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)

Obviously, the analysis of dynamic changes in the hypothalamic activity of corticotropin-releasing factor (CRF) is essential for understanding of the central regulatory mechanism of ACTH secretion. However, the significance of the changes in CRF activity will be extremely lessened if the effect of CRF per se be modified at the pituitary level. In fact, Yates et al. (1971) reported that the CRF effect was potentiated by the presence of vasopressin. Therefore, in this study we attempted first to determine if vasopressin does potentiate the CRF action. Next, we analyzed some aspects of CRF dynamics in the rat hypothalamus under prolonged stress. (1) Potentiation of CRF action by vasopressin. This possibility was examined by the following approaches: i) Adrenocortical responses to various mild stressors (exposure to sound, i.p. injection of saline solution, tail cut) were greater in dehydrated rats than in normal controls. ii) Similarly, the adrenocortical response to intravenous injection of stalk-median eminence extract (SME) through the tail vein under Nembutal anesthesia was larger in the dehydrated rat than in control. iii) Prior to SME administration, vasopressin in a subthreshold dose was injected intravenously to assay rats pretreated with chlorpromazine (CPZ)-morphine (M)-Nembutal (Nb). The adrenocortical response to SME, injected into the carotid artery 1 min later, was found significantly to increase due to prior administration of vasopressin. iv) However, no potentiating effect of vasopressin was observed when SME and vasopressin (4 mU) were placed stimultaneously into the anterior pituitary tissue by the intrapituitary injection technique. v) In addition, no potentiating effect was observed in vitro incubation experiments under varying incubation conditions. Thus, it was shown that vasopressin has some potentiating effect on the stress response in vivo, but the effect is not at the pituitary level. (II) Analysis of dynamic changes in hypothalamic CRF activity. CRF activity was estimated by the intrapituitary injection method of Hiroshige, the plasma ACTH and corticosterone levels being followed simultaneously. Plasma ACTH was determined by radioimmunoassay partly with RCC-RIA Kit, and partly with ACTH antisera (kindly supplied by Dr. W.F. Ganong) by the method of Berson and Yalow. i) In intact normal rats, the response pattern of hypothalamic CRF activity under etherlaparotomy stress was characteristically biphasic, i.e., composed of rapid and slow phases, while the plasma ACTH and corticosterone showed a sustained high level over a 2 hr of observation period.
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PMID:[Analysis of dynamics of corticotropin-releasing factor (CRF) activity in the rat hypothalamus under stress]. 18 25

Responsiveness of cyclic adenosine 3':5'-monophosphate (cAMP) to parathyroid hormone, calcitonin, and vasopressin was studied in six human renal adenocarcinoma cell lines. Four of six renal adenocarcinoma cell lines showed increased cAMP content in response to calcitonin while the other two did not. Neither parathyroid hormone nor vasopressin increased the concentration of cAMP in each of these cell lines. The growth rate of KU-2 cells, which responded to calcitonin with an increase of cAMP content, was inhibited by calcitonin. On the other hand the growth rate of calcitonin-nonsensitive KH-39 cells was unaltered. The growth inhibitory effect of the hormone on KU-2 cells could be considered to be mediated by the increased cAMP levels from the following results: (a) there was positive correlation between the cellular cAMP content and growth inhibition after various amounts of calcitonin addition; (b) KU-2 growth was also suppressed by N6,O2'-dibutyryl cAMP; and (c) a group of KU-2 cells which had become resistant to calcitonin-induced growth inhibition showed a diminished cAMP increase in response to calcitonin.
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PMID:Calcitonin stimulation of cyclic adenosine 3':5'-monophosphate production with growth inhibition in human renal adenocarcinoma cell lines. 299 68

Vasopressin (AVP) is a hormone with antidiuretic properties that is also involved in cellular proliferation of breast, pulmonary, and pancreatic neoplasias, attributable to the interaction with specific receptors, among which is the V2-R. Using a culture model of CAKI-2 and A498 cancer cells, our study aimed to verify if renal carcinoma cells also express V2-R and whether receptor activation modulates their proliferation. Immunofluorescence and RT-PCR showed that both CAKI-2 and A498 cells effectively synthesize and express the V2-R. Administration of the vasopressin analogue DDAVP induced an evident growth in both CAKI-2 and A498 cell lines. However, this proliferative effect was completely avoided by the preventive addition of the V2-R antagonist SR121463B (satavaptan). Our study shows for the first time that renal cancer may effectively synthesize and express the V2-R. Furthermore, AVP exerts in vitro a proliferative effect by acting on this receptor, as the selective V2-R blockage is able to completely prevent the cellular growth. A validation of these findings with in vivo models is required to ascertain if the eventual presence of V2-R could influence the aggressiveness of human renal neoplasias. From this point of view, a new, interesting therapeutical application of V2-R antagonists in the treatment of renal cancer could also be proposed, similar to that successfully described in the treatment of autosomal polycystic kidney disease (ADPKD).
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PMID:Aquaretic inhibits renal cancer proliferation: Role of vasopressin receptor-2 (V2-R). 1921 6

Autosomal dominant polycystic kidney disease affects over 12 million people in the world and is the fourth cause of ESRD. It is the main monogenic kidney disease and causes the progressive formation of cysts leading to renal failure after a few decades. The main manifestations of the disease are observed even at a young age. The early sign of ADPKD is impaired urinary concentrating capacity, due to medullary alteration by cysts, and resistance to vasopressin. These anatomical alterations determine hyperfiltration, altered ammonium transport, nephrolithiasis, and, above all, hypertension even in pediatric age. Activation of the renin-angiotensin-aldosterone system has been shown responsible for the maintenance of high pressure values as well as the growth of cysts and renal fibrosis. Arterial hypertension would be responsible for ventricular hypertrophy. Many recent studies have confirmed the role of pressure control, especially if rigorous, in decreasing the progression of renal disease, and the use of ACE inhibitors seems to have higher efficacy than other antihypertensive drugs. The progression of renal disease is evidenced by the reduction of glomerular filtration which may be minimal in the early years, due to hyperfiltration, but, then, may even exceed 5 ml / min per year, especially when the total kidney volume (TKV) exceeds 1500 ml. In more rapid progression forms, ESRD may appear at about 55 years of age. The main risk factors are age, genetic mutation, familiarity with ESRD, macrohematuria episodes, and early onset hypertension. Some authors have proposed both genetic and clinical scores that can provide guidance on the probability of rapid progression. Other renal manifestations include kidney pain, nephrolithiasis, urinary tract infections and cyst hemorrhage. Renal cell carcinoma is a very rare event.
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PMID:[Renal manifestation of Autosomal Dominant Polycystic Kidney Disease]. 2958 57