Sodium surfeit and potassium deficit: Keys to the pathogenesis of hypertension

被引:31
|
作者
Adrogue, Horacio J. [1 ,2 ]
Madias, Nicolaos E. [3 ,4 ]
机构
[1] Baylor Coll Med, Methodist Hosp, Dept Med, Houston, TX 77030 USA
[2] Vet Affairs Med Ctr, Renal Sect, Houston, TX 77030 USA
[3] Tufts Univ, Sch Med, Dept Med, Boston, MA 02111 USA
[4] St Elizabeths Med Ctr, Div Nephrol, Boston, MA 02135 USA
关键词
Sodium sensitivity; sympathetic activity; aldosterone; angiotensin II; endogenous ouabain; potassium channels; calcium signaling; VASCULAR SMOOTH-MUSCLE; ANGIOTENSIN-ALDOSTERONE SYSTEM; BLOOD-PRESSURE; SALT SENSITIVITY; ENDOGENOUS OUABAIN; NA+/CA2+ EXCHANGER; OXIDATIVE STRESS; PLASMA SODIUM; FLUID; CHANNEL;
D O I
10.1016/j.jash.2013.09.003
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
The pathogenic role of Na+ in primary hypertension is widely recognized but that of K+ remains unappreciated. Yet, extensive evidence indicates that together, the body's dominant cations constitute the chief environmental factor in the pathogenesis of hypertension and its cardiovascular sequelae. In this Review, we provide a synthesis of the determinants of Na+ retention and K+ loss developing in the body as the Na+-rich and K+-poor modem diet interacts with kidneys intrinsically poised to conserve Na+ and excrete K+; and the molecular pathways utilized by these disturbances in the central nervous system and the periphery to increase sympathetic tone and vascular resistance, and establish hypertension. These fresh insights point to new directions for targeted pharmacotherapy of hypertension. The interdependency of Na+ and K+ in the pathogenesis of hypertension indicates that Na+ restriction and increased K+ intake are important strategies for the primary prevention and treatment of hypertension and its cardiovascular consequences. (C) 2014 American Society of Hypertension. All rights reserved.
引用
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页码:203 / 213
页数:11
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