Influence of endothelium on β-adrenoceptor-mediated mechanical and electrical functions in rat pulmonary artery

The effect of isoprenaline on mechanical and electrical functions was studied in intact and denuded rat isolated pulmonary arteries. In intact blood vessels, isoprenaline-induced relaxation was significantly attenuated by acidification of buffer, presence of Ba2+ and/or ouabain. Isoprenaline produced hyperpolarisation of vascular muscle cells increasing Em from − 61.0± 0.44 (n = 190 cells) to − 70.0 ± 0.74 mV (n = 31 cells; mean ± SE). The latter effect was inhibited by acidification of buffer, tetraethylammonium (TEA), Ba2+ and/or ouabain. Isoprenaline-mediated relaxation was also significantly inhibited by the removal of endothelial cells. Acidification of buffer, or the presence of Ba2+, or ouabain alone did not result in further inhibition of relaxation to isoprenaline in denuded tissues. However, Ba2+ and ouabain combined caused further inhibition of the relaxant responses to isoprenaline in denuded tissues analogous to intact tissue. Combined Ba2+, TEA and ouabain also caused substantial inhibition of relaxant response to isoprenaline. Inclusion of Ba2+, TEA or ouabain in acidic buffer did not further inhibit relaxation to isoprenaline when compared to Ba2+, TEA and ouabain combined in regular buffer. Denudation of blood vessels resulted in a significant hyperpolarisation of vascular muscle (− 67.4 ± 0.35 mV; n = 195 cells) due to the activation of K channels and Na+/K+-ATPase. In denuded tissue, isoprenaline was unable to further increase Em (− 68.8 ± 0.44 mV n = 36). Isoprenaline-induced hyperpolarisation involves activation of K channels and Na+/K+-ATPase of smooth muscle cells possibly in parallel but mutually dependent on the presence of endothelial cells.

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