Abstract
The present study was designed to investigate the effects of estradiol-ethylenediamine derivative on perfusion pressure and coronary resistance in rats. An additional aim was to identify the molecular mechanisms involved. The Langendorff model was used to measure perfusion pressure and coronary resistance changes in isolated rat heart after estradiol-ethylenediamine derivative alone and following compounds; tamoxifen (estrogen receptor antagonist), prazosin (alpha1 adrenoreceptor antagonist), metoprolol (selective beta1 receptor blocker), indomethacin (prostanglandin synthesis inhibitor) and nifedipine (L-type calcium-channel inhibitor). The results show that estradiol-ethylenediamine derivative [10(-9) mmol] significantly increased perfusion pressure (p = 0.005) and coronary resistance (p = 0.006) in isolated rat heart. Additionally, the effect of estradiolethylenediamine on perfusion pressure [10(-9) to 10(-4) mmol] was only blocked in the presence of the L-type calcium-channel (nifedipine). These data suggest that the effect of estradiol-ethylenediamine on perfusion pressure and vascular coronary involves activation of the L-type calcium channel through a non-genomic molecular mechanism.
Highlights
High blood pressure contributes substantially to cardiovascular disease incidence and premature mortality[1,2,3]
The results showed that estradiol derivative [10–9 mmol] significantly increased the perfusion pressure (p = 0.005) in comparison with the control. (Fig. 3) shows that coronary resistance calculated as the ratio of perfusion pressure at the coronary flow assayed (10 ml/min) was higher (p = 0.006) in the presence of estradiol-ethylenediamine derivative [10–9 mmol] than in controls. (Fig. 4) shows that estradiol-ethylenediamine derivative, increased the perfusion pressure in a dose dependent manner [10–9 to [] mmol] and that this effect was not inhibited by tamoxifen [10–6 mmol]
In isolated rat heart: L-type calcium channel the effect of estradiol-ethylenediamine derivative [10–9 to [] mmol] on perfusion pressure was not blocked by indomethacin [10–6 mmol]
Summary
High blood pressure contributes substantially to cardiovascular disease incidence and premature mortality[1,2,3]. Studies monitoring ambulatory blood pressure have shown that blood pressure is higher in men than in women of similar age[4,5]. Male spontaneously hypertensive rats (SHR) have higher blood pressure than do females of similar age[12,13,14]. These data suggest that among others, estrogen levels may influence blood pressure. In this regard, there is evidence that estrogen replacement in ovariectomized rats reduces arterial pressure response to psychological stress and that these effects are mediated, at least in part by nitric oxide[15]. Estrogens have been shown to protect transgenic hypertensive rats by shifting the vasoconstrictorvasodilator balance of the renin-angiotensin system and induce change in blood pressure[16]
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