Actions of angiotensin II and noradrenaline on smooth muscle cells of the canine mesenteric artery

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Abstract
The actions of angiotensin II (AngII) and noradrenaline (NA) on smooth muscle cells of the canine mesenteric artery were studied by measurement of isometric contractions recorded from muscle strips and the intracellular Ca2+ concentration monitored with quin2-fluorescence from dispersed suspensions of single cells. The Ca2+ transients provoked by the two agonists were monophasic in shape, i.e., after application of each agonist, [Ca2+]i rose immediately within 1 s and decreased to near-basal level within 5 min. The contraction induced by NA was maintained for several minutes whilst that induced by AngII was short-lasting. When NA was repetitively applied to the strip in Ca2+-containing solution, the same amplitude of contractions was always obtained. In contrast, after initial exposure to AngII, subsequently-applied AngII generated small contractions. In Ca2+-free solution, either agonist could induce the large contraction. After initial exposure to NA or AngII in Ca2+-free solution, subsequently-induced contractions by either agonist were reduced. The response induced by AngII was blocked by [Sar1, Ile8]-AngII and that of NA was blocked by phentolamine. Pertussis toxin inhibited contractions induced by both agonists but not those induced by caffeine and high K+. An activator of protein kinase C, 12-O-tetradecanoylphorbol 13-acetate (TPA), produced a slowly-developing contraction without any change in [Ca2+]i, and this agent inhibited the contractions and Ca2+ transients induced by both agonists. These results indicate that NA and AngII each act on a specific receptor and release Ca2+ from common intracellular storage sites through production of inositol 1,4,5-trisphosphate (InsP3). However, the actions of protein kinase C or the Ca2+-releasing mechanisms induced by InsP3 do not seem to be causally related to the generation of homologous desensitization induced by AngII.

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