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)

Neurohypophyseal hormnones and several synthetic analogs stimulate adenyl cyclase prepared from rabbit kidney medullary tissue. [8-Arginine]-vasopressinoic acid inhibits the stimulation of medullary adenyl cyclase by neurohypophyseal peptides but does not influence the action of parathyroid hormone on adenyl cyclase from kidiney cortex.
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PMID:[8-Arginine]-vasopressinoic acid: an inhibitor of rabbit kidney adenyl cyclase. 498 21

Receptors for calcitonin, determined by activation of adenylate cyclase, were found in a distribution among zones of the kidney distinct from that of receptors for parathyroid hormone or vasopressin. Competitive binding studies showed that the receptors for calcitonin are similar in kidney and bone and that their high apparent affinity for salmon calcitonin accounts in part for the high biological potency in vivo of salmon calcitonin.
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PMID:Calcitonin receptors of kidney and bone. 508 70

Adenyl cyclase from plasma membrane fractions of rat renal cortex or medulla was assayed by measuring conversion of adenosine triphosphate labeled at the alpha-phosphate with (32)P to cyclic 3',5'-adenosine monophosphate labeled with 32P. Parathyroid hormone activated the enzyme primarily in cortex; vasopressin acted primarily in medulla. These experiments support the conclusion that cyclic adenosine monophosphate mediates the action of parathyroid hormone on the kidney and show that parathyroid hormone and vasopressin stimulate adenyl cyclase at anatomically separable areas within the kidney.
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PMID:Renal adenyl cyclase: anatomically separate sites for parathyroid hormone and vasopressin. 563 60

The effect of age on the cyclic AMP (cAMP) response to increases in the concentration of arginine vasopressin in the presence of isobutyl methylxanthine (100 mumol/l) was studied in an in-vitro renal cell suspension prepared from C57BL/Icrfat mice at 6, 12, 18, 24, 29 and 35 months of age. Comparison of the response of the preparation to vasopressin, calcitonin and parathyroid hormone suggested that it was enriched with renal medullary cells. Basal cAMP output was similar throughout but the threshold dose of vasopressin increased from 1 X 10(-11) mol/l (6, 12 and 18 months of age) to 1 X 10(-10) mol/l (24, 29 and 35 months of age). The dose-response curve in 35-month-old mice was shifted to the right with the concentration of vasopressin required to give half maximal cAMP increased from 9.4 +/- 0.37 X 10(-11) mol/l (6 months) to 3.5 +/- 1.6 X 10(-10) mol/l (35 months). Maximum cAMP output at 1 X 10(-9) mol/l was also reduced in the same animals (stimulated:basal ratio, 51.22 +/- 19.12 at 6 months; 11.50 +/- 6.02 at 35 months). The results suggest that the lack of renal response to vasopressin in terms of cAMP metabolism may play a role in the well-documented age-related decline in urine-concentrating ability in experimental animals and elderly people.
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PMID:Effect of ageing on cyclic AMP output by renal medullary cells in response to arginine vasopressin in vitro in C57BL/Icrfat mice. 609 6

Effect of Ca2+ and parathyroid hormone (PTH) on 14 CO2 production from certain metabolic substrates by isolated glomeruli of rat kidney were examined. Increasing calcium concentration in the incubation medium inhibited 14CO2 production from 14C-labeled alpha-ketoglutarate and succinate, stimulated 14CO2 production from [1-14C]glucose and [1-14C]glutamate, but was without effect on that from [6-14C]glucose. PTH in the presence but not in the absence of Ca2+ inhibited 14CO2 production from labeled alpha-ketoglutarate and glutamate but not from labeled glucose. Additions of cyclic AMP as well as hormonal agents known to act directly on the glomureli, such as histamine, epinephrine, prostaglandin E2, vasopressin, angiotensin II and insulin, did not alter 14 CO2 production from labeled alpha-ketoglutarate. These data show the presence of calcium-dependent inhibitory actions on PTH on oxidation of alpha-ketoglutarate and glutamate which may be independent of cyclic AMP. These metabolic effects of PTH may underlie the alteration in the glomerular ultrafiltration coefficient and glomerular filtration induced by the hormone.
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PMID:Effect of parathyroid hormone and calcium ions on substrate oxidation by isolated glomeruli of the rat. 611 29

Studies to identify the physiological role of glomerular mesangial cells were undertaken using homogeneous cultures of rat glomerular cells of apparent mesangial origin (MS). Cultured MS cells were treated with arginine vasopressin (AVP), angiotensin II (AGII), prostaglandin E(2), and parathyroid hormone. AVP (0.1 nM) and AGII (1 nM) stimulated contraction of MS cells in vitro that was complete by 2 min at 37 degrees C or 10 min at 23 degrees C as observed by phase contrast and electron microscopy. Relaxation recurred 15 min after hormonal addition at 23 degrees C. Similar experiments in cloned rat glomerular epithelial cells or "renin"-producing cells did not demonstrate a contractile response. The contraction of MS cells was independent of cyclic AMP (cAMP) and cyclic 3',5'-guanosine monophosphate (cGMP) production, even when cyclic nucleotides were measured as early as 30 s after hormonal stimulation. To demonstrate that contraction was a function of hormone-receptor interaction, binding of [(3)H](8-lysine)vasopressin was studied. Specific binding for 1.6 and 5 nM hormone was both time- and dose-dependent. The estimated apparent affinity was 10 nM. In late MS cell passages (>16th) that no longer demonstrated hormone-stimulated contraction, no specific binding of [(3)H](8-lysine)vasopressin was observed. Incubations were modified to optimize the conditions for detecting the effect of hormones on cell cyclic nucleotide content. A supramaximal concentration of AVP (200 nM) increased the cAMP content of MS cells twofold in the presence of a phosphodiesterase inhibitor. Similar experiments with prostaglandin E(2) (1 mug/ml) led to a 1.5-6-fold increase in MS cell cAMP content, but no effect on contraction was observed. Neither hormone altered cGMP content. These data are further support for the independence of contraction and cyclic nucleotide production. Our studies suggest that MS cells are the equivalent of smooth muscle cells in the glomerulus and that their contraction may be important in control of glomerular filtration.
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PMID:Contraction of cultured rat glomerular cells of apparent mesangial origin after stimulation with angiotensin II and arginine vasopressin. 615 93

To investigate the direct actions and the possible cellular mechanisms of parathyroid hormone (PTH) and salmon calcitonin (sCT) action in inducing the desensitization of renal cAMP responses to these hormones, we studied kidney cells in primary culture. Renal cells isolated from neonatal rats were cultured in F-12 medium plus 100 microliters/ml calf serum. The cultured kidney cells reached confluent monolayer in 24 h and remained responsive to hormones, including PTH, sCT, vasopressin, and prostaglandin E1. Pretreatment of the cultured cells with PTH (2.5 X 10(-7) M) or sCT (3 X 10(-7) M) resulted in homologous desensitization in the cAMP responses to these hormones. Both PTH- and sCT-mediated desensitization were time and dose dependent. The EC50 for PTH-mediated desensitization was approximately 3.2 X 10(-9) M, and that for sCT was 2.0 X 10(-10) M. Cells that were desensitized to PTH or sCT showed normal responsiveness to cholera toxin, indicating that the catalytic and coupling units of the adenylate cyclase were not modified, suggesting that the locus for desensitization was at the receptor sites. We also found that the renal cell adenylate cyclase, after stimulation by PTH, was markedly different from that observed with sCT. The cAMP response to PTH was short-lived and readily reversible after removal of the hormone from the medium. Exposure to sCT resulted in stable activation of the adenylate cyclase system which was noted for several hours after the removal of sCT, sCT may form a stable complex with the receptors, thus activating the catalytic unit of the adenylate cyclase for a substantial period of time after removal of the hormone. This mechanism may account for the unique pharmacological efficacy of sCT.
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PMID:Rat kidney cells in primary culture: hormone-mediated desensitization of the adenosine 3',5'-monophosphate response to parathyroid hormone and calcitonin. 617 27

Tubular microperfusion experiments were performed in rats to examine the effects of thyroparathyroidectomy (TPTX), parathyroid hormone (PTH), antidiuretic hormone (ADH), and cyclic AMP (cAMP) on distal tubular Ca, Na, and water reabsorption. TPTX caused a significant decrease in the Ca reabsorptive rate as compared to intact animals. PTH (5 U/kg; 2 U x kg-1 x h-1) replacement in TPTX animals restored Ca transport to control levels. Application of either cAMP (10(-3) M) or 8-(p-chlorophenylthio)-cyclic 3',5'-adenosine monophosphate (10(-5) M) to the surface of the kidney caused a stimulation of Ca reabsorption similar to that produced by PTH. Neither TPTX nor PTH changed Na or water reabsorption significantly, whereas the cyclic nucleotides increased both of these parameters. These later actions of cAMP duplicated effects of ADH observed in these distal tubules.
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PMID:Effects of PTH, ADH, and cyclic AMP on distal tubular Ca and Na reabsorption. 625 79

Many biologically active peptides (e.g., insulin, nerve growth factor, ACTH, endorphin, parathyroid hormone, etc.) appear to be synthesized first as prohormones, which are then converted intracellularly to the biologically active products by various post-translational modifications. Peptides of neuronal origin (e.g., vasopressin and oxytocin) are synthesized by similar mechanisms. The prominent role of post-translational processing in determining the final peptide products allows for the possibility that different peptides will by generated from identical prohormones in different cells.
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PMID:Biosynthesis of neuronal peptides: implications for neurobiology. 625 90

Hormone-dependent adenylate cyclase activity was measured separately in the different nephron portions by combining the microdissection of collagenase-treated rabbit kidneys and the use of a single tubule enzyme microassay. The results obtained in the rabbit for vasopressin, parathyroid hormone, calcitonin, and isoproterenol are given and discussed. Each hormone stimulated adenylate cyclase activity in several well-localized segments of tubule according to a highly specific and reproducible pattern. Sharp transitions were generally noted between responsive and unresponsive nephron portions. In the rat kidney, the functional segmentation of the distal convoluted tubule was not as clearly delineated as in the rabbit kidney. Various nephron segments of the rat kidney were observed to contain glucagon-sensitive adenylate cyclase activity. When the results obtained for vasopressin are compared in rabbit, rat, mouse, and human kidneys, species differences are noted with respect to the responsiveness to arginine vasopressin in the medullary portion of thick ascending limbs of Henle's loops. It is concluded that biochemical approaches can be used as a means of investigating problems dealing with kidney physiology very near the cell level.
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PMID:Sites of hormone action in the mammalian nephron. 625 51


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