LDL receptor
PGF2α simulates an increase in systolic blood pressure in wild type but not FP(−/−) mice. Furthermore, FP(-/-) mice have significantly lower blood pressure, lower plasma renin levels, and lower plasma angiotensin-1 levels than wild-type mice, and FP agonists have a negative inotropic effect to weaken the strength of heart beating in rats. Finally, FP(−/−) mice deficient in the LDL receptor exhibit significantly less atherosclerosis than FP(+/+) LDL receptor-deficient mice. Activation of FP thus has pathophysiological consequences for the cardiovascular system relative to blood pressure, cardiac function, and atherosclerosis in animal models. The mechanism behind these FP effects and their relevancy to humans have not been elucidated.