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  • Title: Influence of endothelium on beta-adrenoceptor-mediated mechanical and electrical functions in rat pulmonary artery.
    Author: Mahajan P, Tabrizchi R.
    Journal: Vascul Pharmacol; 2010; 53(3-4):144-50. PubMed ID: 20570752.
    Abstract:
    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 Ba(2+) and/or ouabain. Isoprenaline produced hyperpolarisation of vascular muscle cells increasing E(m) 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), Ba(2+) and/or ouabain. Isoprenaline-mediated relaxation was also significantly inhibited by the removal of endothelial cells. Acidification of buffer, or the presence of Ba(2+), or ouabain alone did not result in further inhibition of relaxation to isoprenaline in denuded tissues. However, Ba(2+) and ouabain combined caused further inhibition of the relaxant responses to isoprenaline in denuded tissues analogous to intact tissue. Combined Ba(2+), TEA and ouabain also caused substantial inhibition of relaxant response to isoprenaline. Inclusion of Ba(2+), TEA or ouabain in acidic buffer did not further inhibit relaxation to isoprenaline when compared to Ba(2+), 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 E(m) (-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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