Rossi N F, Churchill P C, Churchill M C
Life Sci. 1987 Feb 2;40(5):481-7. doi: 10.1016/0024-3205(87)90114-7.
Adenosine analogs selective for the A1 subclass of adenosine receptors, such as N6-cyclohexyladenosine (CHA), inhibit renin secretion in in vitro preparations. Ca chelation blocks the inhibitory effect, consistent with mediation by increased intracellular free Ca2+, and it has been suggested that intracellular Ca2+ could increase as a result of receptor-induced inhibition of adenylate cyclase followed by decreased Ca efflux from the renin-secreting cells. Pertussis toxin blocks receptor-induced inhibition of adenylate cyclase in many cells, and in others, it blocks receptor-induced phosphotidylinositol response. In the present studies, pertussis toxin treatment stimulated the basal renin secretory rate of rat renal cortical slices and blocked the inhibitory effect of CHA but not the inhibitory effect of K-depolarization. These data support the hypothesis that a pertussis toxin substrate, such as Ni, is involved in CHA-, but not in K-depolarization, -induced inhibition of renin secretion.
对腺苷受体A1亚类具有选择性的腺苷类似物，如N6-环己基腺苷（CHA），可在体外制剂中抑制肾素分泌。钙螯合可阻断这种抑制作用，这与细胞内游离钙离子增加介导的作用一致，并且有人提出，细胞内钙离子的增加可能是由于受体诱导的腺苷酸环化酶抑制，随后肾素分泌细胞的钙外流减少所致。百日咳毒素可阻断许多细胞中受体诱导的腺苷酸环化酶抑制作用，而在其他细胞中，它可阻断受体诱导的磷脂酰肌醇反应。在本研究中，百日咳毒素处理可刺激大鼠肾皮质切片的基础肾素分泌率，并阻断CHA的抑制作用，但不阻断钾去极化的抑制作用。这些数据支持这样一种假说，即百日咳毒素底物，如Ni，参与了CHA诱导而非钾去极化诱导的肾素分泌抑制。
