions and membrane conductance were reduced. In contrast, ouabain (10(-5) M) did not block the effect of isoprenaline on membrane potential and membrane conductance. These results suggest that beta-adrenergic inhibition of lymphatic smooth muscle involves an increase in an outward K+ current, though an additional metabolic effect cannot be ruled out.

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