Mar 11, 2015

Molecular-based mechanisms of Mendelian forms of salt-dependent hypertension: questioning the prevailing theory

Theodore W KurtzR Curtis Morris


This critical review directly challenges the prevailing theory that a transient increase in cardiac output caused by genetically mediated increases in activity of the ENaC in the aldosterone sensitive distal nephron, or of the NCC in the distal convoluted tubule, accounts entirely for the hemodynamic initiation of all Mendelian forms of salt-dependent hypertension (Figure 1). The prevailing theory of how genetic mutations enable salt to hemodynamically initiate Mendelian forms of salt-dependent hypertension in humans (Figure 1) depends on the results of salt-loading studies of cardiac output and systemic vascular resistance in nongenetic models of hypertension that lack appropriate normal controls. The theory is inconsistent with the results of studies that include measurements of the initial hemodynamic changes induced by salt loading in normal, salt-resistant controls. The present analysis, which takes into account the results of salt-loading studies that include the requisite normal controls, indicates that mutation-induced increases in the renal tubular activity of ENaC or NCC that lead to transient increases in cardiac output will generally not be sufficient to enable increases in salt intake to initiate the increased BP t...Continue Reading

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  • Citations18


Mentioned in this Paper

Epithelial sodium channel
Mendelian Randomization Analysis
Aldosterone Measurement
Vascular Motor Function
Total Peripheral Resistance
Vascular Resistance
Blood Vessel
Diastolic Blood Pressure

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