Key result
Subtle renal injury causing a physiological defect in sodium excretion is proposed as a common mechanism for salt-sensitive essential hypertension.
Discusses the hypothesis that subtle renal injury and defects in sodium excretion are common mechanisms underlying salt-sensitive essential hypertension.
Does not change hypertension management; leaves open prospective validation of renal sodium excretion defects.
Despite the fact that essential hypertension was originallydescribed as hypertension occurring in the absence of clinical renal disease,1 Dahl et al later showed by transplan-tation studies in experimental models of hypertension that the kidney is ultimately responsible for the elevation in blood pressure,2 a finding that was verified later in humans.3 Most authorities believe that the mechanism by which the kidney causes hypertension involves a physiological defect in so-dium excretion as championed by Guyton et al.4 Support for this mechanism is extensive and includes both epidemiolog-ical5 and physiological6 studies. Several hypotheses have been proposed to explain the mechanism responsible for the defect in renal sodium handling. A favored hypothesis is that hypertension results from a polygenic defect in which there are alterations in the regulation or expression in tubular transport systems
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Johnson et al. (2005) conducted a review in Salt-Sensitive Essential Hypertension. Subtle renal injury was evaluated. Subtle renal injury causing a physiological defect in sodium excretion is proposed as a common mechanism for salt-sensitive essential hypertension.
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