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Angiotensin-converting enzyme 2 is an essential regulator of heart function
These genetic data for ACE2 show that it is an essential regulator of heart function in vivo and targeted disruption of ACE2 in mice results in a severe cardiac contractility defect, increased angiotensin II levels, and upregulation of hypoxia-induced genes in the heart. Expand
Counterregulatory actions of angiotensin-(1-7).
The accumulating evidence suggests that Ang-(1-7) may oppose the actions of Ang II either directly or by stimulation of prostaglandins and nitric oxide, which may explain the effective antihypertensive action of converting enzyme inhibitors in a variety of non-renin-dependent models of experimental and genetic hypertension as well as most forms of human hypertension. Expand
Advances in biochemical and functional roles of angiotensin-converting enzyme 2 and angiotensin-(1–7) in regulation of cardiovascular function
Key findings are discussed such as the elucidation of the regulatory mechanisms participating in the expression of ACE2 and angiotensin-(1–7) in the control of the circulation and the first example of a feedforward mechanism directed toward mitigation of the actions of ang Elliotensin II. Expand
Management of high blood pressure in African Americans: consensus statement of the Hypertension in African Americans Working Group of the International Society on Hypertension in Blacks.
The purpose of this consensus statement is to offer primary care providers a practical, evidence-based clinical tool for achieving blood pressure goals in African American patients. Expand
Role of the renin-angiotensin-aldosterone system and proinflammatory mediators in cardiovascular disease.
Large-scale trials are still required to determine the effects of the long-term suppression of inflammation on CVDs through the use of RAAS modulating agents, as well as to determine how closely markers of inflammatory activity may correlate with CVD outcomes. Expand
Angiotensin-(1-7) inhibits growth of cardiac myocytes through activation of the mas receptor.
Peptide hormones such as ANG II and endothelin contribute to cardiac remodeling after myocardial infarction by stimulating myocyte hypertrophy and myofibroblast proliferation. In contrast,Expand
Angiotensin-converting enzyme 2 and angiotensin-(1-7): an evolving story in cardiovascular regulation.
The chronology and rationale that led to the discovery of angiotensin-(1-7) as a hormone that, in its own right, opposes the vasoconstrictor and proliferative actions of ang Elliotensin II are summarized. Expand
Angiotensin-(1-7) dilates canine coronary arteries through kinins and nitric oxide.
The results suggest that increases in circulating levels of Ang-(1-7) accompanying long-term administration of converting enzyme inhibitors or Ang II receptor blockers may contribute to the cardioprotective actions of these drugs. Expand
Upregulation of Angiotensin-Converting Enzyme 2 After Myocardial Infarction by Blockade of Angiotensin II Receptors
Evidence is provided 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). Expand
Metabolism of angiotensin-(1-7) by angiotensin-converting enzyme.
It is suggested that increased levels of Ang-(1-7) following ACE inhibition may be due, in part, to decreased metabolism of the peptide. Expand