Abstract
Recently we demonstrated that the NO pathway, not the prostanoid pathway is involved in flow-dependent relaxation in rat thoracic duct (TD). There are no direct investigations on the role of EDHF in the flow-mediated regulation of lymphatic contractility. Experiments on blood vessels suggest that the action of EDHF often involves the activation of K+ channels. We tested the hypothesis that potassium channels may be involved in the imposed flow-dependent modulation of lymphatic contractility. Diameters of isolated, cannulated and pressurized segments of rat TD were measured. Indices of the active lymph pump were determined. The influences of incrementally increased transmural pressure (from 1 to 5 cm H2O) and imposed flow (1 and 5 cm H2O transaxial pressure gradient) were examined before and after treatment by a non-selective K channel blocker - tetraethylammonium (TEA 10−4M and 10−3M). We found that TEA increased the contraction frequency and amplitude of contractions in TD segments in a dose-dependent manner, consistent with a role for K+ channels in determining the contraction frequency. During periods of imposed flow, TEA did not block the imposed flow-dependent inhibition of the active lymph pump. These findings demonstrate that potassium channels are not involved in the imposed flow-dependent modulation of lymphatic contractility, therefore potassium cannot be identified as EDHF in rat TD. NIH HL070308
Published Version
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