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Evidence for a functional interaction of the angiotensin-(1-7) receptor Mas with AT1 and AT2 receptors in the mouse heart.
Hypertension. 2005 Oct; 46(4):937-42.H

Abstract

The aim of this study was to evaluate the angiotensin (Ang)-(1-7) effects in isolated mouse hearts. The hearts of male C57BL/6J and knockout mice for the Ang-(1-7) receptor Mas were perfused by the Langendorff method. After a basal period, the hearts were perfused for 20 minutes with Krebs-Ringer solution (KRS) alone (control) or KRS containing Ang-(1-7) (0.22 pmol/L), the Mas antagonist A-779 (115 nmol/L), the angiotensin type 1 receptor antagonist losartan (2.2 micromol/L), or the angiotensin type 2 receptor antagonist PD123319 (130 nmol/L). To evaluate the involvement of Ang receptors, prostaglandins, and nitric oxide in the Ang-(1-7) effects, the hearts were perfused for 20 to 30 minutes with KRS containing either A-779, losartan, PD123319, indomethacin, or NG-nitro-L-arginine methyl ester (L-NAME) alone or in association with subsequent Ang-(1-7) perfusion. In addition, hearts from Mas-knockout mice were perfused for 20 minutes with KRS containing Ang-(1-7) (0.22 pmol/L) and losartan. Ang-(1-7) alone did not change the perfusion pressure. Strikingly, in the presence of losartan, 0.22 pmol/L Ang-(1-7) induced a significant decrease in perfusion pressure, which was blocked by A-779, indomethacin, and L-NAME. Furthermore, this effect was not observed in Mas-knockout mice. In contrast, in the presence of PD123319, Ang-(1-7) produced a significant increase in perfusion pressure. This change was not modified by the addition of A-779. Losartan reduced but did not abolish this effect. Our results suggest that Ang-(1-7) produces complex vascular effects in isolated, perfused mouse hearts involving interaction of its receptor with angiotensin type 1- and type 2-related mechanisms, leading to the release of prostaglandins and nitric oxide.

Authors+Show Affiliations

Department of Physiology and Biophysics, Federal University of Minas Gerais, Belo Horizonte, Brazil.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16157793

Citation

Castro, Carlos Henrique de, et al. "Evidence for a Functional Interaction of the Angiotensin-(1-7) Receptor Mas With AT1 and AT2 Receptors in the Mouse Heart." Hypertension (Dallas, Tex. : 1979), vol. 46, no. 4, 2005, pp. 937-42.
Castro CH, Santos RA, Ferreira AJ, et al. Evidence for a functional interaction of the angiotensin-(1-7) receptor Mas with AT1 and AT2 receptors in the mouse heart. Hypertension. 2005;46(4):937-42.
Castro, C. H., Santos, R. A., Ferreira, A. J., Bader, M., Alenina, N., & Almeida, A. P. (2005). Evidence for a functional interaction of the angiotensin-(1-7) receptor Mas with AT1 and AT2 receptors in the mouse heart. Hypertension (Dallas, Tex. : 1979), 46(4), 937-42.
Castro CH, et al. Evidence for a Functional Interaction of the Angiotensin-(1-7) Receptor Mas With AT1 and AT2 Receptors in the Mouse Heart. Hypertension. 2005;46(4):937-42. PubMed PMID: 16157793.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Evidence for a functional interaction of the angiotensin-(1-7) receptor Mas with AT1 and AT2 receptors in the mouse heart. AU - Castro,Carlos Henrique de, AU - Santos,Robson Augusto Souza dos, AU - Ferreira,Anderson José, AU - Bader,Michael, AU - Alenina,Natalia, AU - Almeida,Alvair Pinto de, Y1 - 2005/09/12/ PY - 2005/9/15/pubmed PY - 2005/12/16/medline PY - 2005/9/15/entrez SP - 937 EP - 42 JF - Hypertension (Dallas, Tex. : 1979) JO - Hypertension VL - 46 IS - 4 N2 - The aim of this study was to evaluate the angiotensin (Ang)-(1-7) effects in isolated mouse hearts. The hearts of male C57BL/6J and knockout mice for the Ang-(1-7) receptor Mas were perfused by the Langendorff method. After a basal period, the hearts were perfused for 20 minutes with Krebs-Ringer solution (KRS) alone (control) or KRS containing Ang-(1-7) (0.22 pmol/L), the Mas antagonist A-779 (115 nmol/L), the angiotensin type 1 receptor antagonist losartan (2.2 micromol/L), or the angiotensin type 2 receptor antagonist PD123319 (130 nmol/L). To evaluate the involvement of Ang receptors, prostaglandins, and nitric oxide in the Ang-(1-7) effects, the hearts were perfused for 20 to 30 minutes with KRS containing either A-779, losartan, PD123319, indomethacin, or NG-nitro-L-arginine methyl ester (L-NAME) alone or in association with subsequent Ang-(1-7) perfusion. In addition, hearts from Mas-knockout mice were perfused for 20 minutes with KRS containing Ang-(1-7) (0.22 pmol/L) and losartan. Ang-(1-7) alone did not change the perfusion pressure. Strikingly, in the presence of losartan, 0.22 pmol/L Ang-(1-7) induced a significant decrease in perfusion pressure, which was blocked by A-779, indomethacin, and L-NAME. Furthermore, this effect was not observed in Mas-knockout mice. In contrast, in the presence of PD123319, Ang-(1-7) produced a significant increase in perfusion pressure. This change was not modified by the addition of A-779. Losartan reduced but did not abolish this effect. Our results suggest that Ang-(1-7) produces complex vascular effects in isolated, perfused mouse hearts involving interaction of its receptor with angiotensin type 1- and type 2-related mechanisms, leading to the release of prostaglandins and nitric oxide. SN - 1524-4563 UR - https://www.unboundmedicine.com/medline/citation/16157793/Evidence_for_a_functional_interaction_of_the_angiotensin__1_7__receptor_Mas_with_AT1_and_AT2_receptors_in_the_mouse_heart_ L2 - https://www.ahajournals.org/doi/10.1161/01.HYP.0000175813.04375.8a?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -