CONTRIBUTION OF ALPHA(2)-ADRENOCEPTORS IN CAUDAL VENTROLATERAL MEDULLA TO CARDIOVASCULAR REGULATION IN RAT

The inhibitory action of alpha(2)-agonists on the cardiovascular neuro ns has been elucidated in the rostral ventrolateral medulla (RVLM) but not in the caudal ventrolateral medulla (CVLM). Our study aimed to cl arify whether microinjection of clonidine into the CVLM elicits any ca rdiovascular effect and whether endogenous alpha(2)-adrenoceptor-media ted mechanisms contribute to the tonic activity of the CVLM neurons. I n male Sprague-Dawley rats (7-9 wk old, 270-320 g) anesthetized with u rethan, unilateral microinjection of 8 nmol of clonidine into the CVLM (n = 10) increased mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) by 12.1 +/- 1.8 mmHg (mean +/- SE, P < 0.01) an d 25.8 +/- 4.8% (P < 0.01), while heart rate (KR) remained unaltered. Unilateral microinjection of 2 nmol of SKF-86466, a selective blocker of the az-adrenoceptors, into the CVLM (n = 10) decreased MAP, HR, and RSNA(-11.6 +/- 2.6 mmHg, -26 +/- 7 beats/min, and -15.3 +/- 1.7%, res pectively, P < 0.01 for each). Artificial cerebrospinal fluid caused n either a cardiovascular effect nor a sympathetic response. Prior injec tion of SKF-86466 into the ipsilateral CVLM attenuated the effects of clonidine. Bilateral microinjection of muscimol into the RVLM abolishe d the effects of both clonidine and SKF-86466 injected into the CVLM. The presser and sympathoexcitatory effects of clonidine injected into the CVLM suggest a neuroinhibitory action of the drug on the CVLM neur ons. In addition,the depressor and sympathoinhibitory effects of SKF-8 6466 injected into the CVLM indicated that activation of alpha(2)-adre noceptors by endogenous ligand inhibits CVLM neurons. The effects of c lonidine and the alpha(2)-adrenoceptor antagonist in the CVLM require the integrity of the RVLM.