Abstract

Acute stimulation of forebrain osmoreceptors increases sympathetic nerve activity (SNA) and arterial blood pressure (ABP). The present study sought to determine whether the sympathetic nervous system contributes to this pressor response and whether sympathetic-regulatory neurons of the RVLM mediate the increase in SNA and ABP. In urethane/chloralose anesthetized rats (n=5), intracarotid injection of hypertonic NaCl (150, 375, and 750 mM in 150 μl) dose-dependently increased mean ABP, and this was eliminated by administration of the ganglionic blocker chlorisondamine (2 mg/kg, iv) at 150mM (1±1 vs 1±0 mmHg), 375mM (16±3 vs 1±0 mmHg, p<0.05), and 750mM (27±4 vs 2±1 mmHg, p<0.01). In a second group (n=5), inhibition of the RVLM with microinjection of the GABAA receptor agonist muscimol (250 pmol/100 nl) significantly reduced the increase in mean ABP (150 mM: −3±2 vs 1±1 mmHg; 375mM: 14±5 vs 0±4 mmHg; 750mM: 31±5 vs 2±8 mmHg, p<0.05), renal SNA (150 mM: −1±2 vs −2±2%; 375mM: 50±18 vs −17±6%; 750mM: 80±13 vs −13±16%, p<0.05), and splanchnic SNA (150mM: −6±4 vs −1±1%; 375mM: 54±14 vs −5±14%; 750mM: 99±12 vs 14±20%, p<0.05). The present findings demonstrate that stimulation of forebrain osmoreceptors produces a sympathetically-mediated increase in ABP that depends on the tonic activity of RVLM neurons.

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

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.