We compared the effects of an ACE inhibitor, captopril, with those of a DA(2)-dopaminergic/alpha (2)-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 <mu>g/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 DA(2)/<alpha>(2) agonist CHF-1024 effectively blunts adrenergic drive and cardiac fibrosis in a rat model of pressure overload.

Masson, S., Chimenti, S., Salio, M., Torri, M., Limana, F., Bernasconi, R., et al. (2001). CHF-1024, a DA2/alpha2 Agonist, blunts Norepinephrine Excretion and Cardiac Fibrosis in pressure Overload. CARDIOVASCULAR DRUGS AND THERAPY, 15(2), 131-138 [10.1023/A:1011170812267].

CHF-1024, a DA2/alpha2 Agonist, blunts Norepinephrine Excretion and Cardiac Fibrosis in pressure Overload

ANNONI, GIORGIO;
2001

Abstract

We compared the effects of an ACE inhibitor, captopril, with those of a DA(2)-dopaminergic/alpha (2)-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 g/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 DA(2)/(2) agonist CHF-1024 effectively blunts adrenergic drive and cardiac fibrosis in a rat model of pressure overload.
Articolo in rivista - Articolo scientifico
renovascular hypertension; alpha(2)-adrenoceptor agonist; DA(2)-dopaminergic agonist; norepinephrine; fibrosis
English
mar-2001
15
2
131
138
none
Masson, S., Chimenti, S., Salio, M., Torri, M., Limana, F., Bernasconi, R., et al. (2001). CHF-1024, a DA2/alpha2 Agonist, blunts Norepinephrine Excretion and Cardiac Fibrosis in pressure Overload. CARDIOVASCULAR DRUGS AND THERAPY, 15(2), 131-138 [10.1023/A:1011170812267].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10281/579
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