Abstract

Renal sympathetic nerve activity (rSNA) at a low frequencyinfluences handling of sodium and water by the kidneys, without changing renal blood flow and glomerular filtration rate. Accordingly, we have previously demonstrated that renal nerve stimulation increases NHE3mediated sodium reabsorption due to an increased intrarenal reninangiotensin-system (RAS), independent of hemodynamic changes. In the present study, we evaluated how sympathoexcitation accompanied by blood pressure elevation would impact renal function and proximal tubule NHE3 regulation. To this end, we disinhibited the paraventricular nucleus of the hypothalamus (PVN) by microinjecting the antagonist GABA receptor bicuculline in anesthetized Wistar rats. We found that bicuculline injected unilaterallywithin the PVN caused a rapid increase in blood pressure compared with the baseline period (± 45%), which was accompanied by a great increase in urinary volume (more than 300%). This increase in urinary volumewas associatedwith an increase onNHE3 phosphorylation levels, suggesting that the diuretic effect of PVN disinhibition and blood pressure elevation are, at least in part, due to a decrease in NHE3 activity. Ongoing experiments from our laboratory are directed toward investigating the effects of bicuculline within the PVN in other apical sodium transporters along the renal tubule and evaluating the possible role of both systemic and intrarenal RAS in mediating these effects. Supported by CAPES, CNPq and FAPESP.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call