Evaluation of positive inotropic activity induced by a triazole derivative using an isolated heart model

Figueroa Valverde Lauro, Díaz Cedillo Francisco, García Cervera Elodia, Pool Gómez Eduardo, López Ramos Maria, Rosas Nexticapa Marcela, Hau Heredia Lenin, Sarabia Alcocer Betty, Betty M. Velázquez-Sarabia

Research output: Contribution to journalArticle

Abstract

There are some reports which indicate that several triazole derivatives have inotropic activity; however, the cellular site and mechanism of action at cardiovascular level is very confusing. In order, to have a clear understanding of these phenomena, a triazole derivative was synthesized to evaluate its biological activity on left ventricular pressure and characterize the molecular mechanism. The Langendorff technique was used to measure changes on perfusion pressure and coronary resistance in an isolated rat heart model in absence or presence of the triazole derivative. Additionally, the molecular mechanism involved in the inotropic activity induced by the triazole derivative was evaluated by measuring left ventricular pressure in absence or presence of the following compounds; prazosin, metoprolol, nifedipine, indomethacin and the compound BM-531. The results showed that the triazole derivative significantly increased the perfusion pressure and coronary resistance in comparison with the control conditions. Other data indicate that the triazole derivative increase left ventricular pressure in a dose-dependent manner (0.001 to 100 nM); nevertheless, this phenomenon was significantly inhibited only by indomethacin and BM-531 at a dose of 1 nM. Therefore, experimental results suggest that positive inotropic activity induced by the triazole derivative is via activation of TXA2. This phenomenon is particularly interesting because the inotropic activity induced by the triazole derivative involves a molecular mechanism different in comparison with other positive inotropic drugs.
Original languageAmerican English
Pages (from-to)183-191
Number of pages163
JournalBiomedical Research (India)
StatePublished - 1 Jan 2014

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Triazoles
Derivatives
Ventricular Pressure
Indomethacin
Perfusion
Pressure
Metoprolol
Prazosin
Nifedipine
Bioactivity
Rats
Chemical activation

Cite this

Lauro, F. V., Francisco, D. C., Elodia, G. C., Eduardo, P. G., Maria, L. R., Marcela, R. N., ... Velázquez-Sarabia, B. M. (2014). Evaluation of positive inotropic activity induced by a triazole derivative using an isolated heart model. Biomedical Research (India), 183-191.
Lauro, Figueroa Valverde ; Francisco, Díaz Cedillo ; Elodia, García Cervera ; Eduardo, Pool Gómez ; Maria, López Ramos ; Marcela, Rosas Nexticapa ; Lenin, Hau Heredia ; Betty, Sarabia Alcocer ; Velázquez-Sarabia, Betty M. / Evaluation of positive inotropic activity induced by a triazole derivative using an isolated heart model. In: Biomedical Research (India). 2014 ; pp. 183-191.
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abstract = "There are some reports which indicate that several triazole derivatives have inotropic activity; however, the cellular site and mechanism of action at cardiovascular level is very confusing. In order, to have a clear understanding of these phenomena, a triazole derivative was synthesized to evaluate its biological activity on left ventricular pressure and characterize the molecular mechanism. The Langendorff technique was used to measure changes on perfusion pressure and coronary resistance in an isolated rat heart model in absence or presence of the triazole derivative. Additionally, the molecular mechanism involved in the inotropic activity induced by the triazole derivative was evaluated by measuring left ventricular pressure in absence or presence of the following compounds; prazosin, metoprolol, nifedipine, indomethacin and the compound BM-531. The results showed that the triazole derivative significantly increased the perfusion pressure and coronary resistance in comparison with the control conditions. Other data indicate that the triazole derivative increase left ventricular pressure in a dose-dependent manner (0.001 to 100 nM); nevertheless, this phenomenon was significantly inhibited only by indomethacin and BM-531 at a dose of 1 nM. Therefore, experimental results suggest that positive inotropic activity induced by the triazole derivative is via activation of TXA2. This phenomenon is particularly interesting because the inotropic activity induced by the triazole derivative involves a molecular mechanism different in comparison with other positive inotropic drugs.",
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Lauro, FV, Francisco, DC, Elodia, GC, Eduardo, PG, Maria, LR, Marcela, RN, Lenin, HH, Betty, SA & Velázquez-Sarabia, BM 2014, 'Evaluation of positive inotropic activity induced by a triazole derivative using an isolated heart model', Biomedical Research (India), pp. 183-191.

Evaluation of positive inotropic activity induced by a triazole derivative using an isolated heart model. / Lauro, Figueroa Valverde; Francisco, Díaz Cedillo; Elodia, García Cervera; Eduardo, Pool Gómez; Maria, López Ramos; Marcela, Rosas Nexticapa; Lenin, Hau Heredia; Betty, Sarabia Alcocer; Velázquez-Sarabia, Betty M.

In: Biomedical Research (India), 01.01.2014, p. 183-191.

Research output: Contribution to journalArticle

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T1 - Evaluation of positive inotropic activity induced by a triazole derivative using an isolated heart model

AU - Lauro, Figueroa Valverde

AU - Francisco, Díaz Cedillo

AU - Elodia, García Cervera

AU - Eduardo, Pool Gómez

AU - Maria, López Ramos

AU - Marcela, Rosas Nexticapa

AU - Lenin, Hau Heredia

AU - Betty, Sarabia Alcocer

AU - Velázquez-Sarabia, Betty M.

PY - 2014/1/1

Y1 - 2014/1/1

N2 - There are some reports which indicate that several triazole derivatives have inotropic activity; however, the cellular site and mechanism of action at cardiovascular level is very confusing. In order, to have a clear understanding of these phenomena, a triazole derivative was synthesized to evaluate its biological activity on left ventricular pressure and characterize the molecular mechanism. The Langendorff technique was used to measure changes on perfusion pressure and coronary resistance in an isolated rat heart model in absence or presence of the triazole derivative. Additionally, the molecular mechanism involved in the inotropic activity induced by the triazole derivative was evaluated by measuring left ventricular pressure in absence or presence of the following compounds; prazosin, metoprolol, nifedipine, indomethacin and the compound BM-531. The results showed that the triazole derivative significantly increased the perfusion pressure and coronary resistance in comparison with the control conditions. Other data indicate that the triazole derivative increase left ventricular pressure in a dose-dependent manner (0.001 to 100 nM); nevertheless, this phenomenon was significantly inhibited only by indomethacin and BM-531 at a dose of 1 nM. Therefore, experimental results suggest that positive inotropic activity induced by the triazole derivative is via activation of TXA2. This phenomenon is particularly interesting because the inotropic activity induced by the triazole derivative involves a molecular mechanism different in comparison with other positive inotropic drugs.

AB - There are some reports which indicate that several triazole derivatives have inotropic activity; however, the cellular site and mechanism of action at cardiovascular level is very confusing. In order, to have a clear understanding of these phenomena, a triazole derivative was synthesized to evaluate its biological activity on left ventricular pressure and characterize the molecular mechanism. The Langendorff technique was used to measure changes on perfusion pressure and coronary resistance in an isolated rat heart model in absence or presence of the triazole derivative. Additionally, the molecular mechanism involved in the inotropic activity induced by the triazole derivative was evaluated by measuring left ventricular pressure in absence or presence of the following compounds; prazosin, metoprolol, nifedipine, indomethacin and the compound BM-531. The results showed that the triazole derivative significantly increased the perfusion pressure and coronary resistance in comparison with the control conditions. Other data indicate that the triazole derivative increase left ventricular pressure in a dose-dependent manner (0.001 to 100 nM); nevertheless, this phenomenon was significantly inhibited only by indomethacin and BM-531 at a dose of 1 nM. Therefore, experimental results suggest that positive inotropic activity induced by the triazole derivative is via activation of TXA2. This phenomenon is particularly interesting because the inotropic activity induced by the triazole derivative involves a molecular mechanism different in comparison with other positive inotropic drugs.

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