خشم و واکنش وحشت زده قلبی عروقی در مردان جوان سالم
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|33408||2011||7 صفحه PDF||سفارش دهید||محاسبه نشده|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : International Journal of Psychophysiology, Volume 79, Issue 3, March 2011, Pages 364–370
Anger has been implicated in the etiology of hypertensive disease. Trait anger has been linked to enhanced cardiovascular responsiveness. However, whether this association reflects differences in context appraisal or a general hyper-reactivity of the cardiovascular system remains unclear. We studied the cardiovascular response to acoustic startle probes in 76 healthy Caucasian males in different affective contices (pleasant, neutral, and unpleasant). All participants completed the State-Trait-Anger-Expression-Inventory (STAXI) by Spielberger and the results were analysed with stepwise regression analysis according to the anger scores and traditional risk factors for hypertension. Our study reveals differential modulation of the cardiovascular response to startle stimuli by affective pictures in the dimensions “valence” for heart rate and “arousal” for blood pressure. Anger-in was identified as the most important determinant for blood pressure responses in unpleasant context, while anger-out was associated with less cardiovascular activation in neutral context. This is the first study that relates trait anger to cardiovascular reactivity and affective reflex modulation in normotensive subjects. We could demonstrate an interaction of affective context and trait anger for cardiovascular (hyper-)reactivity. Increased cardiovascular reactivity for higher scores of anger-in in unpleasant context may indicate enhanced sympathetic reactivity and constitute a risk factor for the development of essential hypertension.
The prevalence of hypertension has been rising continuously in modern society. The contribution of psychosocial factors such as suppressed anger has been suggested early in hypertension research (Alexander, 1939). Anger has repeatedly been linked with the etiology of essential hypertension (Deter et al., 2001 and Dimsdale et al., 1986). A recent review found a consistent association of trait anger and ambulatory blood pressure (Schum et al., 2003). It has been hypothesized that trait anger causes increased physiological arousal by interacting with situational factors (Jorgensen et al., 1996). In line with this, trait anger has been linked to enhanced cardiovascular reactivity (Bongard et al., 1998 and Vogele et al., 1997) and increased sympathetic activity (McCraty et al., 1995). Indeed, a functional blood pressure rise in stressful situations can precede a permanently elevated blood pressure that is solidified by structural changes of the arteries (Schlaich et al., 2004). Furthermore, enhanced sympathetic activity can promote later hypertension without preceding blood pressure elevations. Enhanced sympathetic activity unfolds deleterious effects on the cardiovascular system (Mancia et al., 1999), promoting media sclerosis and heightened vascular resistance (Ferriss, 1978 and Markovitz et al., 1993). However, little is known about the affective modulation of blood pressure responsiveness and the relationship between anger and cardiovascular reactivity in a healthy population. Especially “anger-in”, i.e. anger directed towards the own person, held or suppressed anger feelings, and “anger out”, i.e. overtly and directly expressed anger towards other persons or environmental objects (Forgays et al., 1997) appear to be positively correlated with resting systolic blood pressure (Bongard and al'Absi, 2005, Igna et al., 2009 and Vogele and Steptoe, 1992). Negative correlations with resting diastolic blood pressure have been reported (Schum et al., 2003 and Spicer and Chamberlain, 1996), but contradictory findings exist (Holroyd and Gorkin, 1983, Igna et al., 2009 and Shapiro et al., 1997). “Anger-in” is also positively correlated with systolic blood pressure reactivity during stressful tasks (Burns, 1995, Holroyd and Gorkin, 1983, Mills and Dimsdale, 1993 and Vogele and Steptoe, 1992), while mixed results exist for “anger-out”. Although consistently associated with higher systolic blood pressure at rest, both positive (Burns, 1995, Faber and Burns, 1996 and Vogele and Steptoe, 1992) and negative (Haeri et al., 1996, Holroyd and Gorkin, 1983 and Vogele and Steptoe, 1992) correlations with systolic blood pressure reactivity to stress have been reported. Assessing cardiovascular stress reactivity in subjects differing in trait anger may potentially be biased by differences in task perception. The startle reflex represents a valuable tool for the investigation of cardiovascular responses to external stimulation and the modulation of such responses by affective context. In contrast to other stimuli that are commonly used to elicit a cardiovascular reaction (e.g. math task, cold pressor, interview stress, etc.), the startle reflex is brainstem relayed and therefore does not require higher cognitive processing of the eliciting stimulus itself. The startle reflex is part of the defensive reflex system and accompanied by a cardiovascular response consisting of a rise in heart rate and blood pressure (Girard et al., 2001, Holand et al., 1999a and Holand et al., 1999b). The amplitude of the motor response (as measured by electromyogram of the musculus orbicularis oculi) is enhanced in negative affective context (match condition: when the context matches the aversive character of the reflex) and diminished in positive affective context (mismatch condition). The same pattern of modulation has been found for heart rate responses to startle stimuli (Bradley et al., 1990, Cook et al., 1992 and Gautier and Cook, 1997). Although some studies reported inconsistent results for reactions in pleasant context (Bradley and Lang, 2000 and Sanchez et al., 2002), these studies demonstrate an affective modulation of the heart rate reaction that is elicited by the brainstem mediated startle reflex. The affective modulation of the blood pressure response to startle stimuli has, to our knowledge, not been investigated yet, but there is evidence that enhanced affective startle modulation is associated with generally enhanced blood pressure reactivity. Gautier and Cook found enhanced affective startle modulation in individuals with enhanced blood pressure response to mental stress (Gautier and Cook, 1997). Also, enhanced affective startle modulation has been linked to physiological characteristics such as salt sensitivity and psychological states or traits such as anxiety, irritability, and anger (Buchholz et al., 2001) that in turn are considered risk factors for hypertension. In this study, we investigated the affective modulation of heart rate and blood pressure responses to startle stimuli in normotensive subjects. We furthermore investigated how anger affects the cardiovascular response to startle stimuli. Trait "anger expression" (with the dimensions “anger-out" and “anger-in”) as well as trait “anger control” were assessed with the German version of the State-Trait-Anger-Expression-Inventory (STAXI). Pictures of different emotional content (valence) and acoustic startle stimuli were presented to the participants while startle magnitude, heart rate, and blood pressure were recorded. Self-ratings of the visual stimuli were obtained to control for differences in perceived affective stimulation and correlated with anger scores. We hypothesized that the startle reflex would be accompanied by a significant cardiovascular response (i.e. an increase of heart rate and blood pressure) modulated by affective context (i.e. an increase in unpleasant context, and a decrease in pleasant context). We furthermore assumed that trait anger would have a significant effect on the cardiovascular response to startle stimuli. We hypothesized that this effect would be independent of affective context in case of a general hyper-reactivity of the cardiovascular system, or depending on affective context in case of an underlying difference in context appraisal.