Hypertension, Na+/Ca2+ exchanger, and Na+, K+-ATPase

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Presentation transcript:

Hypertension, Na+/Ca2+ exchanger, and Na+, K+-ATPase T. Iwamoto, S. Kita Kidney International Volume 69, Issue 12, Pages 2148-2154 (June 2006) DOI: 10.1038/sj.ki.5000421 Copyright © 2006 International Society of Nephrology Terms and Conditions

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 2006 69, 2148-2154DOI: (10.1038/sj.ki.5000421) Copyright © 2006 International Society of Nephrology Terms and Conditions