Activation of Transient Receptor Potential Vanilloid‐1 (TRPV1) Channels in the Rostral Ventrolateral Medulla (RVLM) Produces Renal Sympathoinhibition

Abstract

The RVLM plays an important role in the regulation of sympathetic nerve activity (SNA) and arterial blood pressure (ABP). The TRPV1 channel is sensitive to temperature, chemical and mechanical stimuli, but recent evidence suggests that TRPV1 channels also modulate neurotransmission. The present study examined whether activation of TRPV1 channels in the RVLM altered SNA and ABP. In urethane‐chloralose anesthetized rats, unilateral injection (60nL) of the TRPV1 agonist capsaicin into the RVLM dose‐dependently decreased renal SNA (0.5nmol: ‐9±1%; 1.0nmol: ‐44±6%; n>4) and mean ABP (0.5nmol: ‐4±1; 1 nmol: ‐15±2 mmHg; n>4). The sympathoinhibitory response to 1nmol capsaicin was eliminated by pretreatment with 600pmol of the TRPV1 antagonist capsazepine (renal SNA: ‐1±1%; mean ABP: 0±0 mmHg, n=6). Blockade of GABA receptors by pretreatment with bicuculline (60pmol) and CGP35348 (400pmol) did not prevent, but rather enhanced the sympathoinhibitory response to 1nmol capsaicin (renal SNA: ‐58±1%; mean ABP: ‐51±3; n=3). Blockade of ionotropic glutamate receptors by injection of kynurenic acid (3nmol) did not alter the capsaicin‐induced decrease in renal SNA (‐42±9%) or mean ABP (‐13±3mmHg, n=4). The present findings suggest that activation of TRPV1 channels in the RVLM inhibit renal SNA and ABP independently of GABAergic or glutamatergic neurotransmission. Supported by NIH HL090826, AHA 0630202N & 0625260B