Navegando por Palavras-chave "VENTROLATERAL MEDULLA"

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    CARDIOVASCULAR EFFECTS PRODUCED BY MICROINJECTION of ANGIOTENSIN-(1-7) ON VASOPRESSOR and VASODEPRESSOR SITES of the VENTROLATERAL MEDULLA
    (Elsevier B.V., 1993-06-11) Silva, LCS; Fontes, MAP; Campagnolesantos, M. J.; Khosla, M. C.; Campos, R. R.; Guertzenstein, P. G.; Santos, RAS; Universidade Federal de Minas Gerais (UFMG); Universidade Federal de São Paulo (UNIFESP); CLEVELAND CLIN EDUC FDN
    In this study, we determined the cardiovascular effects produced by micro-injection of the heptapeptide Angiotensin-(1-7) [Ang-(1-7)] into the rat ventrolateral medulla (VLM). Micro-injection of Ang-(1-7) into the rostral VLM and the caudal pressor area of the VLM produced significant increases in arterial pressure, comparable to that observed with micro-injection of Ang II. the changes in arterial pressure were associated with more variable changes in heart rate (HR) (usually tachycardia). On the other hand, micro-injection of Ang-(1-7) into the caudal depressor area induced decreases in arterial pressure and HR. the results suggest that, besides Ang II, Ang-(1-7) is involved in the mediation of the cardiovascular actions of the renin-angiotensin system in the VLM.
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    THE CAUDAL VENTROLATERAL MEDULLA IS A SOURCE of TONIC SYMPATHOINHIBITION
    (Elsevier B.V., 1993-09-03) Cravo, S. L.; Morrison, S. F.; NORTHWESTERN UNIV; Universidade Federal de São Paulo (UNIFESP)
    The caudal ventrolateral medulla (CVLM) contains neurons that are essential for the elaboration of the sympathoinhibitory effects of baroreceptor afferent stimulation. To determine if neurons in the CVLM also mediate a tonic inhibition of sympathetic nerve activity (SNA), we examined the effects of lesioning CVLM neurons in baroreceptor-denervated rats. the sustained increases in both arterial pressure (AP; 40 mmHg) and splanchnic SNA (200%) indicate that the discharge of neurons in the CVLM maintains a tonic sympathoinhibition that contributes significantly to the maintenance of normotensive levels of SNA and AP.
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    EVIDENCE THAT ANGIOTENSIN-(1-7) PLAYS A ROLE in the CENTRAL CONTROL of BLOOD-PRESSURE AT the VENTROLATERAL MEDULLA ACTING THROUGH SPECIFIC RECEPTORS
    (Elsevier B.V., 1994-11-28) Fontes, MAP; Silva, LCS; Campagnolesantos, M. J.; Khosla, M. C.; Guertzenstein, P. G.; Santos, RAS; Universidade Federal de Minas Gerais (UFMG); Universidade Federal de São Paulo (UNIFESP); CLEVELAND CLIN FDN
    In this study we determined which angiotensin receptors may mediate the cardiovascular effects elicited by angiotensin-(1-7) [Ang-(1-7)] in the rostral ventrolateral medulla (RVLM) and caudal presser area (CPA) of the ventrolateral medulla (VLM) of anesthetized rats. Furthermore the role of endogenous angiotensins in these areas was also investigated. the presser effect produced by unilateral microinjection of Ang-(1-7) into the RVLM or CPA was not modified by either the AT(1) receptor antagonist, DuP 753 or by the AT(2) receptor antagonist, CGP 42112A, but was completely blocked by the Ang-(1-7) selective antagonist, A-779. in contrast, the presser effect produced by microinjection of angiotensin II (Ang II) was completely blocked by DuP 753 but was not changed by CGP 42112A or A-779. Bilateral microinjection of A-779 into the RVLM or CPA produced a significant fall in mean arterial pressure and heart rate. Microinjection of DuP 753 produced a presser effect comparable to bilateral injection of vehicle. These results indicate that, although Ang II acts in the VLM through an AT(1) receptor subtype, the cardiovascular effects produced by microinjection of Ang-(1-7) into the RVLM and CPA are mediated by a specific angiotensin receptor (AT(5)?). Furthermore, our data provide evidence that endogenous Ang-(1-7) participates at the VLM in the neural control of arterial blood pressure.
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    A FALL in ARTERIAL BLOOD-PRESSURE PRODUCED BY INHIBITION of the CAUDALMOST VENTROLATERAL MEDULLA - the CAUDAL PRESSER AREA
    (Elsevier B.V., 1994-11-01) Possas, O. S.; Campos, R. R.; Cravo, S. L.; Lopes, O. U.; Guertzenstein, P. G.; Universidade Federal de São Paulo (UNIFESP)
    The caudal edge of the ventrolateral medulla was mapped to localize sites where microinjections of L-glutamate (L-glu) produce presser responses in paralyzed and artificially ventilated urethane-anesthetized rats. Presser responses ranging from 15 to 65 mmHg were obtained when L-Glu (0.25 M, 200 nl) was microinjected in the ventral medullary surface within an area localized between the rootlets of the XII and first cervical nerves, lateral to the pyramids and just medial to the spinal roots of the XI cranial nerve. This area has been called the caudal presser area (CPA). Inhibition of the CPA by microinjection of GABA or glycine resulted in marked falls (15-45 mmHg) of arterial blood pressure (AP). Hypotension in response to CPA inhibition was also obtained in unanesthetized decerebrate animals. Cardiovascular responses to CPA stimulation or inhibition depend on the activity of neurons in the rostral ventrolateral medulla (RVLM). During hypotension provoked by RVLM inhibition, presser responses to CPA stimulation were abolished. Conversely, presser responses to RVLM stimulation were maintained during hypotension produced by inhibition of CPA, Presser response to bilateral carotid occlusion were not reduced by CPA inhibition. We conclude that cells in the caudal most ventrolateral medulla exert a tonic presser activity that contributes to maintenance of basal levels of the vasomotor tone and arterial blood pressure, its inhibition, however, does not prevent the presser response to carotid occlusion.