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