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)

Derangements in leukocyte function occur in patients with primary hyperparathyroidism and in those with uremia, which is a state of secondary hyperparathyroidism, suggesting that parathyroid hormone (PTH) may affect leukocyte function. We examined the interaction between PTH and random migration of human polymorphonuclear leukocytes (PMNL) utilizing a modified Boyden chamber. Intact 1-84 PTH but not its amino-terminal (1-34 PTH) or its carboxy-terminal (53-84 PTH) fragments produced marked and significant (p less than 0.01) stimulation of random migration in a dose-dependent manner. Inactivation of 1-84 PTH abolished its effect and other peptide hormones (calcitonin, glucagon, insulin and vasopressin) did not stimulate migration of PMNL. The effect of PTH on migration was not due to action of the hormone on chemotaxis. PTH did not enhance cAMP or cGMP production by PMNL. The stimulation of PMNL motility by PTH was independent of calcium concentration in media, was not mimicked by calcium ionophore and was not blocked by verapamil. Quinidine also produced significant (p less than 0.01) increase in random migration of PMNL and this effect was not additive to that of PTH. Prolonged exposure to PTH (16-20 h) was associated with significant inhibition of random migration of PMNL. The migration of PMNL from patients with advanced renal failure was significantly (p less than 0.01) reduced and there was a significant (p less than 0.01) inverse relationship between random migration of PMNL and serum levels of PTH. Also PTH produced only modest stimulation of random migration of PMNL in most patients with renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of parathyroid hormone on random migration of human polymorphonuclear leukocytes. 285 73

Quinidine, a compound thought to increase cytosolic calcium ion activity, has been found to inhibit the hydrosmotic response to vasopressin (VP) and adenosine 3',5'-cyclic monophosphate (cAMP) in the toad urinary bladder. To test whether this drug has a similar action in the mammalian nephron, the effect of quinidine on the hydraulic conductivity of the isolated perfused rabbit cortical collecting tubule (CCT) exposed to either 20 microU/ml VP or 10(-4) M 8-(p-chlorophenylthio) - adenosine 3',5' - cyclic monophosphate (8-CPT-cAMP) was studied. Quinidine had no effect on the basal water permeability of the CCT. Quinidine sulfate (10(-4) M) reduced the VP-stimulated water permeability from 280 +/- 50 X 10(-7) to 115 +/- 41 X 10(-7) cm X s-1 X atm-1 (P less than 0.05). The hydrosmotic response to 8-CPTcAMP was likewise reduced following exposure to quinidine. This effect was shown to be dose dependent. In paired experiments, inhibition of the response to 10(-4) M 8-CPTcAMP averaged 11% at 10(-6) M, 27% at 5 X 10(-6) M, 53% at 5 X 10(-5) M, and 50% at 10(-4) M quinidine. Inhibition of the response to 8-CPTcAMP was estimated to be half maximal at approximately 5 X 10(-6) M quinidine. Tubules were protected against the quinidine-induced inhibition by the addition of 6.5 X 10(-5) M quin 2-acetoxymethylester in the presence of low peritubular Ca concentration. These results are consistent with the view that elevated cytosolic Ca ion levels inhibit the increase in water permeability elicited by VP or exogenous cAMP in the mammalian CCT.
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PMID:Quinidine effect on hydrosmotic response of collecting tubules to vasopressin and cAMP. 303 43

The present studies probe the role of Ca2+ and Na+ in the stimulation-permeability coupling sequences by which antidiuretic hormone (ADH) induces a cyclic AMP (cAMP)-mediated increase in urea permeability in toad urinary bladder. The following results were obtained: (a) Removal of mucosal Na+ or Ca2+ or deletion of serosal Ca2+ did not modify ADH action. (b) Reduction of the serosal Na+ concentration to less than 50 mM inhibited the effects of both ADH and cAMP. The minimal concentration of serosal Na+ needed for the hormone to elicit its maximal effect was reduced to approximately 10 mM if serosal Ca2+ was concomitantly deleted. (c) The Na+ ionophore monensin produced an inhibition of ADH and cAMP actions that was dependent on the presence of Na+ and Ca2+ in the serosa. (d) The Ca2+ ionophore A23187 produced a serosal Ca2+-dependent inhibition of ADH effect and did not modify cAMP action. (e) Carbachol, which increases Ca2+ uptake to the same extent that A23187 does, had no effect on ADH action. (f) Quinidine, which releases Ca2+ from intracellular stores, produced a large inhibition of the action of ADH but not that of cAMP; the inhibition was greatly reduced if serosal Ca2+ was deleted. (g) Dinitrophenol and iodoacetate, which also release Ca2+ from intracellular pools, had no effect on ADH action. (h) The Ca2+ channel blocker diltiazem had no effect on ADH action and did not modify the inhibitions produced by deletion of serosal Na+ or monensin. (i) The cyclooxygenase inhibitor indomethacin partially removed the inhibition produced by deletion of serosal Na+ and almost completely impeded the inhibitions produced by either monensin or A23187. It is concluded: (a) Extracellular Ca2+, Na+ transport rates, and serosal Na+, in concentrations between 10 and 110 mM, have no participation in modulating the increase in urea permeability produced by ADH. (b) Increases in cytosolic Ca2+ activity, which are capable of inhibiting the effect of ADH on urea permeability at pre- and/or post-cAMP steps, seem to be highly compartmentalized. (c) Endogenous prostaglandins might play a role in the inhibitions produced by absence of serosal Na+, monensin, or A23187.
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PMID:Roles of Ca2+ and Na+ on the modulation of antidiuretic hormone action on urea permeability in toad urinary bladder. 392 Feb 47

The effect of quinidine on Na and H+ transport by the turtle bladder and water transport by the toad bladder was examined. Quinidine inhibited the short-circuit current and the potential difference in a dose-dependent fashion. The effect of quinidine on the short-circuit was not dependent on extracellular calcium concentration and was not reversible with removal of the drug. Quinidine inhibited H+ secretion in a dose-dependent fashion. The effect of quinidine on H+ secretion also was not dependent on extracellular calcium concentration and was not reversible, either with removal of the drug or with stimulation of H+ secretion with 5% CO2. The effect of quinidine on Na or H+ transport could not be elicited by an equivalent dose of tetracaine, suggesting that the inhibitory effect of quinidine is not dependent on its anesthetic properties. Quinidine also inhibited vasopressin and cyclic AMP stimulated water flow in the toad bladder. Quinidine did not alter calcium uptake by the turtle bladder but increased calcium efflux by the turtle and toad bladders. These observations suggest that a rise in cytosolic calcium is responsible for the inhibitory effect of quinidine on Na, H+, and water transport.
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PMID:Effect of quinidine on Na, H+, and water transport by the turtle and toad bladders. 625 Dec 23