[Hypertension, cardiovascular reactivity to stress and sensibility to pain]. / Hipertensión, reactividad cardiovascular ante el estrés y sensibilidad al dolor.

OBJECTIVE: To provide a review of empirical evidence of decreased pain perception in hypertensive persons or exaggerated cardiovascular reactivity to stress. DEVELOPMENT: To following article will briefly review the existing literature on the association between hypoalgesia and high blood pressure. In particular, evidence of hypoalgesia in normotensive individuals at increased risk for hypertension (exaggerated cardiovascular reactivity to stress) will be offered in support of the notion that high cardiovascular reactivity to stress and decreased pain perception may result from a common physiological dysfunction. Cardiovascular reactivity refers to changes in cardiovascular activity associated primarily with exposure to psychological stress. Different individuals show different amounts of reactivity under the same conditions. The greater cardiovascular reactivity to behavioral stressors may play some role in the development of sustained arterial hypertension. Central opioid hyposensitivity is hypothesized as a mechanism of both hypoalgesia and exaggerated autonomic and neuroendocrine responses to stress in individuals at risk for hypertension. The paraventricular nucleus of the hypothalamus (PVN) serves the crucial function of integrating cardiovascular and painful responses. The central opioid hyposensitivity model of hypoalgesia asserts that attenuation of inhibitory opioid input to the PVN may have important consequences for pain modulation. These consequences includes: 1) greater activation of baroreceptor reflex arcs, 2) enhanced release of endogenous opioids during stress, and 3) increased stimulation of descending pain modulation pathways. CONCLUSIONS: High elevated thresholds to painful thermal stressors might serve as a behavioral marker of risk for hypertension before the onset of high blood pressure levels.

Hipertensión, reactividad cardiovascular ante el estrés y sensibilidad al dolor / Hypertension, cardiovascular reactivity to stress and sensibility to pain

Objetivo. Realizar una revisión de las pruebas empíricas de la percepción disminuida del dolor en las personas hipertensas o de una reactividad cardiovascular al estrés exagerada. Desarrollo. En el artículo siguiente se realizará un breve repaso de la bibliografía existente sobre la asociación entre la hipoalgesia y la hipertensión arterial. Específicamente, se describirán los indicios de la hipoalgesia en sujetos normotensos con un mayor riesgo de padecer hipertensión (reactividad cardiovascular al estrés exagerada) para apoyar la noción de que una reactividad cardiovascular al estrés elevada y una percepción del dolor disminuida pueden ser el resultado de una disfunción fisiológica común. La reactividad cardiovascular hace referencia a los cambios en la actividad cardiovascular asociados, principalmente, con la exposición al estrés psicológico. Diferentes individuos manifiestan distintos grados de reactividad bajo las mismas condiciones. El mayor grado de reactividad cardiovascular a los factores estresantes conductuales puede jugar un papel en el desarrollo de la hipertensión arterial sostenida. Se ha propuesto la hiposensibilidad opioidea central como el mecanismo de acción tanto de la hipoalgesia como de las respuestas autonómicas y neuroendocrinas exageradas al estrés en los individuos con mayor riesgo de padecer hipertensión. El núcleo paraventricular del hipotálamo (NPV) desempeña la función vital de integrar las respuestas cardiovasculares y dolorosas. El modelo de hipoalgesia basado en la hiposensibilidad a los opioides establece que la atenuación de la entrada de los inhibidores de los opioides al NPV puede tener importantes consecuencias en la modulación del dolor. Estas consecuencias incluyen: 1) una mayor activación de los arcos reflejos barorreceptores, 2) un incremento en la liberación de los opioides endógenos durante el estrés, y 3) una estimulación aumentada de las vías de modulación de dolor descendentes. Conclusiones. Los umbrales elevados a los factores estresantes térmicos dolorosos podrían actuar como marcadores conductuales del riesgo de padecer hipertensión antes de la presentación de los niveles elevados de hipertensión arterial (AU)

Objective. To provide a review of empirical evidence of decreased pain perception in hypertensive persons or exaggerated cardiovascular reactivity to stress. Development. To following article will briefly review the existing literature on the association between hypoalgesia and high blood pressure. In particular, evidence of hypoalgesia in normotensive individuals at increased risk for hypertension (exaggerated cardiovascular reactivity to stress) will be offered in support of the notion that high cardiovascular reactivity to stress and decreased pain perception may result from a common physiological dysfunction. Cardiovascular reactivity refers to changes in cardiovascular activity associated primarily with exposure to psychological stress. Different individuals show different amounts of reactivity under the same conditions. The greater cardiovascular reactivity to behavioral stressors may play some role in the development of sustained arterial hypertension. Central opioid hyposensitivity is hypothesized as a mechanism of both hypoalgesia and exaggerated autonomic and neuroendocrine responses to stress in individuals at risk for hypertension. The paraventricular nucleus of the hypothalamus (PVN) serves the crucial function of integrating cardiovascular and painful responses. The central opioid hyposensitivity model of hypoalgesia asserts that attenuation of inhibitory opioid input to the PVN may have important consequences for pain modulation. These consequences includes: 1) greatrer activation of barorreceptor reflex arcs, 2) enhanced release of endogenous opioids during stress, and 3) increased stimulation of descending pain modulation pathways. Conclusions. High elevated thresholds to painful thermal stressors might serve as a behavioral marker of risk for hypertension before the onset of high blood pressure levels (AU)