Hormones

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Introduction and Aims: A series of experimental and clinical data supports the notion that Endogenous Ouabain (EO) may affect blood pressure (BP), plasma sodium concentration, and renal Na excretion.The plasma sodium concentration directly affects BP but the pressor mechanism for elevated BP following an increased salt intake is unclear.A direct relation between plasma EO and plasma Na has been reported.Further, the BP response to a low salt intake is heterogeneous, with BP rising in some patients.Methods: Here we investigated the response of EO, plasma Na and BP to a low salt intake (<100 mEq/day, 15 days) in a cohort of 79 naïve hypertensive patients (EH).Results: The BP response to the low salt intake showed high systolic and diastolic BP variability (range -62.4 to +40 mmHg, respectively).The changes in mean diastolic BP were directly related to the change in plasma EO (r=0.27,p=0.02).Patients were then segregated into quartile sub-groups according to DBP changes.Those with the greatest BP fall were in the 1 st quartile, while those patients that showed an increase in DBP after low salt intake, i.e., reverse salt sensitivity (RSS), were in the 4 th quartile (Figure A panel).RSS showed a greater decrease in plasma [Na + ] (-2.2±0.6 vs + 0,23±0.54mEq/ L, B panel) and simultaneous increases in plasma EO (C panel).Circulating EO was inversely related to plasma [Na + ] (r=-0.316,p=0.005, n=78).Neither plasma aldosterone nor renin were related to RSS.Conclusions: Our findings show that in EH: 1) a low salt diet lowers BP in the vast majority of patients while raising plasma EO and BP primarily in RSS patients.2) While EO upregulates renal Na-K ATPase activity,and might be a useful mechanism minimizing sodium loss, the elevation of EO in RSS patients suggests it may account for the paradox that reduced salt intake may increase the risk for cardiovascular and renal disease in some individuals.

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