TY - JOUR
T1 - Positive inotropic activity induced by a dehydroisoandrosterone derivative in isolated rat heart model
AU - Figueroa-Valverde, L.
AU - Díaz-Cedillo, F.
AU - García-Cervera, E.
AU - Pool Gómez, E.
AU - López-Ramos, M.
AU - Rosas-Nexticapa, M.
AU - Martinez-Camacho, R.
PY - 2013/10
Y1 - 2013/10
N2 - Experimental studies indicate that some steroid derivatives have inotropic activity; nevertheless, there is scarce information about the effects of the dehydroisoandrosterone and its derivatives at cardiovascular level. In addition, to date the cellular site and mechanism of action of dehydroisoandrosterone at cardiovascular level is very confusing. In order, to clarify those phenomena in this study, a dehydroisoandrosterone derivative was synthesized with the objective of to evaluate its activity on perfusion pressure and coronary resistance and compare this phenomenon with the effect exerted by dehydroisoandrosterone. 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 dehydroisoandrosterone and its derivative. Additionally, to characterize the molecular mechanism involved in the inotropic activity induced by dehydroisoandrosterone derivative was evaluated by measuring left ventricular pressure in absence or presence of following compounds; flutamide, prazosin, metoprolol and nifedipine. The results showed that dehydroisoandrosterone derivative significantly increased the perfusion pressure and coronary resistance in comparison with the control conditions and dehydroisoandrosterone. Additionally, other data indicate that dehydroisoandrosterone derivative increase left ventricular pressure in a dose-dependent manner [1 × 10-9-1 × 10-4 mmol]; nevertheless, this phenomenon was significantly inhibited by nifedipine at a dose of 1 × 10-6 mmol. In conclusion, these data suggest that dehydroisoandrosterone derivative induces positive inotropic activity through of activation the L-type calcium channel.
AB - Experimental studies indicate that some steroid derivatives have inotropic activity; nevertheless, there is scarce information about the effects of the dehydroisoandrosterone and its derivatives at cardiovascular level. In addition, to date the cellular site and mechanism of action of dehydroisoandrosterone at cardiovascular level is very confusing. In order, to clarify those phenomena in this study, a dehydroisoandrosterone derivative was synthesized with the objective of to evaluate its activity on perfusion pressure and coronary resistance and compare this phenomenon with the effect exerted by dehydroisoandrosterone. 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 dehydroisoandrosterone and its derivative. Additionally, to characterize the molecular mechanism involved in the inotropic activity induced by dehydroisoandrosterone derivative was evaluated by measuring left ventricular pressure in absence or presence of following compounds; flutamide, prazosin, metoprolol and nifedipine. The results showed that dehydroisoandrosterone derivative significantly increased the perfusion pressure and coronary resistance in comparison with the control conditions and dehydroisoandrosterone. Additionally, other data indicate that dehydroisoandrosterone derivative increase left ventricular pressure in a dose-dependent manner [1 × 10-9-1 × 10-4 mmol]; nevertheless, this phenomenon was significantly inhibited by nifedipine at a dose of 1 × 10-6 mmol. In conclusion, these data suggest that dehydroisoandrosterone derivative induces positive inotropic activity through of activation the L-type calcium channel.
KW - Dehydroisoandrosterone derivative
KW - Inotropic activity
KW - Langendorff
UR - http://www.scopus.com/inward/record.url?scp=84885950245&partnerID=8YFLogxK
U2 - 10.1007/s12272-013-0166-7
DO - 10.1007/s12272-013-0166-7
M3 - Artículo
C2 - 23821476
SN - 0253-6269
VL - 36
SP - 1270
EP - 1278
JO - Archives of Pharmacal Research
JF - Archives of Pharmacal Research
IS - 10
ER -