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10.1016/S0006-291X(02)00542-9

http://scihub22266oqcxt.onion/10.1016/S0006-291X(02)00542-9
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12056828!ä!12056828

suck abstract from ncbi


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pmid12056828      Biochem+Biophys+Res+Commun 2002 ; 294 (3): 710-3
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  • Magnesium influx enhanced by nitric oxide in hypertensive rat proximal tubule cells #MMPMID12056828
  • Ikari A; Kano T; Suketa Y
  • Biochem Biophys Res Commun 2002[Jun]; 294 (3): 710-3 PMID12056828show ga
  • An abnormal handling of renal magnesium has been suggested to cause salt-sensitive hypertension. The filtered magnesium is first reabsorbed in the proximal tubule. Amiloride has been shown to enhance renal magnesium conservation, but the regulatory mechanisms are unknown yet. High-salt (8% NaCl) diet decreased serum magnesium concentration, while increased urinary magnesium in Dahl salt-sensitive (DS) rat. Furthermore, the expression of nitric oxide synthase type 3 and nitric oxide (NO) content were decreased in high-salt loaded DS rat. In isolated proximal tubule cells, amiloride (0.1 mM) increased intracellular free magnesium concentration ([Mg(2+)](i)). However, the net [Mg(2+)](i) increase in the high-salt loaded DS rat was smaller than other groups. NOR1 (0.1 mM), a NO donor, restored the increase of [Mg(2+)](i) to the same level of other groups. On the contrary, L-NMMA (0.1 mM), an inhibitor of NO production, inhibited the increase of [Mg(2+)](i) in all groups. These results suggest that intracellular NO has an important role to up-regulate amiloride-elicited magnesium influx.
  • |Animals[MESH]
  • |Biological Transport/drug effects[MESH]
  • |Enzyme Inhibitors/pharmacology[MESH]
  • |Hypertension/*metabolism[MESH]
  • |In Vitro Techniques[MESH]
  • |Kidney Tubules, Proximal/*metabolism[MESH]
  • |Magnesium/*metabolism[MESH]
  • |Male[MESH]
  • |Nitric Oxide/*metabolism[MESH]
  • |Rats[MESH]
  • |Rats, Inbred Dahl[MESH]


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