Effect of Antihypertensive Agents on Cardiovascular Reactivity to Stress

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If cardiovascular reactivity to stress mediates the stress-hypertension relation, it follows that interventions aimed at lowering blood pressure might also reduce the magnitude of cardiovascular response to stress. Although there is clear evidence that use of diuretics, adrenergic inhibitors, and vasodilators leads to diminished arterial pressures, we have not yet considered whether they exert this effect by dampening cardiovascular responses to stress. Given the differential physiological mechanisms through which these classes of antihypertensive medications exert their blood pressure-lowering effect, it is possible that they impact cardiovascular reactions to stress differently. For example, because beta-blockers lower blood pressure by blocking sympathetic nervous system activation of the heart, it would certainly be expected that heart rate reactions to stress would be tempered by beta-blockade. Conversely, treatment with diuretics might be expected to influence heart rate or blood pressure response to stress less than beta-blockers because of the indirect effect that diuretic action has on the sympathetic nervous system. Let's examine whether any class of antihypertensive medications affects cardiovascular reactivity to stress.

Research examining whether treatment with antihypertensive medications influences acute cardiovascular reactivity to stress is founded on empirical work demonstrating reductions in cardiovascular reactivity with antihypertensive therapy in SHRs (Weiss and Lund-gren, 1978). In this study, blood pressure responses to stress were reduced following treatment with direct vasodilators and a cardiac-selective beta-blocker, metoprolol, but not following treatment with a nonse-lective beta-blocker, propranolol. Presumably, the failure to observe reduced blood pressure reactions to stress with propranolol was associ ated with dual blockade of both cardiac-enhancing and vasodilating beta-adrenergic effects of the nonselective medication. Although these findings suggested that treatment with a number of antihypertensive medications resulted in reductions in both blood pressure and blood pressure response to stress among SHRs, it was unknown whether comparable findings would emerge when these same pharmacologic agents were tested on humans with hypertension.

Because of the obvious involvement of the sympathetic nervous system in eliciting cardiovascular responses to stress, the vast majority of studies conducted on humans have examined adrenergic-inhibiting agents, in particular beta-blockers. Presumably, when the beta-adren-ergic system is blocked pharmacologically, heart rate reactions to stress will be dampened, resulting in lowered cardiac output and blood pressure responses to stress as well as overall reductions in resting blood pressure. Although this hypothesis has appeal due to its simplicity, support for it is generally lacking. Empirical investigations of the influence of beta-blockers on stress-elicited cardiovascular reactions have been mixed, with some studies observing the hypothesized reduction in cardiovascular reactivity to stress during beta-blockade (Schmieder, 1983), some finding no change in cardiovascular reactivity (Nyberg, Graham, and Stokes, 1977), and still others finding reduced cardiovascular reactions, but only to certain types of experimental tasks (Dunn, de Carvalho, and Frohlich, 1978; Floras et al., 1985). Research on other classes of antihypertensive medications has also failed to demonstrate the hypothesized reductions in cardiovascular response to stress associated with effective pharmacologic intervention, including studies employing centrally acting adrenergic agonists (Boyar et al., 1980), alpha-blockers (Mancia et al., 1980), diuretics (Bateman et al., 1979), and calcium channel blockers (Stevinkel et al., 1997). In contrast, use of ACE inhibitors has been shown to be associated with reductions in both SBP and DBP response to stress (Kahan and Eliasson, 1999; Naz-zaro et al., 1994), although this relation has been relatively infrequently studied.

Although evidence indicates that most of the antihypertensive agents, including diuretics, adrenergic inhibitors, and vasodilators, do not appear to impact the degree of blood pressure reactivity to stress, there is clear evidence that administration of beta-blockers results in an attenuated heart rate response to stress (Mills and Dimsdale, 1991). Recognizing that these diminished heart rate responses to stress occurred in conjunction with no change in blood pressure reactivity, several investigators conducted subsequent studies to explore the underlying hemodynamics responsible for the disparate heart rate and blood pressure response alterations (Garavaglia et al., 1988; Ruddel et al., 1988; Schmieder et al., 1987). Consistent findings emerged across all three studies; the attenuated heart rate response that occurred with beta-blockade was accompanied by increased peripheral resistance during stress presentations, thereby maintaining the blood pressure response. Comparison drugs used in these studies (calcium channel blockers, central adrener-gic agonists), in contrast, lowered blood pressure without altering the hemodynamic response profile to stress. Therefore, although the hemodynamic profile associated with blood pressure reactivity to stress is altered through administration of beta-blockers, the magnitude of the blood pressure response remains unaffected.

With perhaps the exception of ACE inhibitors, then, there is very little evidence indicating that antihypertensive medications exert their blood pressure-lowering effect by altering the magnitude or profile of cardiovascular reactivity to stress. Therefore, the blood pressure-lowering effect of these medicines appears to be caused by other mechanisms involved in blood pressure regulation, like altering fluid retention or local vascular effects. Although demonstrating a link between the mechanism of action of antihypertensive agents and diminished cardiovascular reactivity to stress would have clearly supported the hypothesis that cardiovascular reactivity to stress mediates the stresshypertension relation, the lack of evidence does not suggest that this hypothesis should be abandoned. Clearly, there are multiple physiological adjustments that lead to reductions in blood pressure, and exaggerated cardiovascular reactivity to stress has been proposed to explain only one of them, how stress leads to high blood pressure. In a sense, drugs are not intelligent; that is, they do not need to know the cause of a physiological imbalance in order to have a positive treatment outcome. In this regard, any given antihypertensive agent will lower blood pressure to some extent, whether the hypertensive condition is caused by obesity, a high-salt diet, a genetic propensity for hypertension, or a stress-filled life.

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