Effect of progesterone-carbachol derivative on perfusion pressure and coronary resistance in isolated rat heart: via activation of the M&lt;sub&gt;2&lt;/sub&gt; muscarinic receptor

Figueroa‐Valverde, Lauro; Díaz-Cedillo, Francisco; Elodia, García-Cervera; Gómez, E. Pool; María, López-Ramos

doi:10.5507/bp.2012.010

Cited by 4 publications

(4 citation statements)

References 33 publications

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“…The results showed that the effect of estradiol derivative was not inhibited by yohimbine or ICI 118,551, indicating that the molecular mechanism involved is not through adrenergic activity. Analyzing these results and other reports which indicate that some steroid derivatives induces activation of M 2 muscarinic (Figueroa-Valverde et al, 2012) that induces consequently a negative inotropic response and low blood pressure by activation of nitric oxide synthase (NOS) and increased production of cyclic GMP. In this study, the activity of estradiol derivative on left ventricular pressure was evaluated in the absence or presence of atropine.…”

Section: Discussionsupporting

confidence: 55%

Susceptibility to cardiac ischemia/reperfusion injury modulated by an estrogen derivative

Figueroa‐Valverde¹

2012

Afr. J. Pharm. Pharmacol.

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Several studies indicate that some steroid derivatives have activity at cardiovascular level; nevertheless, there is scarce information about the effects of the estradiol derivatives on cardiac injury ischemia/reperfusion (I/R). Therefore, in this study, an estradiol derivative was synthetized with the objective of evaluating its activity on I/R in an ischemia-reperfusion model. In addition, molecular mechanism involved in the activity of effect induced by estradiol derivative on perfusion pressure and coronary resistance was evaluated using the Langendorff technique by measuring left ventricular pressure in absence or presence of the following compounds; tamoxifen, yohimbine, ICI 118,551 and L-NAME. The results showed that estradiol derivative reduced infarct size compared with control. In addition, another results showed that the estradiol derivative significantly decrease the perfusion pressure and coronary resistance in isolated heart. Additionally, another data indicate that estradiol derivative low left ventricular pressure in a dose-dependent manner (1 × 10-9 to 1 × 10-4 mmol); however, this phenomenon was significantly inhibited by tamoxifen at a dose of 1 × 10-6 mmol and L-NAME (1 × 10-6 mmol). In conclusion, these data suggest that cardioprotective effect of estradiol derivative is through the interaction with estrogen receptor and activation of nitric oxide synthase. This phenomenon results in decrease of myocardial necrosis after ischemia and reperfusion.

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Section: Discussionsupporting

confidence: 55%

Susceptibility to cardiac ischemia/reperfusion injury modulated by an estrogen derivative

Figueroa‐Valverde¹

2012

Afr. J. Pharm. Pharmacol.

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“…Doses of ACh and SNP were determined according to previous research (Mourmoura et al 2014). The coronary resistance was determined by the relationship between coronary flow and perfusion pressure (mm Hg/mL/min) (Figueroa-Valverde et al 2012).…”

Section: Coronary Resistancementioning

confidence: 99%

Endothelin-1 and ET receptors impair left ventricular function by mediated coronary arteries dysfunction in chronic intermittent hypoxia rats

Wang

Guo

et al. 2017

Physiol Rep

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Obstructive sleep apnea (OSA) results in cardiac dysfunction and vascular endothelium injury. Chronic intermittent hypoxia (CIH), the main characteristic of OSAS, is considered to be mainly responsible for cardiovascular system impairment. This study is aimed to evaluate the role of endothelin‐1(ET‐1) system in coronary injury and cardiac dysfunction in CIH rats. In our study, Sprague–Dawley rats were exposed to CIH (FiO2 9% for 1.5 min, repeated every 3 min for 8 h/d, 7 days/week for 3 weeks). After 3 weeks, the left ventricular developed pressure (LVDP) and coronary resistance (CR) were measured with the langendorff mode in isolated hearts. Meanwhile, expressions of ET‐1 and ET receptors were detected by immunohistochemical and western blot, histological changes were also observed to determine effects of CIH on coronary endothelial cells. Results suggested that decreased LVDP level combined with augmented coronary resistance was exist in CIH rats. CIH could induce endothelial injury and endothelium‐dependent vasodilatation dysfunction in the coronary arteries. Furthermore, ET‐1 and ETA receptor expressions in coronary vessels were increased after CIH exposure, whereas ETB receptors expression was decreased. Coronary contractile response to ET‐1 in both normoxia and CIH rats was inhibited by ETA receptor antagonist BQ123. However, ETB receptor antagonist BQ788 enhanced ET‐1‐induced contractile in normoxia group, but had no significant effects on CIH group. These results indicate that CIH‐induced cardiac dysfunction may be associated with coronary injury. ET‐1 plays an important role in coronary pathogenesis of CIH through ETA receptor by mediating a potent vasoconstrictor response. Moreover, decreased ETB receptor expression that leads to endothelium‐dependent vasodilatation decline, might be also participated in coronary and cardiac dysfunction.

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“…The effects were obtained in isolated hearts perfused at a constant flow rate of 10 ml/min. Since a constant flow was used, changes in coronary pressure reflected the changes in coronary resistance (Figueroa-Valverde et al, 2012).…”

Section: Evaluation Of Effects Exerted By the Progesterone Derivativementioning

confidence: 99%

“…Recently, a study indicated that a progesterone derivative induce acardioprotective effect on injury by ischaemia/reperfusion via M2 muscarinic receptor and activation of nitric oxide synthase in an animal model (Figueroa-Valverde et al, 2012). Nevertheless, there are reports which indicate that the administration of medroxyprogesterone acetate can inhibit the effects of estradiol that lead to protection of the myocardium from reperfusion injury and that this involves both neutrophildependent and neutrophil-independent mechanisms (Jeanes et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Evaluation of activity exerted by a steroid derivative on injury by ischaemia/reperfusion

Figueroa‐Valverde¹,

DÃaz-Cedillo²,

Marcela³

et al. 2014

Afr. J. Pharm. Pharmacol.

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There are reports which indicate that some steroid derivatives have activity atcardiovascular level; nevertheless, there is scarce information about the effects exerted by the progesterone derivatives on cardiac injury caused by ischemia/reperfusion. In this study, a new steroid (progesterone derivative) was synthetized with the objective of evaluating its activity on ischemia/reperfusion injury. The Langendorff technique was used to evaluate the effect of progesterone derivative on ischemia/reperfusion injury. Additionally, molecular mechanism involved in the activity exerted by the progesterone derivative on perfusion pressure and coronary resistance was evaluated by measuring left ventricular pressure in absence or presence of following compounds; mifepristone, prazosin, metoprolol, indomethacin and nifedipine. The results showed that the progesterone derivative reduces infarct size compared with control. Other results showed that the progesterone derivative significantly increase (p = 0.05) the perfusion pressure and coronary resistance in isolated heart. Other data indicate that the progesterone derivative increase left ventricular pressure in a dose-dependent manner (0.001 to 100 nM); however, this phenomenon was significantly inhibited by nifedipine at a dose of 1 nM (p = 0.05). In conclusion, these data suggest that progesterone derivative exert acardioprotective effect via the calcium channels activation and consequently induces changes in the left ventricular pressure levels. This phenomenon results in decrease of myocardial necrosis after ischemia and reperfusion.

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Effect of progesterone-carbachol derivative on perfusion pressure and coronary resistance in isolated rat heart: via activation of the M<sub>2</sub> muscarinic receptor

Cited by 4 publications

References 33 publications

Susceptibility to cardiac ischemia/reperfusion injury modulated by an estrogen derivative

Susceptibility to cardiac ischemia/reperfusion injury modulated by an estrogen derivative

Endothelin-1 and ET receptors impair left ventricular function by mediated coronary arteries dysfunction in chronic intermittent hypoxia rats

Evaluation of activity exerted by a steroid derivative on injury by ischaemia/reperfusion

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