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The target‐specific transporter and current status of diuretics as antihypertensive
Author(s) -
Ali Syed Salman,
Sharma Pramod Kumar,
Garg Vipin Kumar,
Singh Avnesh Kumar,
Mondal Sambhu Charan
Publication year - 2012
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.2011.01012.x
Subject(s) - distal convoluted tubule , diuretic , transporter , thiazide , loop of henle , nephron , chemistry , pharmacology , organic anion transporter 1 , sodium , endocrinology , convoluted tubule , medicine , kidney , biochemistry , organic chemistry , gene
The currently available diuretics increase the urinary excretion of sodium chloride by selective inhibition of specific sodium transporters in the loop of Henle and distal nephron. In recent years, the molecular cloning of the diuretic‐sensitive sodium transporters at distal convoluted tubule has improved our understanding of the cellular mechanisms of action of each class of diuretics. Diuretics are tools of considerable therapeutic importance. First, they effectively reduce blood pressure. Loop and thiazide diuretics are secreted from the proximal tubule via the organic anion transporter‐1 and exert their diuretic action by binding to the Na + ‐K + ‐2Cl − co‐transporter type 2 in the thick ascending limb and the Na + ‐ Cl − co‐transporter in the distal convoluted tubule, respectively. Recent studies in animal models suggest that abundance of these ion transporters is affected by long‐term diuretic administration. The WHO/ISH guidelines point out that diuretics enhance the efficacy of antihypertensive drugs and will most often be a component of combination therapy.