1. Hypertension, Na+/Ca2+ exchanger, and Na+, K+-ATPase
T. Iwamoto, S. Kita 
Kidney International 
Volume 69, Issue 12, Pages (June 2006)
DOI: /sj.ki
Copyright © 2006 International Society of Nephrology Terms and Conditions

2. Figure 1
Proposed pathway responsible for salt-dependent hypertension. High salt intake (or Na+ retention) and genetic or pathological defects cause the levels of ECGs that inhibit the Na+,K+-ATPase α2-isoform (or α1-isoform) to rise in the plasma (although Na+ retention also increases plasma volume, resulting in elevated blood pressure). This results in the increase in subplasma membrane [Na+] of arterial smooth muscle. The restricted [Na+] accumulation elevates [Ca2+]i by vascular NCX1 isoform (NCX1.3)-mediated Ca2+ entry. This enhances arterial tone and causes hypertension. SEA0400, as well as thiazides and PST2238, blocks this Ca2+ entry and exerts an antihypertensive effect in salt-dependent hypertension. SR; sarcoplasmic reticulum, RyR; ryanodine receptor.
Kidney International  , DOI: ( /sj.ki )
Copyright © 2006 International Society of Nephrology Terms and Conditions