UNIPROT:P01185 - FACTA Search

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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We modified and improved enzyme digestion and density gradient separation procedures to obtain fractions of proximal and distal renal tubules with high yield and viability. Kidneys from two anesthetized adult Wistar rats were flushed with Krebs-Henseleit buffer (KHB) and then perfused in situ with recirculated KHB containing collagenase and hyaluronidase at 125 mmHg. Cortices were excised, minced, and incubated in KHB containing enzymes for 35 min at 37 degrees C. Dissociated tubules were removed at 10-min intervals, rinsed, and placed in KHB containing 10% calf serum, vitamins, and amino acids at 4 degrees C. Separation was achieved by suspending the tissue in 45% isosmotic Percoll layered over an undiluted Percoll cushion and centrifuging. Proximal tubules sedimented near the cushion. Distal segments were isolated in the uppermost bands of a second 35% Percoll separation. Viability was greater than 95% as measured by lactate dehydrogenase leakage and quantitated by oxygen consumption and ATP content. Basal oxygen consumption was greater than 33 nmol O2 X min-1 X mg protein-1 in all fractions and was stimulated by succinate and inhibited by amiloride and ouabain. Basal ATP content averaged 9.7 nmol/mg ATP. An average 3.3-fold separation for the proximal fraction and 24.5-fold separation for the distal fraction was assessed by the enrichment of six specific enzyme markers, with several of the markers indicating separations up to 32-fold. Isolated tubules also displayed functional responses to parathyroid hormone and vasopressin. Distal, but not proximal, segments demonstrated significantly increased adenosine 3',5'-cyclic monophosphate formation with vasopressin.
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PMID:Improved separation method for rat proximal and distal renal tubules. 303 59

We recently demonstrated that parathyroid hormone (PTH) inhibited both vasopressin- and cyclic AMP-stimulated water transport in the toad bladder. This was associated with an increase in calcium uptake by isolated epithelial cells. We postulated that PTH exerts its action on H2O transport by directly stimulating calcium uptake. The current study was designed to compare the effects of PTH and the calcium ionophore, A23187, on H2O and Na transport and H+ secretion in toad and turtle bladders. In toad bladder, PTH and A23187 decreased arginine vasopressin (AVP)-stimulated H2O flow and short-circuit current (SCC) after 60 min serosal incubation. In turtle bladder A23187 decreased SCC to 79.3 +/- 3.6% of base line (P less than 0.05), and significantly decreased RSCC as well. PTH had no effect on SCC or H+ secretion in turtle bladders. Both PTH and A23187 increased 45Ca uptake in toad bladder epithelial cells; only A23187 increased 45Ca uptake in the turtle bladder. The different action of PTH in these two membranes, compared with that of the calcium ionophore, illustrates the selectivity of PTH on membrane transport. PTH increases calcium uptake and decreases transport only in a hormone-sensitive epithelium, whereas the ionophore works in virtually all living membranes. The mode of action of these two agents to increase calcium uptake is, therefore, likely different.
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PMID:Effect of parathyroid hormone on transport by toad and turtle bladder. 310 19

Following ureteral obstruction there is a progressive fall in glomerular filtration rate (GFR) due to a reduction in single nephron glomerular filtration rate (SNGFR) and a reduced number of filtering nephrons. Renal plasma flow also declines after a transient, prostaglandin-dependent increase, due to afferent and efferent arteriolar vasoconstriction. The vasoactive hormones thromboxane A2 and angiotensin II are implicated in the pathogenesis of the vasoconstriction following ureteral obstruction and they also reduce the glomerular ultrafiltration coefficient by causing mesangial contraction. Ureteral obstruction also leads to profound changes in renal tubular cell function. These include altered sodium and water handling resulting in a post-obstructive diuresis and natriuresis and a failure to dilute or concentrate the urine. Potassium and divalent cation exchange is also affected, as is urinary acidification. Furthermore, the response of the tubule to hormones such as antidiuretic hormone and parathyroid hormone is impaired. The pathophysiology of these alterations in renal function is discussed.
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PMID:Effects of obstruction on renal functions. 315 99

LLC-PK1L cells, a kidney-derived cell line, were able to grow in a chemically defined medium. Growth of the cells in the presence of retinol, ergocalciferol, d-alpha-tocopherol, 3,3',5-triiodothyronine, hydrocortisone, l-carnitine, d-l-methionine-S-methylsulfonium chloride, insulin, transferrin, cholesterol, and sodium linoleate increased the number of vasopressin receptors by 20- to 40-fold. All the newly detectable vasopressin receptors were coupled to the adenylate cyclase activity with similar efficiency. The same growth conditions did not alter the basal adenylate cyclase activity or the responses to calcitonin, parathyroid hormone, prostaglandin, adenosine, and GTP. In contrast, the increased responsiveness of the adenylate cyclase to vasopressin was associated with a reduced response to isoproterenol. Such an inverse correlation was also found when the time course of vasopressin receptor induction was studied. The supplemented medium permitted the growth of cells for several weeks. The effects of the enriched medium were fully reversible when we returned to the original cell growth medium. Thus such a cellular system appears as a useful tool for further work in cellular and kidney endocrinology and for detailing the molecular mechanisms of receptor-adenylate cyclase regulations.
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PMID:Regulation of hormonal responsiveness in LLC-PK1L cells grown in defined medium. 315 11

Four male divers were exposed to an environment of 1 ATA air for 7 d, followed by 7 d of 31 ATA He-O2, and following decompression to a postdive 1 ATA air environment for 3 d. Urine and blood were collected for hormonal measurements. Divided 24-h urine collections were obtained during 3 consecutive d at predive 1 ATA conditions, and at 31 ATA conditions. Two consecutive day collections were obtained at early decompression (31-25 ATA), at late decompression (14-8 ATA), and at postdive 1 ATA. Two blood samples were obtained, at predive 1 ATA, at 31 ATA, and at postdive 1 ATA. Plasma antidiuretic hormone (ADH) concentration decreased about 45% (P less than 0.005), while plasma aldosterone concentration and urinary aldosterone excretion were doubled (P less than 0.005) after the subjects were at 31 ATA. Plasma cortisol concentration and plasma parathyroid hormone concentration were not significantly affected by hyperbaria. Urinary excretion of aldosterone was not significantly different between day (0700-1900) and night (1900-0700) at any time, and both day and night excretion rates were increased at 31 ATA through late decompression (P less than 0.005). Urinary ADH excretion was greater during daytime at predive 1 ATA (P less than 0.005), but not thereafter. Both daytime and nighttime ADH excretion rates were decreased from 31 ATA through late decompression (P less than 0.005). It is concluded that hyperbaria eliminates the circadian release pattern of ADH and that the overall reduction of ADH may contribute to the increased free water clearance observed at hyperbaria. Also, increased parathyroid hormone was not associated with the phosphaturia observed at hyperbaria, but increased aldosterone coexisted with the increased kaliuresis observed.
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PMID:Seadragon VI: a 7-day dry saturation dive at 31 ATA. III. Alterations in basal and circadian endocrinology. 331 55

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

Because the rat papilla has parathyroid hormone (PTH)-sensitive adenylate cyclase and because of indirect evidence that PTH may alter collecting duct water and also calcium transport, the effects of PTH on rat papillary collecting duct water and calcium transport have been studied. PTH in concentrations of 50 and 500 ng/ml significantly increased diffusional water permeability by 20 and 38%, respectively, while 5,000 ng/ml had no additional effect. This permeability response was small when compared to a 78% increase in water permeability with a maximal (0.5 ng/ml) concentration of antidiuretic hormone (ADH). The normal increase in water permeability with ADH was depressed in the presence of PTH (500 ng/ml) but was overcome when the ADH concentration was increased from 0.5 to 5 ng/ml. Neither PTH nor ADH altered the permeability of the collecting duct to calcium which was low (0.19 +/- 0.03 micron/s). Increasing either the bath or perfusate calcium concentration from 1 to 5 mM did not alter calcium permeability. These studies suggest that PTH acts as a partial agonist to ADH within the papillary collecting duct and that PTH is unlikely to have a major role in collecting duct calcium transport.
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PMID:Effect of parathyroid and antidiuretic hormone on water and calcium permeability in the rat collecting duct. 338 69

Clearance experiments were performed to characterize the sensitivity to vasopressin of the thick ascending limbs and collecting duct system of the rat kidney. The response of the thick ascending limbs was evaluated by measuring the Mg2+ excretion rate in the urine, since the [arginine-8] vasopressin-mediated effects on Mg2+ excretion are the direct result of a stimulation of Mg2+ reabsorption in this nephron segment, and the response of the collecting ducts was evaluated by changes in urine flow. To avoid the effects of parathyroid hormone, glucagon, and calcitonin, which stimulate Mg2+ reabsorption in the thick ascending limb and distal tubule, and of calcitonin, which increases the permeability of the cortical collecting ducts to water, experiments were performed on Brattleboro D. I. rats (with hereditary diabetes insipidus, due to a lack of [Arg8]vasopressin) acutely deprived of endogenous parathyroid hormone, calcitonin, and glucagon. Vasopressin infused at rates up to 5 pg/min did not reduce the Mg2+ fractional excretion rate, whereas at 5 pg/min water excretion was decreased by 50%. The half-maximal reduction of Mg2+ excretion occurred at vasopressin infusion rates 4-6 times higher than those necessary to diminish the water excretion rate to the same extent. We conclude that in vivo, two segments involved in the production of concentrated urine have different sensitivities to vasopressin and that this difference in sensitivity is very similar for the biological response in vivo and the adenylate cyclase activation in vitro. We suggest that both the magnitude and the nature of the effects of [Arg8]vasopressin on the kidney may vary according to the required antidiuretic response.
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PMID:Sensitivities of rat kidney thick ascending limbs and collecting ducts to vasopressin in vivo. 345 86

We investigated by micropuncture the effects of glucagon and parathyroid hormone (PTH) on thin limbs of juxtamedullary nephrons of rats with reduced plasma concentration of endogenous glucagon, PTH, antidiuretic hormone (ADH) and calcitonin, all four hormones enhancing the adenylate-cyclase activity in the thick ascending limbs and the distal nephron. Such a hormonal depletion suppresses the corticomedullary concentration gradient, making favourable conditions for studying the influence of these hormones on the renal concentrating mechanism. Administration of glucagon (4.4 ng/min-1) or PTH (5 mU/min-1) to these hormone-deprived rats elicited the expected decrease in urinary Mg and Ca fractional excretion without modifying either fractional or absolute excretion of water. At the tip of the loop, glucagon enhanced the loop fluid osmolality by 20%, but left the delivery of water unchanged. The Na and Cl concentrations increased significantly with the osmolality, resulting in a positive correlation between the fractional delivery of either ion and the loop fluid osmolality. PTH increased the fraction of filtered phosphate delivered to the thin limbs, as expected, but, in contrast to glucagon, did not alter either the Na, Cl, or total solute fractional deliveries. The Mg, Ca and K deliveries were unaffected by glucagon and PTH. In conclusion, glucagon, which activates the cyclase system of both the medullary and cortical portion of the thick ascending limb, enhances the delivery of salt to the tip of the loop by net sodium chloride addition to the descending limb. PTH which activates the adenyl-cyclase system only in the cortical thick ascending limb cannot enhance such NaCl delivery. NaCl, when added, might therefore originate from the medullary thick ascending limb.
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PMID:Effects of glucagon and PTH on the loop of Henle of rat juxtamedullary nephrons. 371 66

The effects of synthetic human calcitonin (HCT) on water and electrolyte deliveries to the thin limbs of Henle's loop of juxtamedullary nephrons were investigated by micropuncture in the rat. To avoid undesirable interference with exogenous calcitonin, experiments were performed in hormone-deprived rats with reduced circulating calcitonin, antidiuretic hormone, parathyroid hormone and glucagon, all four of which stimulate the adenylate-cyclase activity in the thick ascending limb and the distal tubule. Administration of HCT (1.0 mU/min X 100 g body wt) to such rats significantly reduced the urinary fractional excretion rate of water, Mg, Ca and K. At the tip of the longlooped nephrons, the fractional delivery of water diminished in the presence of HCT, although the glomerular filtration rate of these nephrons was unaltered. Simultaneously, the loop fluid osmolality rose significantly. HCT, however, did not alter the fraction of total filtered solutes remaining in the thin limbs, nor the NaCl fractional delivery. As previously observed in this laboratory with dDAVP, the reduced fractional delivery of water at the hairpin turn was accompanied by a decrease in Mg and Ca deliveries in rats given HCT, indicating that the handling of these two ions along the descending limb may be linked in part to the water movements in this nephron segment. The fractional deliveries of K at the hairpin turn and in urine were significantly correlated, and both decreased in the presence of HCT. Since, as shown previously, HCT reduces the net addition of K along the superficial distal tubule, it is concluded that calcitonin inhibits the medullary recycling of K between the nephron terminal segments and the loop of Henle of juxtamedullary nephrons.
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PMID:Effects of human calcitonin on water and electrolyte movements in rat juxtamedullary nephrons: inhibition of medullary K recycling. 371 48

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