수소이온농도 변화의 수축물질에 따른 가토신동맥 수축에 미치는 영향과 기전

Effects of H₊ on the Contraction Induced by Various Agonists in the Renal Artery of a Rabbit

The effects of H⁺ on the arterial contraction and their mechanisms were investigated in the renal artery of a rabbit. The helical strips of isolated renal artery were immersed in the HEPES-buffered or CO₂/HCO₃^--buffered Tyrode s solution. The contractions induced by agonists (norepinephrine, histamine, serotonin and angiotensin II) or high K⁺ were observed with change of extracellular or intracellular H⁺ concentration. The contractions induced by norepinephrine, histamine, serotonin, angiotensin II or high K⁺ in HEPES-buffered Tyrode s solution were inhibited by increase in extracellular H⁺ concentration and potentiated by decrease in extracellular H⁺ concentration. The degrees of these effects were most evident in the contraction induced by serotonin and angiotensin II, moderate in those by histamine and high K⁺, and least in those by norepinephrine. Maximal contraction by norepinephrine, histamine and high K⁺ were not influenced by change in extracellular H⁺ concentration, but influenced in those contration by serotonin and angiotensin II. The attenuated contractions by an acidic pH were not returned to the level of contraction at normal pH (7.4) by elevation of extracellular =C²⁺ concentration. The agonists (norepinephrine, histamine and serotonin)-induced contractions in =C²⁺-free Tyrode s solution were also attenuated by increase in extracellular H⁺ concentration and potentiated by decrease in extracellular H⁺ concentration. Elevation of PCO₂ in the CO₂/HCO₃^--buffered Tyrode s solution, which increase the intracellular H⁺ concentration, at constant extracellular pH (7.4), increased the contraction by 30 mM K⁺. From the above results, it is suggested that the decrease in contractions by increase in extracellular H⁺ concentration may be resulted from that H⁺ make the receptors less sensitive to agonists and cell membrane hyperpolarize and then inhibit the =C²⁺ influx as well as =C²⁺ release from intracellular =C²⁺ storage site.