Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In isolated rat hepatocytes PMA, angiotensin II and to a lesser extent other hormones induce an early genetic response (increased expression of c-fos, c-mos, c-myc and beta-actin) without altering the expression of the glyceraldehyde 3-phosphate dehydrogenase gene. PMA, PDB and O-met-PMA, but not alpha-phorbol, stimulated c-fos expression. The effect of angiotensin II was inhibited by the AT1 antagonist, Losartan (DuP 753) (Ki approx. 25 nM), but not by the AT2 antagonist PD123177. Angiotensin II was much more effective than vasopressin or epinephrine in inducing proto-oncogene expression which suggests that angiotensin II receptors may exert actions in addition to those shared with the receptors for the other calcium-mobilizing hormones. The effect of PMA and angiotensin II on c-fos expression took place rapidly, with half times of 7 and 12 min, respectively. Actinomycin D markedly diminished basal c-fos expression whereas cycloheximide had the opposite effect. Actinomycin D diminished the effect of PMA and angiotensin II but it did not block them. PMA and the calcium-mobilizing hormones increased c-fos expression above the level observed with cycloheximide alone. These data suggest that PMA and the calcium-mobilizing hormones increased both transcription of the c-fos gene and stabilization of the proto-oncogene mRNA.
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PMID:Angiotensin II and active phorbol esters induce proto-oncogene expression in isolated rat hepatocytes. 152 Jul 5

Accelerated kidney growth and increased tissue Na content have been observed in rats fed a K-deficient diet. These observations suggest that enhanced Na influx could mediate renal growth, a hypothesis that was tested in cultures of kidney epithelial cells of the BSC-1 line. Reduction of the K concentration in the culture medium from 5.4 to 3.2 mM augmented cell growth and induced a transient increase in the cellular content of Na and a decrease in that of K. That low-K-induced growth was Na dependent was shown by decreasing the medium Na concentration from 155 to 150 mM, which abolished the increases in both growth and cell Na content in a concentration-dependent manner. The stimulation of glyceraldehyde-3-phosphate dehydrogenase (G3PD) activity that occurs in cells exposed to low-K medium for 1 h was similarly prevented by decreasing the medium Na concentration. Thus decreased availability of extracellular Na prevented the increase in cell Na content, stimulation of G3PD activity, and accelerated growth induced by low-K medium. The hypothesis was also tested by adding vasopressin to cultures of BSC-1 cells exposed to low-K medium; the hormone prevented the increments in cell Na content, G3PD activity, and growth to the same extent as did decreased availability of extracellular Na. These results are consistent with the interpretation that transient accumulation of Na is a critical determinant of the initiation of kidney epithelial cell growth.
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PMID:Na regulates growth of kidney epithelial cells induced by lowering extracellular K concentration. 649 22

Brain natriuretic peptide (BNP) messenger RNA was measured with a semiquantitative method from heart auricles and ventricles of vasopressin-deficient Brattleboro rats (DI) and from desmopressin treated Brattleboro rats (DI + DDAVP). Desmopressin had been injected peripherally and Long-Evans rats (LE) served as controls. The 3-day substitution treatment had shifted the fluid balance of DI almost to that of LE. In the present study, the amount of BNP mRNA, normalized to the glyceraldehyde-3-phosphate dehydrogenase mRNA content, was constant in all three groups in the right auricle. No changes were when the right auricular and left auricular mRNA levels were compared within each group. In the left auricle, desmopressin treatment increased significantly (P < 0.05) the amount of BNP mRNA compared with that of LE rats (from 1.09 +/- 0.21, n = 7 to 1.72 +/- 0.17, n = 8, arbitrary units). In all groups, the left ventricle had significantly (P < 0.05) higher mRNA content than the right ventricle (LE: 2.24 +/- 0.23 vs. 0.67 +/- 0.13, n = 6; DI: 2.30 +/- 0.60 vs. 0.33 +/- 0.05, n = 8; DI + DDAVP: 2.36 +/- 0.29 vs. 0.37 +/- 0.07, n = 10). In the right ventricle, both DI and DI + DDAVP rats had significantly (P < 0.05) lower mRNA content than LE rats (0.33 +/- 0.5 vs. 0.67 +/- 0.13 and 0.37 +/- 0.07 vs. 0.67 +/- 0.13, respectively). To conclude, these findings suggest that brain natriuretic peptide gene expression dissociates from, or rapidly adapts to, the chronic effects of peripheral desmopressin treatment which have shifted the fluid balance to almost normal in Brattleboro rats. The left ventricular pressure appears to regulate the brain natriuretic peptide gene expression.
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PMID:Brain natriuretic peptide (BNP) gene expression in the heart of vasopressin-deficient Brattleboro rats. 907 57

Arginine vasopressin (AVP) stimulates cortisol secretion through its vascular type V(1a) receptor in the adrenal glands, in addition to stimulating ACTH secretion through pituitary V(3) receptor. Because hyper-response of plasma cortisol to vasopressin is documented in some patients with Cushing's syndrome due to adrenal adenoma (CS) or ACTH-independent macronodular adrenocortical hyperplasia (AIMAH), we analyzed the expression of V(1a), V(2), V(3) receptor and AVP mRNA in human adrenal tissues by quantitative competitive RT-PCR or real-time PCRs. V(1a) receptor mRNA levels (ratio against glyceraldehyde 3-phosphate dehydrogenase) were 0.378 +/- 0.143 (mean +/- SE) in preclinical CS (n = 5) and 0.630 +/- 0.072 in AIMAH (n = 4), which were significantly higher than those (0.046 +/- 0.012; n = 9) in control adrenals, whereas those in overt CS (0.143 +/- 0.048; n = 10) or aldosterone-producing adenomas (0.069 +/- 0.018; n = 12) were similar to control adrenals. Although ectopic expression of V(2) or V(3) receptor was detected in half of AIMAH cases, the absolute levels were low. Furthermore, V(1a) receptor mRNA levels in the adjacent adrenal glands (0.190 +/- 0.039, n = 9) of aldosterone-producing adenomas were higher than those in control adrenals and in the corresponding tumor portions (0.079 +/- 0.024). In contrast, there were no significant differences in AVP mRNA levels among these groups. These results suggest that eutopic V(1a) receptor overexpression is involved in the etiology of AIMAH and a subset of adrenal adenomas causing overt or preclinical Cushing's syndrome. Our results imply a possible association of V(1a) receptor expression with adrenal hyperplasia.
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PMID:Eutopic overexpression of vasopressin v1a receptor in adrenocorticotropin-independent macronodular adrenal hyperplasia. 1246 75