Key points are not available for this paper at this time.
It has been suggested that heightened cardiovascular responses to behavioral stressors play some role in the development of arterial hypertension. Two aspects of this hypothesis are discussed here: (a) current conceptualizations of cardiovascular reactivity as a dimension of individual differences; and (b) models of potential association between such reactivity and hypertension. Considered first are matters bearing on the quantification of cardiovascular responses to stress and on the stability of individual differences in cardiovascular reactivity, both over time and between laboratory and natural (field) settings. While inter-individual differences on some measures of behaviorally-evoked cardiovascular response are reproducible (stable) on retesting, evidence that these differences predict reactions to stressors encountered during the course of daily activities is scant and inconclusive. We suggest that inconsistencies in the latter literature are due to methodologic deficiencies, to an absence of clearly articulated hypotheses describing expected associations between cardiovascular reactions to laboratory stressors and to naturally-occurring life events, and in part, to a confusion of objectives among investigators. Regarding hypertension, hypertensive individuals and offspring of hypertensives consistently show elevated cardiovascular reactions to laboratory stressors; also, the two existing longitudinal studies involving follow-up intervals of more than twenty years show significant prospective associations between cold pressor reactivity and subsequent hypertension. These findings are consistent with the hypothesis that behaviorally-evoked cardiovascular reactivity plays some role in essential hypertension and justify further research in this area. As a guide to design of such research, five hypothetical relationships are proposed—that an enhanced reactivity: (a) potentiates vascular and end-organ complications of hypertension; (b) is a marker for increased risk conferred by an associated pathogenic factor; (c) directly promotes hypertension; (d) contributes to the development of hypertension only with exposure to psychosocial stressors of sufficient intensity and chronicity, or in conjunction with predisposing dispositional attributes; or (e) modifies the influences of another pathogenic factor. It is also recommended that future research employ more comprehensive assessments of reactivity and investigate factors underlying an enhanced cardiovascular responsivity to stress (particularly in relation to CNS and peripheral mechanisms of relevance to hypertension).
Manuck et al. (Mon,) studied this question.