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Provedor de dados:  BJMBR
País:  Brazil
Título:  Inhibitory effect of high [Mg2+] on the vasopressin-stimulated hydroosmotic permeability of the isolated perfused cortical collecting duct
Autores:  Falkenstein,D.
Ribeiro,C.A.L.
Figueiredo,J.F.
Data:  1999-08-01
Ano:  1999
Palavras-chave:  Cortical collecting ducts
Magnesium
Arginine vasopressin
Osmotic water permeability
Resumo:  High magnesium concentration inhibits the effect of arginine vasopressin (AVP) on smooth muscle contraction and platelet aggregation and also influences hepatocyte AVP receptor binding. The aim of this study was to determine the role of magnesium concentration [Mg2+] in AVP-stimulated water transport in the kidney collecting duct. The effect of low and high peritubular [Mg2+] on the AVP-stimulated osmotic water permeability coefficient (Pf) was evaluated in the isolated perfused rabbit cortical collecting duct (CCD). Control tubules bathed and perfused with standard Ringer bicarbonate solution containing 1 mM Mg2+ presented a Pf of 223.9 ± 27.2 µm/s. When Mg2+ was not added to the bathing solution, an increase in the AVP-stimulated Pf to 363.1 ± 57.2 µm/s (P<0.05) was observed. An elevation of Mg2+ to 5 mM resulted in a decrease in Pf to 202.9 ± 12.6 µm/s (P<0.05). This decrease in the AVP-stimulated Pf at 5 mM Mg2+ persisted when the CCDs were returned to 1 mM Mg2+, Pf = 130.2 ± 20.3 µm/s, and was not normalized by the addition of 8-[4-chlorophenylthio]-adenosine 3',5'-cyclic monophosphate, a cAMP analogue, to the preparation. These data indicate that magnesium may play a modulatory role in the action of AVP on CCD osmotic water permeability, as observed in other tissues.
Tipo:  Info:eu-repo/semantics/other
Idioma:  Inglês
Identificador:  http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1999000800016
Editor:  Associação Brasileira de Divulgação Científica
Relação:  10.1590/S0100-879X1999000800016
Formato:  text/html
Fonte:  Brazilian Journal of Medical and Biological Research v.32 n.8 1999
Direitos:  info:eu-repo/semantics/openAccess
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