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As discussed in Chapter i, incidence of hypertension is influenced by gender. Basically, males exhibit higher incidence rates of essential hypertension than females until menopause. Following this stage in life, females' incidence rates increase and actually exceed incidence rates for males (Wolz et al., 2000). Naturally, this has alerted researchers to the importance of the menstrual cycle in protecting women from onset of high blood pressures until later in life (von Eiff et al., 1971). The relation between blood pressure and gender is clearly age-related. In general, males and females have comparable blood pressure levels in childhood and early adolescence. However, blood pressures in men begin to become higher than in women in mid-adolescence and remain that way until ages in the late 50s (National Center for Health Statistics, 1977). Furthermore, because smaller body sizes are associated with higher heart rates and males are typically larger than females, mean resting heart rates of women are generally higher than mean resting heart rates of men (Berkow, 1982). Although risk for hypertension clearly differs between males and females, the evidence that men who lead stressful lives are more susceptible to hypertension than women who lead such lives is largely based upon data on job stress and strain (Cesana et al., 2003; Schnall et al., 1992). When measures of home and family stress are measured in addition to work-related stress, these gender effects are less compelling (Brisson et al., 1999; James et al., 1993).

In a meta-analysis of 12 studies that compared cardiovascular responses to stress between males and females, Stoney, Davis, and Matthews (1987) found evidence to support gender differences in acute physiological response to stress. Males, in contrast to females, exhibited significantly higher SBP and epinephrine responses, but lower heart rate responses to stress. Measurement of hemodynamic responses of males and females using impedance cardiography has also revealed consistent gender differences, with males showing more of a total peripheral resistance response to mental stress than females, and females showing more of a cardiac output response to mental stress than males (Allen et al., 1993; Girdler et al., 1990). Furthermore, postmenopausal women were shown to exhibit higher heart rate, SBP, and epinephrine responses to stress than premenopausal women, suggesting that after menopause, women more closely resemble male acute physiological response profiles than prior to menopause (Saab et al., 1989). Interestingly, in some studies, postmenopausal women undergoing hormone replacement therapy have been shown to have lower blood pressure responses to mental stress than postmenopausal women not receiving hormone replacement (Matthews et al., 2001; von Eiff et al., 1971). Coupled with observations of elevated heart rate responses to stress in postmenopausal women (Burleson et al., 1998), these findings suggest that hormone replacement therapy returns women to their premenopausal cardiovascular reactivity pattern.

Comparable reductions in cardiovascular reactivity to stress with hormone replacement therapy have also been observed among women at risk for developing essential hypertension (McCubbin et al., 2002). In this study, as in many previous studies, postmenopausal women with either elevated blood pressures or a family history of coronary heart disease exhibited increased blood pressure responses to stress in comparison to women with normal blood pressures and no family history of heart disease. However, this effect was not observed among women on hormone replacement therapy, indicating that hormone replacement normalizes the acute cardiovascular response to stress, presumably lowering women's risk for subsequent development of essential hypertension.

Some contradictory findings regarding the effect of menopause and hormone replacement have also been reported (see Saab, 1989). In a more recent study in which young women were administered hormones to reduce estrogen to postmenopausal levels, no differences in cardiovascular or neuroendocrine responses to stress were detected (Matthews et al., 1998). Although this study did not examine the long-term effect of estrogen loss, the findings clearly failed to support previous work that suggested that normal ovarian functioning served a protective role for both acute physiological responses to stress and incidence of essential hypertension.

Studies investigating gender differences in cardiovascular response to stress, however, have been criticized on the grounds that they typically employ competitive mental tasks that can be characterized as masculine in nature (like mental arithmetic or a handgrip challenge). As such, the heightened cardiovascular responses commonly observed among males may represent the fact that men are more threatened or engaged by these sorts of tasks than women. In fact, studies comparing responses of men and women to tasks that might be characterized as being more challenging to the traditionally female gender role, like interpersonal cooperation with one's spouse or talking about one's physical appearance, have yielded greater cardiovascular responses among women (Fritz, Matthews, and Cohen, 2001; Smith et al., 1998; Stroud, Niaura, and Stoney, 2001).

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