Evidence for ETB receptor regulation of circadian control of sodium excretion (860.1)

Abstract

Lack of renal ETB receptor function exacerbates circadian blood pressure variation in response to a high salt intake. Thus, we hypothesized that ET‐1 maintains normal circadian variation of sodium and water excretion through activation of the ETB receptor. To test this hypothesis, Sprague Dawley (SD) or ETB receptor deficient (sl/sl) rats were given a 900 μEq Na salt load by oral gavage at the beginning of either their active (dark) or inactive (light) cycle (7 pm or 7 am). Urine was collected in 12 hr increments and mean arterial pressure (MAP) measured by telemetry throughout the study. SD rats excreted the salt load during the initial 12 hrs whether given before their active (941 ± 88 baseline active period vs. 1548 ± 76 μEq Na/12 hr active period post gavage) or inactive cycle (362 ± 33 baseline vs. 944 ± 57 μEq Na/12 hr post gavage). Sl/sl rats also excreted the salt load when challenged during their active cycle (609 ± 25 baseline vs. 1119 ± 97 μEq Na/12 hr post gavage). However, sl/sl rats retained the salt load in the first 12 hr post gavage when given prior to the inactive period (364 ± 53 baseline vs. 464 ± 83 μEq Na/12 hr post gavage), but then excreted the salt load during the subsequent active period (684 ± 88 baseline vs. 1342 ± 121 μEq Na/12 hr, 24 hrs post gavage) and was associated with a significant elevation in MAP. These data demonstrate that the ETB receptor contributes to the circadian control of sodium excretion and blood pressure.Grant Funding Source: Supported by NIH grant P01 HL095499