Do stretch sensors expressed by aortic baroreceptors interact with circulating estradiol to mediate baroreflex sensitivity in hypertension?

Hypertension, or high blood pressure, is a major risk factor for cardiovascular disease, the leading cause of mortality worldwide. The incidence and the severity of hypertension is higher in middle-aged men than women. The hallmark of hypertension is an increased sympathetic nerve activity to the cardiovascular organs. One mechanism that regulates sympathetic nerve activity is the homeostatic baroreflex which maintains blood pressure at optimal levels for survival. Baroreceptive nerve endings innervating the aortic arch detect stretch at the vascular wall and convey these signals to the hindbrain which subsequently modulates sympathetic nerve activity. Although the baroreflex was described more than 80 years ago, the specific molecular, structural, and functional phenotype of aortic baroreceptors remain to be fully elucidated. Several recent studies suggest the involvement of various ion channels, termed as "Stretch Sensors", in detecting vascular stretch. Stretch sensors are diverse, and they include