cAMP-dependent control of Na+/H+ antiport by AVP, PTH, and PGE2 in rat medullary thick ascending limb cells
| Autor: | Maurice Bichara, J. Poggioli, P. Borensztein, M. Paillard, Catherine Vernimmen, Philippe Juvin |
|---|---|
| Rok vydání: | 1993 |
| Předmět: |
Male
endocrine system medicine.medical_specialty Vasopressin Sodium-Hydrogen Exchangers Physiology Inositol Phosphates Intracellular pH Parathyroid hormone In Vitro Techniques Dinoprostone Rats Sprague-Dawley chemistry.chemical_compound Cytosol Internal medicine Cyclic AMP medicine Animals Kidney Medulla Forskolin urogenital system Biological Transport Rats Amiloride Arginine Vasopressin Bicarbonates Sodium–hydrogen antiporter Endocrinology chemistry Parathyroid Hormone Second messenger system Loop of Henle Calcium Carrier Proteins hormones hormone substitutes and hormone antagonists Intracellular medicine.drug |
| Zdroj: | American Journal of Physiology-Renal Physiology. 264:F354-F364 |
| ISSN: | 1522-1466 1931-857X |
| Popis: | 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) |
| Databáze: | OpenAIRE |
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