HEALING HYPERTENSION BY MEDITATION

Stress and Hypertension: The relationships between stress and hypertension have been evaluated extensively. Acutely, stress has been shown to increase blood pressure by increasing cardiac output and the heart rate without affecting total peripheral resistance. Acute stress has been found to increase levels of catecholeamines, cortisol, vasopressin, endorphins and aldosterone, which may in part explain the increase in blood pressure. However, a primary role for the activation of the sympathetic nervous system has recently been suggested in several studies. Studies in the rat are beginning to determine specific central nervous system pathways which transform stressful stimuli into signals triggering a cardiovascular response without direct cortical participation. Furthermore, acute stress reduces renal sodium excretion, which contributes to an increase in blood pressure. Several studies suggest that prolonged stress may predispose people and animals to prolonged hypertension and certain populations are at risk for the development of stress-induced hypertension. It is likely that prolonged stress-induced hypertension is the result of neurohormonal trophic factors which cause vascular hypertrophy or atherosclerosis. Because stress can affect measurement of blood pressure due to the phenomenon of 'white-coat hypertension', ambulatory blood pressure monitoring is emerging as an important feature in the evaluation of patients with hypertension. Finally, relaxation techniques are being used increasingly in the treatment of patients with hypertension. Epidemiologic and experimental studies disclosed that the sympathetic nervous system might play a pivotal role in the pathogenesis of essential hypertension. Although systolic pressure exhibits a weak endogenous rhythm, diurnal fluctuations of arterial pressure are provoked primarily by physical or emotional stress factors. The magnitude of the cardiovascular response, however, varies widely from individual to individual. Subjects at high risk of future hypertension,--such as those with a positive history of familial hypertension, high resting heart rate, or transient increase in arterial hypertension--revealed blood pressure hyper-responsiveness to stress stimuli mediated by an over-reactivity of the sympathetic nervous system. Furthermore, cardiovascular reactivity to mental arithmetic tasks and to traffic noise put a patient at high risk of developing arterial hypertension. In women, exaggerated cardiovascular response to stress stimuli appeared to be mitigated by estrogens, whereas oral contraceptives overrode this 'protective' effect of estrogens. At a certain point, repeated episodes of high stress blood pressure could produce structural vascular changes finally inducing sustained hypertension. 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 hyper-reactivity 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 hyper-reactivity and symptom specificity in a single individual increases the risk to develop essential hypertension.