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Vasopeptidase inhibition and Ang-(1-7) in the spontaneously hypertensive rat.
Hypertension-linked decrease in the expression of brain gamma-adducin.
Role of blood pressure reduction in prevention of cardiac and vascular hypertrophy.
Angiotensin-(1-12) is an alternate substrate for angiotensin peptide production in the heart.
Localization of the novel angiotensin peptide, angiotensin-(1-12), in heart and kidney of hypertensive and normotensive rats.
Increased expression of angiotensin converting enzyme 2 in conjunction with reduction of neointima by angiotensin II type 1 receptor blockade.
Decreased cardiac Ang-(1-7) is associated with salt-induced cardiac remodeling and dysfunction.
Uptake and metabolism of the novel peptide angiotensin-(1-12) by neonatal cardiac myocytes.
Angiotensin receptors contribute to blood pressure homeostasis in salt-depleted SHR.
Angiotensin II AT1 receptors regulate ACE2 and angiotensin-(1-7) expression in the aorta of spontaneously hypertensive rats.
Salt-induced renal injury in spontaneously hypertensive rats: effects of nebivolol.
Attenuation of hypertension-mediated glomerulosclerosis in conjunction with increased angiotensin (1-7).
Nebivolol reduces cardiac angiotensin II, associated oxidative stress and fibrosis but not arterial pressure in salt-loaded spontaneously hypertensive rats.
Rats, Inbred SHR
Primacy of angiotensin converting enzyme in angiotensin-(1-12) metabolism.
Primacy of cardiac chymase over angiotensin converting enzyme as an angiotensin-(1-12) metabolizing enzyme.
ANGIOTENSIN 1-7 IN THE SPONTANEOUSLY HYPERTENSIVE
Blunting of cardioprotective actions of estrogen in female rodent heart linked to altered expression of cardiac tissue chymase and ACE2.
Blunting of estrogen modulation of cardiac cellular chymase/RAS activity and function in SHR.
Estrogen modulates the differential expression of cardiac myocyte chymase isoforms and diastolic function.
G-Protein-Coupled Estrogen Receptor Agonist G1 Improves Diastolic Function and Attenuates Cardiac Renin-Angiotensin System Activation in Estrogen-Deficient Hypertensive Rats.
Rats Inbred SHR