Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three patients with the syndrome of inappropriate secretion of antidiuretic hormone had elevated uric acid clearances. Their uric acid clearances decreased markedly after the administration of pyrazinamide. Probenecid was given to two of them and it produced large increases in uric acid clearance. These data suggest that enhanced secretion in the renal tubules was responsible for the increased clearance of uric acid. This article provides evidence that hypouricemia in the syndrome of inappropriate secretion of antidiuretic hormone is due to increased tubular urate secretion.
 ...
PMID:Renal handling of urate in the syndrome of inappropriate secretion of antidiuretic hormone. 406 56

LLC-PK1 is an established porcine renal cell line with epithelial characteristics. Upon hormonal stimulation by vasopressin, LLC-PK1 cells release adenosine 3',5'-cyclic monophosphate (cAMP) into the medium. Release of cAMP is inhibited by the organic anion transport inhibitor probenecid and by cold phosphodiesterase inhibitors and iodoacetate but not by prostaglandins A1 or E1. The kinetics of release are first order, and cAMP analogues do not induce the release of cAMP. When grown on cellulose filters, monolayers of LLC-PK1 have morphological characteristics of transporting epithelia (apical microvilli and intercellular tight junctions) and maintain a transepithelial potential difference. Stimulation of such monolayers by vasopressin elicits probenecid-sensitive release of cAMP into the medium bathing the apical surface. Smaller quantities of cAMP are released from the basolateral surface, but release in this direction is not inhibited by probenecid. In contrast, release of cAMP from the nonepithelial cell line BHK is symmetrical and is symmetrically inhibited by probenecid. Probenecid-sensitive release of cAMP from LLC-PK1 is thus a function of the apical (brush-border) membrane.
 ...
PMID:Release of cAMP from a renal epithelial cell line. 632 92

Fluorescent calcium indicators have been widely used to assess cytoplasmic calcium concentration in cells. To examine the role of calcium ions on different physiological functions (e.g. in case of liver; bile secretion, glucose metabolism, etc.) there is a need for whole organ studies. We have developed a technique to estimate intracellular free calcium changes in perfused rat liver. Krebs-Henseleit perfused livers were loaded with 7 microM or 35 microM Indo-1/AM. An area 3 mm in diameter and approximately 300 microns in depth was illuminated at 340 nm. Fluorescence was monitored with photomultiplier tubes at 3 wavelengths (400 nm for Ca-bound dye, 504 nm for free dye and 464 nm for NADH). The viability of liver preparations was assessed by measurement of the concentrations of lactate dehydrogenase and alanine aminotransferase in the effluent. Loading of the livers with 7 microM Indo-1/AM via the portal vein resulted in a 5-fold increase of fluorescence at 400 nm. However the dye 'leaked' out of the liver with a half-time of 18 min. Probenecid (a specific anion carrier blocker) inhibited loss of dye in a dose dependent fashion (2.5-10 mM). Transient calcium elevations were observed in response to vasopressin (5-50 nM) at physiological levels, ethanol (0.3-0.8 M) and the calcium ionophore, ionomycin. Certain limitations were apparent with this approach: (1) it was necessary to use an anion carrier blocker to maintain a relatively steady dye concentration; (2) endogenous NADH fluorescence interfered with the calcium signal; and (3) absolute values of calcium concentration could not be determined.
 ...
PMID:Monitoring of intracellular free calcium in perfused rat liver. 835 70