Premium
Psychophysiological theories on sympathetic nervous system reactivity in the development of essential hypertension
Author(s) -
FREDRIKSON MATS
Publication year - 1991
Publication title -
scandinavian journal of psychology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.743
H-Index - 72
eISSN - 1467-9450
pISSN - 0036-5564
DOI - 10.1111/j.1467-9450.1991.tb00876.x
Subject(s) - psychology , sympathetic nervous system , reactivity (psychology) , neuroscience , autonomic nervous system , essential hypertension , blood pressure , medicine , heart rate , alternative medicine , pathology
Psychophysiological theories on the development of essential hypertension are reviewed and evaluated. Two interconnected theories that relate behavior to essential hypertension and account for individual differences in susceptibility to disease are the “hyperreactivity” theory and "the symptom specificity" theory. The “hyperreactivity” theory identifies individual differences in autonomic nervous system reactivity as the pathophysiological mechanism and the "symptom specificity" theory suggests that inflexible, stereotypical responding increases the risk to develop hypertension. Based on a literature review, these theories are examined. There exist both case/control and prospective studies on autonomic nervous system reactivity and the development of hypertension. It is concluded that a neurogenically mediated hyperreactivity to stress is a precursor and not an effect of hypertension. Tasks that call for active but not passive coping efforts are more efficient elicitors of reactivity differences between those at high and low risk to develop hypertension in case/control studies. In prospective studies, active tasks may also have a predictive advantage over passive with respect to blood pressure development. In the early phase of hypertension, an increased cardiovascular reactivity is accompanied by increased neuroendocrine activation. In the later phase, heightened reactivity is confined to the cardiovascular system. This does not prove but is consistent with the notion that transient episodes of increased cardiac output translate into essential hypertension by causing vascular hypertrophy. Case/control studies suggest that an increased “symptom specificity”, with stereotypical responding across multiple stressors, is independent of cardiovascular reactivity and a precursor of hypertension. The literature lacks prospective studies on the clinical relevance of stereotypical responding. It is suggested that the presence of both hyperreactivity and symptom specificity in a single individual increases the risk to develop essential hypertension.