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Increased expression of angiotensin converting enzyme 2 in conjunction with reduction of neointima by angiotensin II type 1 receptor blockade.
Hypertens Res. 2008 Mar; 31(3):553-9.HR

Abstract

Angiotensin converting enzyme 2 (ACE2), a newly recognized homolog of ACE that converts angiotensin II (Ang II) to angiotensin-1-7 (Ang-(1-7)), is found in vascular smooth muscle cells. Expression of ACE2 may be a local determinant of vascular Ang-(1-7) production and, when increased, may augment the increasingly recognized protective effects of this peptide within injured tissues. We previously showed that treatment with the angiotensin II type 1 (AT1) receptor blocker (ARB) olmesartan increased aortic ACE2 and Ang-(1-7) in conjunction with improved vascular remodeling in spontaneously hypertensive rats (SHR). In the present study, we investigated balloon injury-related ACE2 in the vasculature by determining the effect of sustained AT1 blockade on ACE2 protein expression in the carotid arteries of 12-week-old male SHR treated with either vehicle (n=5) or 10 mg/kg olmesartan (n=5) in drinking water for 14 days. Olmesartan treatment caused a 61% reduction in the cross-sectional area of the neointima, from 0.27+/-0.01 mm2 in vehicle-treated rats to 0.11+/-0.01 mm2 in olmesartan-treated rats. In contrast, olmesartan treatment had no effect on the medial area of injured or uninjured carotid arteries compared to that in vehicle-treated rats. Quantitative analysis of ACE2 immunostaining intensity in the carotid artery of SHR was significantly greater (p<0.05) in the neointima of olmesartan-treated SHR compared to that in vehicle-treated animals. In contrast, ACE2 immunostaining intensity was not quantitatively different in uninjured carotid arteries of olmesartan and vehicle-treated animals. These studies suggest that changes in ACE2 within the vascular system of SHR are regulated by a factor other than arterial pressure.

Authors+Show Affiliations

Department of Geriatric Medicine, Ehime University School of Medicine, Toon, Japan. migase@m.ehime-u.ac.jpNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

18497476

Citation

Igase, Michiya, et al. "Increased Expression of Angiotensin Converting Enzyme 2 in Conjunction With Reduction of Neointima By Angiotensin II Type 1 Receptor Blockade." Hypertension Research : Official Journal of the Japanese Society of Hypertension, vol. 31, no. 3, 2008, pp. 553-9.
Igase M, Kohara K, Nagai T, et al. Increased expression of angiotensin converting enzyme 2 in conjunction with reduction of neointima by angiotensin II type 1 receptor blockade. Hypertens Res. 2008;31(3):553-9.
Igase, M., Kohara, K., Nagai, T., Miki, T., & Ferrario, C. M. (2008). Increased expression of angiotensin converting enzyme 2 in conjunction with reduction of neointima by angiotensin II type 1 receptor blockade. Hypertension Research : Official Journal of the Japanese Society of Hypertension, 31(3), 553-9. https://doi.org/10.1291/hypres.31.553
Igase M, et al. Increased Expression of Angiotensin Converting Enzyme 2 in Conjunction With Reduction of Neointima By Angiotensin II Type 1 Receptor Blockade. Hypertens Res. 2008;31(3):553-9. PubMed PMID: 18497476.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Increased expression of angiotensin converting enzyme 2 in conjunction with reduction of neointima by angiotensin II type 1 receptor blockade. AU - Igase,Michiya, AU - Kohara,Katsuhiko, AU - Nagai,Tokihisa, AU - Miki,Tetsuro, AU - Ferrario,Carlos M, PY - 2008/5/24/pubmed PY - 2008/7/2/medline PY - 2008/5/24/entrez SP - 553 EP - 9 JF - Hypertension research : official journal of the Japanese Society of Hypertension JO - Hypertens Res VL - 31 IS - 3 N2 - Angiotensin converting enzyme 2 (ACE2), a newly recognized homolog of ACE that converts angiotensin II (Ang II) to angiotensin-1-7 (Ang-(1-7)), is found in vascular smooth muscle cells. Expression of ACE2 may be a local determinant of vascular Ang-(1-7) production and, when increased, may augment the increasingly recognized protective effects of this peptide within injured tissues. We previously showed that treatment with the angiotensin II type 1 (AT1) receptor blocker (ARB) olmesartan increased aortic ACE2 and Ang-(1-7) in conjunction with improved vascular remodeling in spontaneously hypertensive rats (SHR). In the present study, we investigated balloon injury-related ACE2 in the vasculature by determining the effect of sustained AT1 blockade on ACE2 protein expression in the carotid arteries of 12-week-old male SHR treated with either vehicle (n=5) or 10 mg/kg olmesartan (n=5) in drinking water for 14 days. Olmesartan treatment caused a 61% reduction in the cross-sectional area of the neointima, from 0.27+/-0.01 mm2 in vehicle-treated rats to 0.11+/-0.01 mm2 in olmesartan-treated rats. In contrast, olmesartan treatment had no effect on the medial area of injured or uninjured carotid arteries compared to that in vehicle-treated rats. Quantitative analysis of ACE2 immunostaining intensity in the carotid artery of SHR was significantly greater (p<0.05) in the neointima of olmesartan-treated SHR compared to that in vehicle-treated animals. In contrast, ACE2 immunostaining intensity was not quantitatively different in uninjured carotid arteries of olmesartan and vehicle-treated animals. These studies suggest that changes in ACE2 within the vascular system of SHR are regulated by a factor other than arterial pressure. SN - 0916-9636 UR - https://www.unboundmedicine.com/medline/citation/18497476/Increased_expression_of_angiotensin_converting_enzyme_2_in_conjunction_with_reduction_of_neointima_by_angiotensin_II_type_1_receptor_blockade_ L2 - https://medlineplus.gov/highbloodpressure.html DB - PRIME DP - Unbound Medicine ER -