RENALASE PLASMA LEVELS ARE ASSOCIATED WITH SYSTOLIC BLOOD PRESSURE IN PATIENTS WITH RESISTANT HYPERTENSION: 9C.01

Abstract

Evidence from experimental studies suggest that renalase, a soluble FAD-dependent protein, is involved in blood pressure regulation, possibly via degradation of catecholamines including noradrenaline. To investigate whether renalase is associated with blood pressure levels and/or indices of noradrenaline disposition in humans we studied a cohort of 22 patients with resistant hypertension (at least 3 antihypertensive drugs including a diuretic) and 4 healthy, normotensive control subjects. Radiotracer dilution methodology and arterial blood sampling was applied to measure whole body noradrenaline (NA) spillover. Arterial plasma levels of renalase were measured by Western blot analysis using a monoclonal anti-renalase antibody and quantified using a gel documentation system (Bio-Rad Quantity One Software). Split half analysis of the hypertensive cohort according to systolic blood pressure levels (mean: 186 ± 22 vs 156 ± 9mmHg; p < 0.001) revealed that mean arterial renalase levels were substantially lower in the group with higher systolic blood pressure (62 ± 31 vs 125 ± 82 arbitrary units; p < 0.05), whereas whole body NA spillover tended to be higher in the group with higher systolic blood pressure without reaching statistical significance (645 ± 445 vs 407 ± 195ng/min; p = 0.12). Arterial renalase levels were higher (238 ± 174 arbitrary units) and whole body NA spillover was lower (168 ± 78ng/min) in the normotensive control subjects (mean systolic blood pressure: 123 ± 7mmHg)(all p < 0.05). Correlation analysis revealed an inverse relationship between arterial renalase plasma levels and systolic blood pressure for the entire cohort (r = -0.52; p < 0.05). These data suggest that arterial plasma levels of renalase are inversely associated with systolic blood pressure in a cohort of patients with resistant hypertension. Whether this relation can in part be explained by alleviated degradation of noradrenaline or whether alternative pathways are involved requires further investigation.