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http://scihub22266oqcxt.onion/ 2987608!ä!2987608 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Klin+Wochenschr 1985 ; 63 Suppl 3 (ä): 125-8 Nephropedia Template TP {{tp|p=2987608|t=1985. Mechanism of diuretic-induced hypopotassemia in human hypertension |pdf=|usr=}}{{2987608}} gab.com Text Mechanism of diuretic-induced hypopotassemia in human hypertension JO: Klin Wochenschr http://www.kidney.de/pget.php?&tw=1&pmid=2987608 #FOAvip Diuretic treatment (hydrochlorothiazide) induced a marked decrease of red cell membrane Na+K+ ATPase activity in excessive potassium loser hypertensive patients. The decreased activity occurred within 2-4 weeks of treatment and returned to baseline in 4-6 weeks after cessation of treatment. Simultaneously, red cell sodium increased, potassium decreased together with increased 24-h urinary excretion. The persistent low serum potassium may be due to impaired absorption of potassium from the gut as a result of suppressed enzyme activity since total body potassium appears also to decrease. The decreased Na+K+ ATPase activity may be due to a direct effect of the diuretic on cell membrane. Twit Text FOAVip Mechanism of diuretic-induced hypopotassemia in human hypertension ????Klin Wochenschr http://www.kidney.de/pget.php?&tw=1&pmid=2987608 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=2987608 #FOAvip English Wikipedia <ref>{{Cite pmid|2987608}}</ref> Mechanism of diuretic-induced hypopotassemia in human hypertension #MMPMID2987608 Kezdi P; Danopulos D; Stanley EL; Mullins M Klin Wochenschr 1985[]; 63 Suppl 3 (ä): 125-8 PMID2987608show ga Diuretic treatment (hydrochlorothiazide) induced a marked decrease of red cell membrane Na+K+ ATPase activity in excessive potassium loser hypertensive patients. The decreased activity occurred within 2-4 weeks of treatment and returned to baseline in 4-6 weeks after cessation of treatment. Simultaneously, red cell sodium increased, potassium decreased together with increased 24-h urinary excretion. The persistent low serum potassium may be due to impaired absorption of potassium from the gut as a result of suppressed enzyme activity since total body potassium appears also to decrease. The decreased Na+K+ ATPase activity may be due to a direct effect of the diuretic on cell membrane. |Calcium/blood/urine[MESH] |Erythrocyte Membrane/enzymology[MESH] |Erythrocytes/metabolism[MESH] |Humans[MESH] |Hydrochlorothiazide/*adverse effects/therapeutic use[MESH] |Hypertension/blood/*drug therapy[MESH] |Hypokalemia/*chemically induced[MESH] |Magnesium/blood/urine[MESH] |Potassium/blood/urine[MESH] |Prospective Studies[MESH] |Sodium-Potassium-Exchanging ATPase/blood[MESH]Mechanism of diuretic-induced hypopotassemia in human hypertension (epmc).pdf DeepDyve Pubget Overpricing