ROLE OF ALPHA-1-ADRENERGIC RECEPTORS IN THE INTERMEDIOLATERAL COLUMN IN MEDIATING THE PRESSOR-RESPONSES ELICITED BY THE STIMULATION OF VENTROLATERAL MEDULLARY PRESSOR AREA

Citation
V. Malhotra et al., ROLE OF ALPHA-1-ADRENERGIC RECEPTORS IN THE INTERMEDIOLATERAL COLUMN IN MEDIATING THE PRESSOR-RESPONSES ELICITED BY THE STIMULATION OF VENTROLATERAL MEDULLARY PRESSOR AREA, Brain research, 626(1-2), 1993, pp. 278-286
Citations number
37
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00068993
Volume
626
Issue
1-2
Year of publication
1993
Pages
278 - 286
Database
ISI
SICI code
0006-8993(1993)626:1-2<278:ROARIT>2.0.ZU;2-T
Abstract
Microinjections of alpha1-adrenergic receptor agonists into the interm ediolateral cell column of the spinal cord (IML) elicit sympathoexcita tory responses. This observation, together with the identification of projections of epinephrine-containing cells in the rostral ventrolater al medullary pressor area (VLPA) to the IML, has prompted speculation that epinephrine may mediate pressor responses to the stimulation of t he VLPA. This hypothesis was tested in pentobarbital-anesthetized, art ificially ventilated, male Wistar rats. A mesenteric arterial branch w as cannulated for monitoring blood pressure. Pressor responses were el icited predominantly from T8-T10 by injections (1.7 nmol/20 nl) of L-g lutamate into the IML; maximum pressor responses (29.3 +/- 4 mmHg) wer e elicited from T9. Pressor responses were also elicited by injections of epinephrine into the IML at T9; maximum pressor effect (16.3 +/- 1 .2 mmHg) was elicited by a dose of 0.05 pmol/20 nl. This effect of epi nephrine at T9 was blocked by prior injections of prazosin (a selectiv e alpha1-adrenergic receptor blocker; 0.125 pmol/20 nl) at the same si te. Stimulation of the VLPA by unilateral microinjections of glutamate elicited pressor responses (56 +/- 12 mmHg). Bilateral injections of prazosin at T8-T10, in the dose (0.125 pmol) that blocked a maximally effective dose of epinephrine, did not block the pressor responses to subsequent injections of glutamate into the VLPA. On the other hand, b ilateral microinjections of AP-7 (an NMDA receptor blocker; 1 nmol/20 nl), but not DNQX (10 pmol; a non-NMDA receptor blocker), into the IML at T8-T10 blocked the pressor effects of the subsequent injections of glutamate into the VLPA. At the dose used, AP-7 did not alter pressor responses to injections of kainic acid or AMPA into the IML at T9. Th ese results suggest that under the experimental conditions in this stu dy, the pressor responses following the stimulation of VLPA are not me diated by alpha1-adrenergic receptors in the IML. On the other hand, N MDA receptors in the IML do mediate these pressor responses.