Abstract

Our study aimed at elucidating the effects of acute central hypervolemia induced by water immersion (WI) on renal hemodynamics, hormonal responses and on cardiovascular control in hypertensive patients, as well as at evaluating the possible role of the opioidergic system (OS) in determining these effects. Thirteen essential hypertensives were studied for 2 h before and for 2 h during WI. This was done twice, without and with i.v. injection of the OS antagonist naloxone. Before and during WI alone, glomerular filtration rate (GFR), effective renal plasma flow (ERPF), renal vascular resistance (RVR), mean arterial pressure (MAP), pulse interval (PI), spontaneous baroreflex sensitivity (BRS), Low frequency to High frequency (LF/HF) ratio in PI spectra, hematocrit, urinary sodium excretion, plasma renin activity (PRA) and aldosterone (PA) were assessed. Based on their response to WI, hypertensives were subdivided into two groups: ERPF+ (n = 7) in whom WI increased ERPF, and ERPF– (n = 6) in whom WI reduced ERPF. ERPF+ displayed a higher BRS than ERPF– at baseline and during WI. A suppression of PRA and PA and an increase in MAP and urinary sodium excretion were found in both groups. In ERPF+ naloxone caused RVR and MAP to increase during WI and this response was associated with a blockade of the increase in ERPF in this group, while BRS and natriuresis were unchanged. In ERPF– naloxone did not affect WI-induced MAP, ERPF, RVR and BRS changes, while it blunted sodium excretion. Our data provide the first evidence of a differentiate renal hemodynamic response to WI in hypertension; they also suggest that while OS may significantly potentiate the renal vasodilatory response to WI in ERPF+, it does not affect the natriuretic response nor the changes in systemic cardiovascular regulation induced by central hypervolemia.

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