Division of BioMedical Sciences, Faculty of Medicine, Memorial University, St. John's, NL, Canada.
Vascul Pharmacol. 2010 Sep-Oct;53(3-4):144-50. doi: 10.1016/j.vph.2010.05.005. Epub 2010 Jun 4.
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.
在完整和去内皮的大鼠离体肺动脉中，研究了异丙肾上腺素对机械和电功能的影响。在完整的血管中，缓冲液酸化、存在钡（Ba2+）和/或哇巴因显著减弱了异丙肾上腺素诱导的松弛。异丙肾上腺素使血管平滑肌细胞超极化，将 E(m)从-61.0+/-0.44（n=190 个细胞）增加到-70.0+/-0.74 mV（n=31 个细胞；平均值+/-SE）。后一种效应被缓冲液酸化、四乙铵（TEA）、Ba2+和/或哇巴因抑制。异丙肾上腺素介导的松弛也被内皮细胞去除显著抑制。单独缓冲液酸化、Ba2+或哇巴因的存在并未导致去内皮组织中对异丙肾上腺素的松弛进一步抑制。然而，Ba2+和哇巴因联合使用导致去内皮组织中对异丙肾上腺素的松弛反应进一步抑制，类似于完整组织。联合使用 Ba2+、TEA 和哇巴因也导致对异丙肾上腺素的松弛反应显著抑制。与 Ba2+、TEA 和哇巴因联合在常规缓冲液中相比，将 Ba2+、TEA 或哇巴因包含在酸性缓冲液中并不会进一步抑制对异丙肾上腺素的松弛。血管去内皮导致血管平滑肌显著超极化（-67.4+/-0.35 mV；n=195 个细胞），这是由于 K 通道和 Na+/K+-ATP 酶的激活。在去内皮组织中，异丙肾上腺素无法进一步增加 E(m)（-68.8+/-0.44 mV n=36）。异丙肾上腺素诱导的超极化涉及平滑肌细胞 K 通道和 Na+/K+-ATP 酶的激活，可能是平行的，但相互依赖于内皮细胞的存在。
