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)

A new system was established using primary cultured mouse kidney epithelial cells to study the effect of PTH on renal tubular phosphate transport. The cells used in our study had alkaline phosphatase activity. They showed increased cAMP content in response to PTH, calcitonin, and vasopressin. Thus, these cells were thought to be a mixture of cells originating from the proximal and distal renal tubules. To explore the mechanism of phosphate handling in these cells, the accumulation of radioactive phosphate from the medium into the cells and the spaces between the cell layer and culture plate (submonolayer spaces) was measured. The accumulation of phosphate by the cells was a sodium-dependent, energy-dependent process, which was demonstrated by inhibition both in the absence of sodium and in the presence of ouabain or 2,4-dinitrophenol. Furthermore, phosphate accumulation was decreased significantly by PTH presumably acting through cAMP. PTH inhibited phosphate accumulation not by affecting the efflux process, but by affecting the uptake process through the apical membrane of the cultured cells without altering the compartmental mental distribution of the accumulated phosphate. These characteristics of phosphate accumulation resemble those of renal tubular phosphate transport.
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PMID:Establishment of a parathyroid hormone-responsive phosphate transport system in vitro using cultured renal cells. 302 32

LLC-PK1 cells, a permanent cell line of renal tubule origin, which has vasopressin (VP) receptors and an adenosine 3',5'-cyclic monophosphate (cAMP) response to VP were grown to confluence on glass cover slips and loaded for 30-45 min with fura-2. Exposure to fura-2 did not affect cell viability (greater than 99%), K+, or ATP levels. Free cytosolic Ca2+ (Caf) was estimated spectrofluorometrically on washed cover slips. Basal levels averaged 73 +/- 3 nM. Peak Caf levels induced were: 10(-8) M VP - 128 +/- 24 nM, 10(-7) M VP - 301 +/- 51 nM, 10(-6) M VP - 537 +/- 117 nM. Peak Caf after 10(-6) M VP was reached in 42 +/- 5 s, followed by a return toward basal levels. Addition of a second dose of 10(-6) M VP following an initial dose of 10(-6) M VP did not raise Caf. Chelation of medium Ca2+ with ethyleneglycol-bis(beta-aminoethylether)-N,N'-tetraacetic acid just prior to 10(-6) M VP did not reduce the response of Caf (peak of 359 +/- 53). In contrast to VP, 10(-6) M calcitonin and PTH did not significantly increase Caf. The response to 10(-6) M VP was not significantly modified by prior prostaglandin E2 (3 microM) or dibutyryl-cAMP (100 microM). The response to 1-desamino-8-D-arginine vasopressin was less than that to VP. However, studies with VP-receptor antagonists did not allow definitive delineation of receptor type. These data provide evidence for VP-induced increases of Caf via release from intracellular stores in a renal epithelial cell.
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PMID:Vasopressin-induced increases of cytosolic calcium in LLC-PK1 cells. 302 4

Both the native hormone and the aminoterminal 1-34 peptide of parathyroid hormone [PTH-(1-34)] are potent vasodilators of the coronary and hepatic circulations and, relatedly, produce marked hypotensive effects in a variety of animal species. In this report, a new technique for studying vasoactive substances was used to determine the nature of the vasodilator response of the aminoterminal peptide. The technique, an alternative to classical cylindrical segment or helical strip approaches, involved perfusion of a 4 to 5 cm segment of rat thoracic aorta at a constant flow rate with a circumferentially applied pulsatile "systolic" pressure of 100 mm Hg. Changes in perfusion pressure were indicative of changes in vascular resistance. The perfusate consisted of oxygenated physiological salt solution. Aortas were precontracted with high [KCl], norepinephrine, phenylephrine or arginine vasopressin. PTH-(1-34) elicited a concentration-related relaxation of vessels precontracted with the alpha agonists or [arg8]-vasopressin, but did not inhibit high K+ (3.5 x 10(-2) M)-induced contractions over the same dose range. Inhibition of prostaglandin biosynthesis with indomethacin did not alter the vasorelaxant properties of the peptide fragment. Endothelium-dependency of the PTH-(1-34)-induced vasorelaxant effect was assessed in untreated aortas and in tissues pretreated with saponin. Aortas pretreated with saponin, in which both scanning and transmission electron microscopy revealed extensive damage to or loss of endothelium, relaxed in a manner indistinguishable from nontreated control vessels. Thus, PTH-(1-34) relaxed precontracted perfused rat aortas in dose-dependent fashion. The vasorelaxant effects of the peptide fragment involved preferential relaxation of pharmacomechanically coupled vessels, and were not mediated by vasodilator prostaglandins or other specific endothelium-dependent mechanisms.
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PMID:Use of a new pulsatile perfused rat aorta preparation to study the characteristics of the vasodilator effect of parathyroid hormone. 336 14

There are a variety of water and electrolyte disorders in patients with cancer. These disorders occur during the growth of tumors, generally as a consequence of inadequate intake and absorption of electrolytes, renal failure secondary to tumor or rapid tumor destruction and production of metabolically active substances by the tumor. In this paper, the electrolyte abnormalities associated with cancer were reviewed. Hyponatremia is one of the most common clinical electrolyte abnormalities in advanced cancer. Some patients may have hyponatremia, in spite of increased total body sodium and absence of a defect in water diuresis. This status is designated as "sick cell syndrome" or "essential hyponatremia". In addition, the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in association with various tumors has been described. This syndrome is principally due to water retention, but can also be due to continuous urinary loss of sodium, and hypo-osmolality. Hypercalcemia is associated with coexistent primary hyperparathyroidism, prostaglandin (PGE2) or osteoclast-activating factor. It now seems likely that ectopic PTH is rarely the cause of hypercalcemia in nonparathyroid cancer. There are no data supporting the ectopic production of vitamin D-like substance as an important factor in the hypercalcemia of cancer. There are three general categories in which patients with hypercalcemia and cancer may be placed: those with bone metastases, those without bone metastases of solid tumors and those with hematologic malignancies. Hypokalemia is associated with ectopic ACTH- and insulin--producing tumors, and is often found in patients with mucin-secreting, potassium-losing adenocarcinoma of the colon.
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PMID:[Electrolyte abnormalities associated with cancer: a review]. 352 93

The biologically active PTH fragment 1-34 induces mononuclear leukocytes to produce a substance(s) capable of increasing bone resorption, as assayed in an organ culture system. The onset of the effect is evident at 2 days and lasts at least 7 days. The cell responsible for this effect appears to be an activated nonadherent lymphocyte (probably T-cell). PTH-(1-34) induces these cells to secrete this factor(s). The presence of adherent mononuclear leukocytes or appropriate conditioned medium appears to augment this response. Secretion of this factor(s) is specific for PTH-(1-34); it is not induced by biologically inactive PTH fragments, nor can it be induced by incubating mononuclear leukocytes with other hormones, including human PRL or lysine vasopressin. On the other hand, PTH-(1-34), human PRL, and lysine vasopressin all activate mononuclear leukocytes, as determined by [3H]thymidine incorporation. Biologically inactive PTH fragments do not. Thus, while lymphocyte activation may be a necessary prerequisite to lymphocyte modulation of bone resorption, it is not sufficient of itself. The PTH fragment 1-34 activates mononuclear leukocytes and specifically induces nonadherent lymphocytes to produce a substance(s) capable of increasing bone resorption. Preliminary characterization of this substance(s) shows that cellular components of the organ culture are necessary to demonstrate the increased resorptive capacity of PTH-stimulated lymphocyte supernatants. Secondly, this resorptive capacity is heat sensitive. Finally, this substance(s) appears to have a nominal molecular radius greater than 14,000 daltons, but less than 50,000 daltons.
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PMID:Parathyroid hormone-lymphocyte interactions modulate bone resorption. 376 72

The effect of endogenous renal prostaglandins on calcium and magnesium reabsorption was investigated. Renal tubular handling of calcium and magnesium was studied by clearance methods in anesthetized Sprague-Dawley and Brattleboro rats, either intact or thyroparathyroidectomized (ATPTX), before and during prostaglandin synthesis inhibition by meclofenamate, indomethacin, or piroxicam infusion. These three inhibitors had similar effects on calcium and magnesium excretion: A significant decrease in absolute and fractional excretions of both cations was observed in intact Sprague-Dawley rats, and in ATPTX rats of both strains, but not in intact Brattleboro rats. These results suggest an inhibitory effect of prostaglandins on vasopressin-, glucagon-, but not PTH-mediated calcium and magnesium reabsorption. This effect is likely to occur in the thick ascending limb of Henle, which is both a target site for these polypeptidic hormones, and a segment where the bulk of calcium and magnesium is reabsorbed.
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PMID:Decreased calcium and magnesium urinary excretion during prostaglandin synthesis inhibition in the rat. 387 57

The effects of glucagon and PTH on electrolyte reabsorption in the distal tubule were investigated in rats deprived of vasopressin, calcitonin, PTH, and glucagon. Micropunctures of distal tubule, at a late and an early site of a same nephron, have been performed in 23 rats, nine control, seven infused with glucagon (5 ng X min-1 X 100 g-1 b.w.) and seven with PTH (5 mU X min-1 X 100 g-1 b.w.). The Ca and Mg reabsorptive capacity of the distal segment was increased by glucagon and by PTH. Moreover, fractional Na and Cl reabsorption was significantly higher than in control during PTH administration. A K secretion appeared during the administration of both hormones. No phosphate net transport was observed in any group. Finally, the data presented here, together with those previously reported, indicate that the increase of Ca and Mg renal reabsorption observed with glucagon and PTH results from an effect located in both Henle's loop, where the bulk of Ca and Mg is reabsorbed, and the distal tubule.
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PMID:Stimulation by glucagon and PTH of Ca and Mg reabsorption in the superficial distal tubule of the rat kidney. 398 56

Circulating levels of calcium (Ca) and immunoreactive parathyroid hormone (IPTH), and the renal cyclic AMP responses to PTH, calcitonin (CT), and vasopressin (VP) were measured in fetal and neonatal rats. Serum Ca increased from a mean value of 9.1 mg/dl on the 19th day of gestation to 10.9 on day 20. Circulating IPTH decreased from 875 pg/ml to 213. Serum Ca declined rapidly after birth to a nadir of 7.6 by 3 h and IPTH increased to 2,006 pg/ml, indicating that fetal and newborn parathyroids are capable of responding appropriately to changes in circulating Ca. Renal responsiveness to hormones was assessed in vitro in the presence of methylisobutylxanthine, a phosphodiesterase inhibitor. The tissue cyclic AMP response to PTH and CT (15- to 18-fold over basal) was greatest at gestational days 18 and 19, progressively declined throughout the remainder of gestation, and remained low during the first 24 h after birth (6- to 7-fold). Renal cyclic AMP response to VP remained consistently low throughout this period. The depressed renal cyclic AMP response to PTH at the time of birth may contribute to the hypocalcemia found in newborn rats.
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PMID:Regulation of calcium homeostasis in the fetal and neonatal rat. 626 86

Using the single tubule adenylate cyclase microassay, we investigated in vitro in three different segments of the rat nephron whether the effects of various hormones are additive when these hormones are tested in combination. In the cortical portion of the thick ascending limb (CAL), no additivity of the effects of glucagon, calcitonin, and PTH was observed. In the medullary portion of the thick ascending limb (MAL), the effects of vasopressin and glucagon were only partly additive, and the effects of vasopressin and calcitonin were fully additive. In the cortical collecting tubule (CCT), the effects of calcitonin and vasopressin were nonadditive in the kidneys in which vasopressin alone induced a high cyclase stimulation, whereas they were fully additive when vasopressin induced a low cyclase stimulation. The data suggest that in each segment, the hormones tested stimulated the same cells: no additivity was observed when cyclase Vmax acted as the limiting factor of the response; partial or full additivity was observed when the number of hormone receptors acted as the limiting factor of the response. As a consequence, calcitonin, glucagon, and PTH should induce the same effects in CAL; vasopressin, glucagon, and calcitonin, the same effects in MAL; and vasopressin and calcitonin, the same effects in CCT.
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PMID:Multiple hormonal control of adenylate cyclase in distal segments of the rat kidney. 628 98

The effects of Tramadol-N2O-anaesthesia on the per- and postoperative change in blood concentrations of cortisol, prolactin, thyroxine, triiodothyronine, cyclic AMP, glucagon, antidiuretic hormone, PTH-peptide (44-68), glucose, lactate, pyruvate and free fatty acids (FFA) were investigated in connection with elective orthopaedic surgery. Anaesthesia in man with Tramadol and nitrous oxide were found to be associated with a significant elevation of plasma cortisol and plasma prolactin in man. However, cortisol secretion during anaesthesia is associated with an inhibition in T4-T3 conversion. No significant alterations in plasma glucagon concentrations were observed. Generally, surgical trauma induced a significant increase in plasma cyclic AMP with intraoperative levels between 26.4 and 34.3 pmol/ml. At the end of surgery a significant fall in plasma PTH-peptide (44-68) occurred. There was also a significant change in plasma ADH levels following induction of anaesthesia. During surgery we found plasma ADH levels up to 56 pg/ml. In addition stress and surgical trauma increased blood glucose and FFA while plasma pyruvate and plasma lactate nearly remained unchanged. The data would suggest that the non-specific stress response attributed to anaesthesia may in fact be reflecting a response to relatively light anaesthesia.
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PMID:[Endocrine reaction pattern in the course of a one-phase tramadol-N2O combination anesthesia]. 629 29


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