Involvement of central alpha(1)- and mu(2)-adrenoceptors on cardiovascular responses to moxonidine

Involvement of central alpha(1)- and mu(2)-adrenoceptors on cardiovascular responses to moxonidine

Author Moreira, Thiago S. Google Scholar
Takakura, Ana C. Google Scholar
Menani, Jose V. Google Scholar
Colombari, Eduardo Google Scholar
Institution Universidade Federal de São Paulo (UNIFESP)
Univ Estadual Paulista
Abstract In the present study we compared the effects produced by moxonidine (alpha(2)-adrenoceptor/imidazoline agonist) injected into the 4th cerebral ventricle and into the lateral cerebral ventricle on mean arterial pressure, heart rate and on renal, mesenteric and hindquarter vascular resistances, as well as the possible action of moxonidine on central alpha(1)- or alpha(2)-adrenoceptors to produce cardiovascular responses. Male Holtzman rats (n = 7-8) anesthetized with urethane (0.5 g/kg, intravenously - i.v.) and alpha-chloralose (60 mg/kg, i.v.) were used. Moxonidine (5, 10 and 20 nmol) injected into the 4th ventricle reduced arterial pressure (-19 +/- 5, -30 +/- 7 and -43 +/- 8 mmHg vs. vehicle: 2 +/- 4 mmHg), heart rate (-10 +/- 6, - 16 +/- 7 and -27 +/- 9 beats per minute - bpm, vs. vehicle: 4 +/- 5 bpm), and renal, mesenteric and hindquarter vascular resistances. Moxonidine (5, 10 and 20 nmol) into the lateral ventricle only reduced renal vascular resistance (-77 +/- 17%, - 85 +/- 13%, -89 +/- 10% vs. vehicle: 3 +/- 4%), without changes on arterial pressure, heart rate and mesenteric and hindquarter vascular resistances. Pre-treatment with the selective alpha(2)-adrenoceptor antagonist yohimbine (80, 160 and 320 nmol) injected into the 4th ventricle attenuated the hypotension (-32 +/- 5, -25 +/- 4 and -12 +/- 6 mmHg), bradycardia (-26 +/- 11, -23 +/- 5 and -11 +/- 6 bpm) and the reduction in renal, mesenteric and hindquarter vascular resistances produced by moxonidine (20 nmol) into the 4th ventricle. Pretreatment with yohimbine (320 nmol) into the lateral ventricle did not change the renal vasodilation produced by moxonidine (20 nmol) into the lateral ventricle. the alpha(1)-adrenoceptor antagonist prazosin (320 nmol) injected into the 4th ventricle did not affect the cardiovascular effects of moxonidine. However, prazosin (80, 160 and 320 nmol) into the lateral ventricle abolished the renal vasodilation (-17 +/- 4, -6 +/- 9 and 2 +/- 11%) produced by moxonidine. the results indicate that the decrease in renal vascular resistance due to moxonidine action in the forebrain is mediated by alpha(1)-adrenoceptors, while the cardiovascular effects produced by moxonidine acting in the brainstern depend at least partially on the activation of coadrenoceptors. (c) 2007 Elsevier B.V. All rights reserved.
Keywords arterial pressure
vascular resistance
alpha(1)- and alpha(2)-adrenoceptors
hypotension
anti-hypertensive
sympathetic activity
Language English
Date 2007-06-01
Published in European Journal of Pharmacology. Amsterdam: Elsevier B.V., v. 563, n. 1-3, p. 164-171, 2007.
ISSN 0014-2999 (Sherpa/Romeo, impact factor)
Publisher Elsevier B.V.
Extent 164-171
Origin http://dx.doi.org/10.1016/j.ejphar.2007.02.002
Access rights Closed access
Type Article
Web of Science ID WOS:000246608300021
URI http://repositorio.unifesp.br/handle/11600/29798

Show full item record




File

File Size Format View

There are no files associated with this item.

This item appears in the following Collection(s)

Search


Browse

Statistics

My Account