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High blood pressure is associated with decreased sensitivity to pain in humans and animals. Interestingly, hypoalgesia has also been observed in normotensive organisms at risk for hypertension, suggesting that it may be related to processes involved in the development of hypertension rather than with elevations of blood pressure per se. Sensitivity to laboratory and naturalistic daily aches and pains was assessed in young normotensive women and men with or without a parental history of hypertension and varying degrees of resting blood pressure. In women, risk for hypertension, as defined by a parental history of hypertension, relatively elevated systolic blood pressure, or a combination of the two, was associated with decreased pain reports and increased pain threshold for mechanical finger pressure, but not for the cold pressor test. Offspring of hypertensives also exhibited a reduced response to the pain stimuli compared to offspring of normotensives as assessed by the objective physiological measure of respiratory sinus arrhythmia (RSA). Group differences observed in the laboratory were generally maintained in reports of daily pain, with significant correlations emerging between laboratory and naturalistic pain reports. To assess the role of cardiopulmonary baroreceptor stimulation in blood pressure-related hypoalgesia, young men varying in risk for hypertension were exposed to finger pressure during a period of passive leg elevation and two control periods. Men with relatively elevated systolic blood pressure exhibited reduced pain during the period of leg elevation but not while in a supine position, nor following the valsalva manoeuver. The results of these studies support an association between risk for hypertension and pain sensitivity. This relation appears to extend to naturalistic pain encountered in daily life. Further, there is promising evidence suggesting that this relationship is influenced by cardiopulmonary baroreceptor activity.

A growing literature has reported a significant reduction in pain sensitivity among hypertensioe animals and humans. One of the key questions about this finding is whether a reduced sensitivity to pain can be observed in normotensive individuals who go on to develop high blood pressure. Blood pressure was re-assessed in one hundred and fifteen 19 year-old boys initially tested at age 14, when they were also presented with a pain stimulus (mechanical finger pressure). Analyses indicated that information regarding pain sensitivity improved prediction of changes in blood pressure beyond that afforded by differences in blood pressure at age 14, parental history of hypertension, and body mass index. Similar results were found in comparable analyses predicting 24-hour blood pressure recorded in one hundred and seventeen of the young men at age 22. Significant associations were also observed between pain sensitivity in 14 year-olds and 24-hour heart rate variability in various frequency bands at age 22, suggesting increased sympathetic and reduced parasympathetic tone among individuals less sensitive to pain. In order to further assess the relationship between autonomic function and pain sensitivity, one hundred and sixteen adolescent boys were assessed for pain sensitivity and autonomic responses to orthostatic challenge. Analyses indicated that exaggerated autonomic responses to postural change were associated with reduced pain sensitivity. Finally, to examine the potential role of endogenous opioids in blood pressure-related hypoalgesia, a group of young normotensive men were administered low-frequency transcutaneous electrical nerve 5 stimulation (TENS), which has been demonstrated to elicit endogenous opioid release, prior to being presented with two painful stimuli (electric shock and arm ischemia). A negative association between pain and resting blood pressure was significantly strengthened by administration of low-frequency TENS. The resu

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Hypertension is associated with a reduction in sensitivity to pain in both animals and humans. Changes in nociception pre-date elevations in blood pressure in animals genetically predisposed to hypertension, and preliminary findings with male offspring of hypertensives indicate that genetic risk for hypertension is related to decreased pain sensitivity in humans. Sensitivity to naturalistic and laboratory pain stimuli was compared in normotensive females with and without a parental history of hypertension in three studies. Genetic risk for hypertension was associated with decreased sensitivity for blood donation venipuncture pain and electric shock, but not for menstrual pain or the cold pressor test. These findings provide modest support for the notion that hypoalgesia is present in females at risk for hypertension. Issues for future research include extension of these findings to other pain stimuli, use of multiple indices of risk, assessment of the effects of cyclic hormonal changes on the relationship between pain sensitivity and risk for hypertension, and further study of the mechanisms and pathophysiological implications of this effect.

Psychological stress may be a risk factor for essential hypertension. While several variables have been implicated as mediators or moderators of the relationship between stress and high blood pressure, their exact roles and level of importance remain to be elucidated. A key moderating variable may be family history of hypertension. A series of five studies examined the cardiovascular and emotional reactions to stress of normotensive individuals with and without a parental history of hypertension. In an attempt to facilitate the generalizability of the results, the studies used stressors with greater ecological validity than those used in most previous studies of this topic. This aspect of the research aided the examination of a possible mediator of group differences in cardiovascular reactivity, i.e., emotionality. Several studies observed significant group differences in cardiovascular reactivity to stress, suggesting that stress may be more likely to contribute to the development of hypertension in those with a genetic predisposition for the disorder. However, the exaggerated cardiovascular responsivity of individuals with a parental history of hypertension did not appear to be mediated by greater trait or state emotionality.

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Bibliography: leaves 67-75

published_or_final_version / Medicine / Doctoral / Doctor of Philosophy