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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0001629,
umls-concept:C0007634,
umls-concept:C0012472,
umls-concept:C0015385,
umls-concept:C0025148,
umls-concept:C0034693,
umls-concept:C0034721,
umls-concept:C0205385,
umls-concept:C0597484,
umls-concept:C1153198,
umls-concept:C1366535,
umls-concept:C1419072,
umls-concept:C1550278,
umls-concept:C2587213
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pubmed:issue |
2 Pt 2
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pubmed:dateCreated |
1993-4-6
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pubmed:abstractText |
Antidiuretic hormone and parathyroid hormone (PTH) inhibit HCO3- absorption by the rat medullary thick ascending limb (MTAL). Studies were performed on rat MTAL tubule suspension to specify the H(+)-HCO3- membrane transporters affected by these hormones and the implicated intracellular second messengers. Arginine vasopressin (AVP) and PTH stimulated cell adenosine 3',5'-cyclic monophosphate (cAMP) production with a relative rank order potency of AVP > rat PTH-(1-34) > bovine PTH-(1-84). Significant cell acidification in HCO3- -CO2-free medium, monitored in 2'7'-bis(carboxyethyl)-5(6')-carboxyfluorescein-loaded cells, was caused by 0.1 nM AVP, 1 nM rat PTH-(1-34), but not by < 100 nM bovine PTH-(1-84), as well as by 10(-4) M 8-bromo-cAMP and 2 x 10(-5) M forskolin; 10 nM AVP or rat PTH-(1-34) did not alter the intracellular pH when Na+/H+ antiport was inhibited by 2 mM amiloride. Prostaglandin E2 (PGE2, 10(-6) M), which inhibited AVP-stimulated cell cAMP production, reduced by 35% the cell acidification response to 10 nM AVP. AVP and 8-bromo-cAMP inhibited Na+/H+ antiport-dependent cell pH recovery from intracellular acidification, which was explained by a decrease in the Vmax of the antiporter. AVP did not directly affect K(+)-HCO3- cotransport and plasma membrane H(+)-ATPase of rat MTAL cells. Cytosolic calcium ([Ca2+]i), monitored in fura-2-loaded cells, was unaffected by up to 1 nM AVP, 100 nM PTH, glucagon, calcitonin, and oxytocin, and 1 microM PGE2; however, 100 nM AVP, but not 1-desamino-8-D-AVP (dDAVP), caused a peak increase in [Ca2+]i, even in the absence of extracellular Ca2+, and stimulated cell accumulation of [3H]inositol phosphates.(ABSTRACT TRUNCATED AT 250 WORDS)
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Arginine Vasopressin,
http://linkedlifedata.com/resource/pubmed/chemical/Bicarbonates,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/Dinoprostone,
http://linkedlifedata.com/resource/pubmed/chemical/Inositol Phosphates,
http://linkedlifedata.com/resource/pubmed/chemical/Parathyroid Hormone,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium-Hydrogen Antiporter
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
264
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
F354-64
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8383452-Animals,
pubmed-meshheading:8383452-Arginine Vasopressin,
pubmed-meshheading:8383452-Bicarbonates,
pubmed-meshheading:8383452-Biological Transport,
pubmed-meshheading:8383452-Calcium,
pubmed-meshheading:8383452-Carrier Proteins,
pubmed-meshheading:8383452-Cyclic AMP,
pubmed-meshheading:8383452-Cytosol,
pubmed-meshheading:8383452-Dinoprostone,
pubmed-meshheading:8383452-Inositol Phosphates,
pubmed-meshheading:8383452-Kidney Medulla,
pubmed-meshheading:8383452-Loop of Henle,
pubmed-meshheading:8383452-Male,
pubmed-meshheading:8383452-Parathyroid Hormone,
pubmed-meshheading:8383452-Rats,
pubmed-meshheading:8383452-Rats, Sprague-Dawley,
pubmed-meshheading:8383452-Sodium-Hydrogen Antiporter
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pubmed:year |
1993
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pubmed:articleTitle |
cAMP-dependent control of Na+/H+ antiport by AVP, PTH, and PGE2 in rat medullary thick ascending limb cells.
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pubmed:affiliation |
Physiologie et Endocrinologie Cellulaire Rénale, Institut National de la Santé et de la Recherche Médicale, Unité 356, Université Pierre et Marie Curie, Paris, France.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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