BLOCKADE OF ANGIOTENSIN RECEPTORS IN RAT ROSTRAL VENTROLATERAL MEDULLA REMOVES EXCITATORY VASOMOTOR TONE

Authors
Citation
S. Ito et Af. Sved, BLOCKADE OF ANGIOTENSIN RECEPTORS IN RAT ROSTRAL VENTROLATERAL MEDULLA REMOVES EXCITATORY VASOMOTOR TONE, American journal of physiology. Regulatory, integrative and comparative physiology, 39(6), 1996, pp. 1317-1323
Citations number
39
Categorie Soggetti
Physiology
ISSN journal
03636119
Volume
39
Issue
6
Year of publication
1996
Pages
1317 - 1323
Database
ISI
SICI code
0363-6119(1996)39:6<1317:BOARIR>2.0.ZU;2-R
Abstract
The rostral ventrolateral medulla (RVLM) plays a primary role in the t onic and phasic control of arterial blood pressure. Stimulation of ang iotensin receptors in this region appears to contribute to the tonic e xcitatory drive of RVLM neurons involved in the control of blood press ure, but the extent of this contribution has not been previously evalu ated. The present study used bilateral microinjections of angiotensin receptor antagonists into the RVLM of chloralose-anesthetized rats to determine the degree to which tonic blood pressure was dependent upon this angiotensin-mediated input. Bilateral injection into the RVLM of 1 nmol of [Sar(1),Thr(8)]angiotensin II or [Sar(1),IIe(8)] angiotensin II decreased blood pressure similar to 40 mmHg. The decrease in blood pressure elicited by these angiotensin antagonists was nearly as grea t as that elicited by complete bilateral inhibition of the RVLM produc ed by local injections of muscimol or elicited by inhibition of the au tonomic nervous system by intravenous injection of chlorisondamine. Th e decrease in blood pressure caused by injection of these angiotensin antagonists was localized to the RVLM and was dose related. Responses elicited by [Sar(1),Thr(8)]angiotensin II were eliminated by coinjecti on of angiotensin. In addition to markedly decreasing resting blood pr essure, 1 nmol of [Sar(1),Thr(8)]angiotensin II injected into the RVLM also completely antagonized the increase in blood pressure elicited b y blocking the tonic inhibitory influence exerted on the RVLM by neuro ns in the caudal ventrolateral medulla. These results demonstrate that tonic stimulation of angiotensin receptors in the RVLM accounts for m uch of the excitatory sympathetic vasomotor drive emanating from the R VLM.