chf-1024 and Cardiomyopathy--Hypertrophic

chf-1024 has been researched along with Cardiomyopathy--Hypertrophic* in 1 studies

Other Studies

1 other study(ies) available for chf-1024 and Cardiomyopathy--Hypertrophic

Article	Year
CHF-1024, a DA2/alpha2 agonist, blunts norepinephrine excretion and cardiac fibrosis in pressure overload. Cardiovascular drugs and therapy, 2001, Volume: 15, Issue:2 We compared the effects of an ACE inhibitor, captopril, with those of a DA2-dopaminergic/alpha2-adrenergic receptor agonist (CHF-1024) on neuroendocrine activation and cardiac fibrosis in a model of pressure-overload hypertrophy. Interrenal aortic stenosis was performed in 89 rats, treated with CHF-1024 (0.33, 2 or 6 mg kg(-1) day(-1)), or captopril (1 g/L). Hemodynamic variables were recorded. Cardiac and renal weights, plasma aldosterone, renin activity and urinary catecholamine excretion were measured, as well as cardiac collagen. Blood pressure was lower in stenotic animals treated with CHF-1024 compared to vehicle (161 +/- 10 vs 219 +/- 10 mmHg, p < 0.01), but LV weight was similar. CHF-1024 elicited a marked dose-dependent attenuation of urinary norepinephrine excretion (1.80 +/- 0.18 in controls compared to 0.40 +/- 0.14 microg/24 h at the highest dose, p < 0.01) and of LV perivascular fibrosis. Captopril provoked a marked hypotension, reduced cardiac and body weights, plasma aldosterone concentration, dopamine excretion and perivascular collagen. The DA2/alpha2 agonist CHF-1024 effectively blunts adrenergic drive and cardiac fibrosis in a rat model of pressure overload. Topics: Adrenergic alpha-Agonists; Analysis of Variance; Angiotensin-Converting Enzyme Inhibitors; Animals; Aortic Valve Stenosis; Captopril; Cardiomyopathy, Hypertrophic; Dose-Response Relationship, Drug; Hemodynamics; Hypertension, Renal; Ligation; Male; Norepinephrine; Rats; Rats, Sprague-Dawley; Tetrahydronaphthalenes	2001

Article

Year

CHF-1024, a DA2/alpha2 agonist, blunts norepinephrine excretion and cardiac fibrosis in pressure overload.

Cardiovascular drugs and therapy, 2001, Volume: 15, Issue:2

We compared the effects of an ACE inhibitor, captopril, with those of a DA2-dopaminergic/alpha2-adrenergic receptor agonist (CHF-1024) on neuroendocrine activation and cardiac fibrosis in a model of pressure-overload hypertrophy. Interrenal aortic stenosis was performed in 89 rats, treated with CHF-1024 (0.33, 2 or 6 mg kg(-1) day(-1)), or captopril (1 g/L). Hemodynamic variables were recorded. Cardiac and renal weights, plasma aldosterone, renin activity and urinary catecholamine excretion were measured, as well as cardiac collagen. Blood pressure was lower in stenotic animals treated with CHF-1024 compared to vehicle (161 +/- 10 vs 219 +/- 10 mmHg, p < 0.01), but LV weight was similar. CHF-1024 elicited a marked dose-dependent attenuation of urinary norepinephrine excretion (1.80 +/- 0.18 in controls compared to 0.40 +/- 0.14 microg/24 h at the highest dose, p < 0.01) and of LV perivascular fibrosis. Captopril provoked a marked hypotension, reduced cardiac and body weights, plasma aldosterone concentration, dopamine excretion and perivascular collagen. The DA2/alpha2 agonist CHF-1024 effectively blunts adrenergic drive and cardiac fibrosis in a rat model of pressure overload.

Topics: Adrenergic alpha-Agonists; Analysis of Variance; Angiotensin-Converting Enzyme Inhibitors; Animals; Aortic Valve Stenosis; Captopril; Cardiomyopathy, Hypertrophic; Dose-Response Relationship, Drug; Hemodynamics; Hypertension, Renal; Ligation; Male; Norepinephrine; Rats; Rats, Sprague-Dawley; Tetrahydronaphthalenes

2001