Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/34068
Title: Vascular mechanisms involved in angiotensin II-induced venoconstriction in hypertensive rats
Authors: Loiola, Rodrigo Azevedo [UNIFESP]
Fernandes, Liliam [UNIFESP]
Eichler, Rosangela
Tostes Passaglia, Rita de Cassia
Fortes, Zuleica Bruno
Carvalho, Maria Helena Catelli de
Universidade de São Paulo (USP)
Universidade Federal de São Paulo (UNIFESP)
Keywords: Angiotensin II
Venous system
Hypertension
Angiotensin receptors
Issue Date: 1-Oct-2011
Publisher: Elsevier B.V.
Citation: Peptides. New York: Elsevier B.V., v. 32, n. 10, p. 2116-2121, 2011.
Abstract: To investigate the venoconstrictor effect of angiotensin II (Ang II) in spontaneously hypertensive rats (SHR), we used preparations of mesenteric venular beds and the circular muscle of the portal veins. Vessels were tested with Ang II in the presence or absence of losartan, PD 123319, HOE 140, L-NAME, indomethacin, or celecoxib. in the mesenteric venular bed of SHR, the effect of Ang II (0.1 nmol) was nearly abolished by losartan and enhanced by HOE 140, indomethacin, and celecoxib, while PD1 23319 and L-NAME had no effect. in portal vein preparations, cumulative-concentration response curves (CCRC) to Ang II (0.1-100 nmol/L) exhibited a lower maximal response (E(max)) in SHR compared to Wistar rats. AT(1) receptor expression was similar in the two strains, while AT(2) receptor levels were lower in SHR portal veins when compared to Wistar. in SHR portal veins, losartan shifted the CCRC to Ang II to the right, while indomethacin and HOE 140 increased the E (max) to Ang II. PD 123319, celecoxib, and L-NAME had no effect. Taken together, our results suggest that Ang II-induced venoconstriction in SHR is mediated by activation of AT(1) receptors and this effect may be counterbalanced by kinin B(2) receptor and COX metabolites. Furthermore, our data indicate that there are different cellular and molecular mechanisms involved in the regulation of venous tonus of normotensive and hypertensive rats. These differences probably reflect distinct factors that influence arterial and venous bed in hypertension. (C) 2011 Elsevier Inc. All rights reserved.
URI: http://repositorio.unifesp.br/handle/11600/34068
ISSN: 0196-9781
Other Identifiers: http://dx.doi.org/10.1016/j.peptides.2011.09.011
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