Now that the foundations for both essential hypertension and stress have been established, we can begin to address the primary question of the book, namely, what is the relation between a psychophysiological construct like stress and the physical manifestation of essential hypertension? It has probably become apparent that many of the bodily organs, systems, and mechanisms responsible for regulating arterial pressure are the same organs, systems, and mechanisms that have served usefully in explaining how environmental stress leads to physical disease.
These include the branches of the autonomic nervous system, hormone and steroid release from the neuroendocrine system, and various brain regions like the hypothalamus, brain stem, and limbic system. All in all, there is a great deal of overlap between the physiological mechanisms described in section 1 and section 3 ; thus there is good reason to consider that an association exists between stress and hypertension.
In examining the evidence for the relation between stress and hypertension, the model of stress depicted in Figure 3.3 can be applied specifically to the condition of essential hypertension.
An application of this model to essential hypertension, shown in Figure 4.1, serves as the foundation for research presented in this section and the three sections that follow. In this section, we will consider research supporting a link between environmental stressors and essential hypertension.
The model linking stress with essential hypertension shown in Figure 4.1 is quite similar to several existing models (for example, see Beilin, 1997, Jorgensen et al., 1996, and Pickering, 1997), in that all recognize that the relation between stress and essential hypertension is not simple or direct. There are multiple intervening variables that need to be measured and tested regarding their roles in the stress???hypertension relation. Because of the numerous organ systems involved in blood pressure regulation, it is quite likely that multiple etiologic pathways exist that lead to the onset of essential hypertension, and the search for the single cause of the medical condition is misguided. The present model recognizes the potential multiple pathways to essential hypertension as well as the variety of intervening variables that influence disease onset.
Additionally, this model, as well as previous models, recognizes the bidirectional relation among many intervening variables. For example, in the model presented in Figure 4.1, both the acute stress response and physiological changes that maintain elevated blood pressure result from stress in addition to contributing to the level of stress an individual experiences.
Jorgensen et al. (1996) proposed a more complicated synergistic model suggesting that individual difference personality variables were linked bidirectionally to all other components of the model, including stressors, acute stress responses, and the physiological changes that maintain elevated blood pressure. Although these synergistic relations may indeed exist, the model presented in Figure 4.1 provides a useful structure for organizing the results from empirical research presented in the next several sections. Regardless of the exact directionality of the proposed linkages in these various models, all models highlight the importance of individual difference variables in determining who will or who will not develop essential hypertension. Before we consider the research examining the role of various intervening variables in explaining the onset of hypertension, however, it is important to examine evidence for the fundamental stress???hypertension relation.