Roy C
FEBS Lett. 1984 Apr 24;169(2):133-7. doi: 10.1016/0014-5793(84)80304-x.
LLC-PK1L cells, a kidney-derived cell line grown in defined medium, possess a vasopressin-sensitive adenylate cyclase. Somatostatin was able to inhibit the vasopressin-induced increase in adenylate cyclase activity, without affecting the basal enzyme activity. This inhibition was competitive. No effect of somatostatin could be detected on [3H]vasopressin binding suggesting an interaction of somatostatin with the vasopressin-sensitive system distal to the hormone-receptor interaction. At variance with N6-L-2-phenylisopropyladenosine (PIA), GTP did not potentiate the inhibition by somatostatin. The inhibition of the vasopressin stimulation by somatostatin and that by PIA were additive. Changing the composition of the cell growth medium increased the number of vasopressin receptors per cell. Cells with a high number of vasopressin receptors were less sensitive to inhibition by somatostatin. Such results suggested that somatostatin and vasopressin receptors and/or the inhibitory (Ni) and stimulatory (Ns) regulatory transducing components are regulated by different mechanisms.
LLC - PK1L细胞是一种在限定培养基中生长的肾源细胞系，具有对血管加压素敏感的腺苷酸环化酶。生长抑素能够抑制血管加压素诱导的腺苷酸环化酶活性增加，而不影响基础酶活性。这种抑制是竞争性的。未检测到生长抑素对[3H]血管加压素结合有影响，这表明生长抑素与血管加压素敏感系统在激素 - 受体相互作用远端存在相互作用。与N6 - L - 2 - 苯基异丙基腺苷（PIA）不同，GTP不能增强生长抑素的抑制作用。生长抑素和PIA对血管加压素刺激的抑制作用是相加的。改变细胞生长培养基的成分会增加每个细胞上血管加压素受体的数量。具有大量血管加压素受体的细胞对生长抑素的抑制作用不太敏感。这些结果表明，生长抑素和血管加压素受体和/或抑制性（Ni）和刺激性（Ns）调节转导成分受不同机制调节。
