Sex differences in primary hypertension

Sex differences in biology arise from differences in sex chromosome dosage (2X vs. 1X or 0Y vs. 1Y) [1]. It is the transcription factor Sry located on the Y chromosome that causes differentiation of testes and leading to a rise in the levels of testosterone (T) in utero. Since one's sex is defined phenotypically (i.e., whether one is born with testes or ovaries), a functioning Sry leads to the birth of a male while in its absence (e.g., an XX or XO individual), ovaries develop and a female is born. Thus, Y dosage (0Y or 1Y) dictates the hormonal milieu in utero and throughout the life span. Physiological sex differences can also arise from differences in X dosage (2X or 1X) as a result of differences in parental imprinting, escape from X-inactivation and X-mosacism. This review will focus not only on the impact of the gonadal hormone milieu but also on the other effects that differences in the sex chromosome complement can exert on blood pressure control. The current state of knowledge regarding sex differences in the pathophysiology of human hypertension as well as the clinical implications of studies conducted in experimental animal models of hypertension will be addressed.Many organizations including the leading United States authority on blood pressure - the Joint National Committee on the Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC) - define hypertension as a systolic blood pressure (SBP) ≥ 140 or a diastolic blood pressure (DBP) of ≥ 90 mm Hg. According to the 7th and the latest report of the JNC [2], high blood pressure is divided into three categories (in mm Hg): Prehypertension (SBP of 120-139 or DBP between 80-89); Stage 1 hypertension (SBP of 140-159 or DBP between 90-99); and, Stage 2 hypertension (SBP ≥ 160 or DBP ≥ 100).High blood pressure can lead to substantial morbidity by damaging the function of critical organs including the brain, heart, blood vessels and kidney [3]. Hypertension is a leading cause of stroke [4,5]