Andriantsitohaina R, Andre P, Stoclet J C
Laboratoire de Pharmacologie, Cellulaire et Moléculaire, Unité de Recherche Associée Centre National de la Recherche Scientifique D0600, Université Louis Pasteur de Strasbourg, Faculté de Pharmacie, Illkirch, France.
Am J Physiol. 1990 Nov;259(5 Pt 2):H1427-32. doi: 10.1152/ajpheart.1990.259.5.H1427.
Pertussis toxin (PTX) was used to investigate the possible involvement of a G protein in the mechanism of action of neuropeptide Y (NPY) on rat mesenteric arterioles. ADP ribosylation of membrane protein was assessed by gel electrophoresis followed by autoradiography. The effect of NPY was studied on contractions elicited either by addition of calcium to depolarized vessels or by the calcium agonist BAY K 8644. Under conditions in which PTX ADP-ribosylated a 40-41 kDa protein, the potentiation of contractions induced by NPY in both protocols was abolished. In contrast, the contraction induced by norepinephrine was unaffected by PTX. It is concluded that a G protein mediates the potentiating effect of NPY on external calcium-dependent contractions in rat mesenteric arterioles.
百日咳毒素（PTX）被用于研究G蛋白是否可能参与神经肽Y（NPY）对大鼠肠系膜小动脉的作用机制。通过凝胶电泳和放射自显影评估膜蛋白的ADP核糖基化。研究了NPY对去极化血管中添加钙或钙激动剂BAY K 8644所引发收缩的影响。在PTX使一种40 - 41 kDa蛋白发生ADP核糖基化的条件下，两种实验方案中NPY诱导的收缩增强作用均被消除。相反，去甲肾上腺素诱导的收缩不受PTX影响。结论是，G蛋白介导了NPY对大鼠肠系膜小动脉中外源性钙依赖性收缩的增强作用。
