Navegando por Palavras-chave "alpha-2 adrenoceptors"

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    Diabetic Hypertensive Leptin Receptor-Deficient db/db Mice Develop Cardioregulatory Autonomic Dysfunction
    (Lippincott Williams & Wilkins, 2009-02-01) Goncalves, Andrey C. da Costa; Tank, Jens; Diedrich, Andre; Hilzendeger, Aline Mourão [UNIFESP]; Plehm, Ralph; Bader, Michael [UNIFESP]; Luft, Friedrich C.; Jordan, Jens; Gross, Volkmar; Max Delbruck Ctr Mol Med; Hannover Med Sch; Universidade Federal de São Paulo (UNIFESP); Vanderbilt Univ; HELIOS Klin
    Leptin receptor-deficient db/db mice develop human type 2 diabetes mellitus, hypertension, and obesity with disrupted circadian blood pressure (BP) rhythm. Whether leptin is the sole mechanism mediating autonomic imbalance and hypertension is unclear. To explore this notion further, we measured BP by radiotelemetry combined with fast Fourier transformation and assessed autonomic function pharmacologically before and after renin-angiotensin system blockade with enalapril. the resting period BP (117 +/- 3 versus 108 +/- 1.0 mm Hg) and heart rate (HR; 488 +/- 12 versus 436 +/- 8 bpm) were higher in db/db mice compared with db/+ mice. BP and HR amplitudes were lower in db/db mice compared with db/+ mice. BP response to trimetaphan (-43 +/- 5 versus -27 +/- 3 mm Hg) and HR response to metoprolol (-59 +/- 12 versus -5 +/- 4 bpm) were greater in db/db mice than in db/+ mice. the HR response to atropine was blunted in db/db mice (59 +/- 17 versus 144 +/- 24 bpm), as were baroreflex sensitivity and HR variability. Enalapril improved autonomic regulation in db/db mice. Stimulation of central alpha-2 adrenoreceptors enhanced both parasympathetic HR control and baroreflex sensitivity in db/db mice. We suggest that functional, rather than structural, alpha-2 adrenoceptor changes and the renin-angiotensin system are involved in the increased sympathetic and decreased parasympathetic tones in db/db mice. Our data suggest that db/db mice exhibit features found in humans with type 2 diabetic autonomic neuropathy and could serve as a model for this complication. (Hypertension. 2009; 53[part 2]: 387-392.)
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    Impaired function of alpha-2 adrenoceptors in smooth muscle of mesenteric arteries from spontaneously hypertensive rats
    (Stockton Press, 1998-11-01) Feres, Teresa [UNIFESP]; Borges, Antonio Carlos Romao [UNIFESP]; Silva, Eneida de Gusmão [UNIFESP]; Paiva, Antonio Cechelli de Mattos [UNIFESP]; Paiva, Therezinha Bandiera [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    1 the alpha(2)-adrenoceptor function in mesenteric arteries of spontaneously hypertensive rats (SHR) was investigated by comparing membrane potential changes in response to adrenergic agonists in preparations from female SHR, Wistar-Kyoto (WKY) and normotensive Wistar rats (NWR).2 Resting membrane potential was found to be less negative in mesenteric arteries from SHR than in those from NWR and WKY. Apamin induced a decrease in the membrane potential of mesenteric artery rings without endothelium from NWR and WKY, but had no effects in those from SHR. Both UK 14,304 and adrenaline, in the presence of prazosin, induced a hyperpolarization that was significantly lower in de-endothelialized mesenteric rings from SHR than in those from NWR and WKY. in mesenteric rings with endothelium, however, similar hyperpolarization was observed in the three strains.3 in NWR mesenteric rings with endothelium the hyperpolarization induced by activation of alpha(2)-adrenoceptors was abolished by apamin, whereas in intact SHR mesenteric rings this hyperpolarization was slightly reduced by apamin and more efficiently reduced by N-omega-nitro-L-arginine.4 It is concluded that the activity of potassium channels coupled to alpha(2)-adrenoceptors is altered in the smooth muscle cells of SHR mesenteric arteries, contributing to their less negative membrane potential. On the other hand, the endothelial alpha(2)-receptors are functioning in mesenteric vessels from SHR and their stimulation induces a hyperpolarization mainly through the release of nitric oxide.
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    Recovery of impaired K+ channels in mesenteric arteries from spontaneously hypertensive rats by prolonged treatment with cholecalciferol
    (Stockton Press, 1999-06-01) Borges, Antonio Carlos R; Feres, Teresa; Vianna, Lucia M.; Paiva, Therezinha B. [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    1 the mechanism responsible for blood pressure reduction in spontaneously hypertensive rats (SHR) after prolonged cholecalciferol treatment was studied. Two-week treatment of SHR with 0.125 mg cholecalciferol kg(-1) body weight per day orally caused significant reductions of systolic blood pressure and of the resting perfusion pressure of the mesenteric vascular bed at constant flow.2 in addition, the treated animals presented a normalization of the maximum vasoconstriction response to noradrenaline and a reduction of the maximum effect of the adrenaline concentration-response curves. This latter effect probably was due to recovery of the impaired Ca2+-dependent K+ channels coupled to alpha(2)-adrenoceptors since it was prevented by apamin.3 the treatment with cholecalciferol also normalized the smooth muscle cell membrane potential of de-endothelialized mesenteric arteries of SHR and their hyperpolarizing responses to alpha(2)-adrenergic agonists, which were depressed in untreated SHR.4 in mesenteric rings with endothelium, alpha(2)-adrenergic agonists caused similar hyperpolarizing responses in the SHR and in normotensive Wistar (NWR) and Wistar Kyoto (WKY). in non cholecalciferol-treated SHR the hyperpolarizing mediator involved in this effect was NO, while in NWR it was the endothelium-derived hyperpolarizing factor (EDI-IF). After cholecalciferol treatment, the hyperpolarization induced by alpha(2)-adrenergic agonists in SHR smooth muscle cells was mediated by EDHF, as in NWR.5 Our results indicate that the hypotensive effect of cholecalciferol in the SHR is probably due to the normalization of vascular reactivity, by restoring the functioning of apamin- and ATP-sensitive K+ channels located in the vascular smooth muscle cell membrane, which are impaired in the SHR.