Endogenous ouabain and acute salt loading in low-renin hypertension.

Background: Endogenous ouabain (EO), which is structurally identical to the cardiac glycoside ouabain, has been isolated in human plasma. The substance EO has been implicated in states of volume expansion and in some types of arterial hypertension, especially as a factor of salt sensitivity of blood pressure. On the other hand, salt sensitivity has been described in low-renin hypertension. The aim of this study was to determine the response of plasma EO to acute sodium expansion in low-renin hypertension.
Methods: We performed an acute intravenous sodium load (2 L of saline in 4 h) in 13 hypertensive subjects with low renin values (<0.65 ng/mL/h). We measured EO in plasma extracts by a radioimmunoassay and compared it with other endocrine parameters including atrial natriuretic peptide (ANP), aldosterone (ALDO), cortisol (CORT), adrenocorticotropic hormone (ACTH), and plasma renin activity (PRA).
Results: We found that EO showed only a mild nonsignificant decrease after saline infusion (from 938.8+/-218.8 pmol/L to 781.4+/-181.4 pmol/L ouabain equivalents), whereas ALDO and PRA significantly decreased (P<.0001; P<.05 respectively). The ANP significantly increased, as a marker of effective volume expansion (P<.01). At the end of the infusion, we found that EO was positively related to ACTH levels and to ALDO changes from baseline.
Conclusions: Our results do not support the hypothesis that EO is stimulated in low-renin hypertension by acute salt-volume expansion. ACTH could be a factor modulating EO secretion in this condition.