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Upregulation of angiotensin-converting enzyme 2 after myocardial infarction by blockade of angiotensin II receptors.
Hypertension. 2004 May; 43(5):970-6.H

Abstract

We investigated in Lewis normotensive rats the effect of coronary artery ligation on the expression of cardiac angiotensin-converting enzymes (ACE and ACE 2) and angiotensin II type-1 receptors (AT1a-R) 28 days after myocardial infarction. Losartan, olmesartan, or the vehicle (isotonic saline) was administered via osmotic minipumps for 28 days after coronary artery ligation or sham operation. Coronary artery ligation caused left ventricular dysfunction and cardiac hypertrophy. These changes were associated with increased plasma concentrations of angiotensin I, angiotensin II, angiotensin-(1-7), and serum aldosterone, and reduced AT1a-R mRNA. Cardiac ACE and ACE 2 mRNAs did not change. Both angiotensin II antagonists attenuated cardiac hypertrophy; olmesartan improved ventricular contractility. Blockade of the AT1a-R was accompanied by a further increase in plasma concentrations of the angiotensins and reduced serum aldosterone levels. Both losartan and olmesartan completely reversed the reduction in cardiac AT1a-R mRNA observed after coronary artery ligation while augmenting ACE 2 mRNA by approximately 3-fold. Coadministration of PD123319 did not abate the increase in ACE 2 mRNA induced by losartan. ACE 2 mRNA correlated significantly with angiotensin II, angiotensin-(1-7), and angiotensin I levels. These results provide evidence for an effect of angiotensin II blockade on cardiac ACE 2 mRNA that may be due to direct blockade of AT1a receptors or a modulatory effect of increased angiotensin-(1-7).

Authors+Show Affiliations

Hypertension and Vascular Disease Center, Wake Forest University Health Science Center, Winston-Salem, NC 27157, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15007027

Citation

Ishiyama, Yuichiro, et al. "Upregulation of Angiotensin-converting Enzyme 2 After Myocardial Infarction By Blockade of Angiotensin II Receptors." Hypertension (Dallas, Tex. : 1979), vol. 43, no. 5, 2004, pp. 970-6.
Ishiyama Y, Gallagher PE, Averill DB, et al. Upregulation of angiotensin-converting enzyme 2 after myocardial infarction by blockade of angiotensin II receptors. Hypertension. 2004;43(5):970-6.
Ishiyama, Y., Gallagher, P. E., Averill, D. B., Tallant, E. A., Brosnihan, K. B., & Ferrario, C. M. (2004). Upregulation of angiotensin-converting enzyme 2 after myocardial infarction by blockade of angiotensin II receptors. Hypertension (Dallas, Tex. : 1979), 43(5), 970-6.
Ishiyama Y, et al. Upregulation of Angiotensin-converting Enzyme 2 After Myocardial Infarction By Blockade of Angiotensin II Receptors. Hypertension. 2004;43(5):970-6. PubMed PMID: 15007027.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Upregulation of angiotensin-converting enzyme 2 after myocardial infarction by blockade of angiotensin II receptors. AU - Ishiyama,Yuichiro, AU - Gallagher,Patricia E, AU - Averill,David B, AU - Tallant,E Ann, AU - Brosnihan,K Bridget, AU - Ferrario,Carlos M, Y1 - 2004/03/08/ PY - 2004/3/10/pubmed PY - 2004/10/9/medline PY - 2004/3/10/entrez SP - 970 EP - 6 JF - Hypertension (Dallas, Tex. : 1979) JO - Hypertension VL - 43 IS - 5 N2 - We investigated in Lewis normotensive rats the effect of coronary artery ligation on the expression of cardiac angiotensin-converting enzymes (ACE and ACE 2) and angiotensin II type-1 receptors (AT1a-R) 28 days after myocardial infarction. Losartan, olmesartan, or the vehicle (isotonic saline) was administered via osmotic minipumps for 28 days after coronary artery ligation or sham operation. Coronary artery ligation caused left ventricular dysfunction and cardiac hypertrophy. These changes were associated with increased plasma concentrations of angiotensin I, angiotensin II, angiotensin-(1-7), and serum aldosterone, and reduced AT1a-R mRNA. Cardiac ACE and ACE 2 mRNAs did not change. Both angiotensin II antagonists attenuated cardiac hypertrophy; olmesartan improved ventricular contractility. Blockade of the AT1a-R was accompanied by a further increase in plasma concentrations of the angiotensins and reduced serum aldosterone levels. Both losartan and olmesartan completely reversed the reduction in cardiac AT1a-R mRNA observed after coronary artery ligation while augmenting ACE 2 mRNA by approximately 3-fold. Coadministration of PD123319 did not abate the increase in ACE 2 mRNA induced by losartan. ACE 2 mRNA correlated significantly with angiotensin II, angiotensin-(1-7), and angiotensin I levels. These results provide evidence for an effect of angiotensin II blockade on cardiac ACE 2 mRNA that may be due to direct blockade of AT1a receptors or a modulatory effect of increased angiotensin-(1-7). SN - 1524-4563 UR - https://www.unboundmedicine.com/medline/citation/15007027/Upregulation_of_angiotensin_converting_enzyme_2_after_myocardial_infarction_by_blockade_of_angiotensin_II_receptors_ L2 - https://www.ahajournals.org/doi/10.1161/01.HYP.0000124667.34652.1a?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -