Premium
Inhibition by somatostatin of the vasopressin‐stimulated adenylate cyclase in a kidney‐derived line of cells grown in defined medium
Author(s) -
Roy Christian
Publication year - 1984
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(84)80304-x
Subject(s) - vasopressin , somatostatin , somatostatin receptor 3 , medicine , cyclase , endocrinology , vasopressin receptor , arginine vasopressin receptor 1b , arginine vasopressin receptor 2 , adenylate kinase , delta cell , somatostatin receptor , somatostatin receptor 1 , somatostatin receptor 2 , receptor , neuropeptide , chemistry , biology , stimulation , hormone , antagonist , glucagon
LLC‐PK 1L 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 [ 3 H]vasopressin binding suggesting an interaction of somatostatin with the vasopressin‐sensitive system distal to the hormone—receptor interaction. At variance with N 6‐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.