G-protein-coupled estrogen receptor as a new therapeutic target for treating coronary artery disease

Table 1 Primary effects of G-protein-coupled estrogen receptor activation on coronary arteries

Effect	Species	Drug
Relaxation	Porcine	G-1[36,46]
		ICI182,780[35,36]
		Raloxifene[37]
		Tamoxifen[73]
	Rabbit	Raloxifene[54]
		Tamoxifen[74]
Endothelial NO production	Porcine	G-1[36]
		Raloxifene[54]
		Tamoxifen[74]
CASMC BKCa channel opening	Porcine	G-1[46]
		Raloxifene[37]
		Tamoxifen[10]
	Human	G-1[46]
Inhibition of CASMC proliferation	Porcine	G-1[47]
	Human	G-1[47]
Inhibition of CASMC migration	Porcine	G-1[47]

CASMC: Coronary artery smooth muscle cells; BK_Ca: G-1 opens calcium-activated potassium; NO: Nitric oxide.

Table 2 Evidence for possible therapeutic effects of G-protein-coupled estrogen receptor agonists and selective estrogen receptor modulators

	Species	Drug
Coronary artery relaxation
Endothelium-dependent, in vitro	Porcine	G-1[36]
	Rabbit	Raloxifen[54]
		Tamoxifen[73,74]
Endothelium-independent, in vitro	Porcine	G-1[46]
		Raloxifen[37]
Reduced cardiac ischemic injury/infarct	Rat	G-1[75,76]
Reduced cerebral ischemic injury/infarct	Mice	G-1[77]
Middle cerebral artery relaxation, in vitro	Rat	G-1[78]
Systemic artery relaxation, in vitro	Mice	G-1[40]
		G-1[49]
		G-1[50]
		G-1[79]
	Rat	G-1[51]
		G-1[52]
	Human	G-1[50]
Reduced systemic blood pressure, infusion	Rats	G-1[49]
		G-1[50]
Inhibit VSM cell proliferation	Porcine	G-1[47]
	Human	G-1[50]
Inhibit endothelial cell proliferation	Mice	G-1[70]
Prevents calcium-induced increases in plasma cholesterol	Rats	G-1[80]

VSM: Vascular smooth muscle.