Psychologic distress as a predictor of mortality.

In a 12-year follow-up study of 610 persons (239 black and 371 white) in Evans County, Georgia, psychologic distress as measured by total score on the Health Opinion Survey, a 20-item questionnaire, was a predictor of mortality. The hazard ratio, comparing the 95th percentile score with the median, was 1.93 (97.5% confidence interval (CI) 1.42-2.62), controlling for age, race, and sex; there was no interaction with these variables. A purer measure of distress symptomatology, based on 18 of the questionnaire items, was also predictive of mortality. The hazard ratio was 1.94 (97.5% Cl 1.33-2.82), controlling for age, race, sex, and the item, "Do you have any sickness or illness problems at the present time?"; no interactions with the latter variables were found. This pattern was not affected in any major way by several modifications of the analyses: 1) controlling also for smoking, serum cholesterol, Quetelet index (weight (kg)/height (m)2), diastolic blood pressure, a social network index, and a social class index; 2) excluding persons with a diagnosis (in 1968) of chronic heart disease, angina pectoris, myocardial infarction, stroke, transient cerebral ischemic attach, or diabetes mellitus, or whose deaths were due to neoplastic disease; and 3) restricting the analyses to the last half of the follow-up period to explore the role of incipient or early physical illness in producing the association. With the restricted samples, confidence intervals included 1.00, which may be attributed to both the substantially smaller samples and the slightly reduced strength of the effect. The evidence is consistent with a causal role for psychologic distress, as measured by the Health Opinion Survey, in subsequent mortality rates.

Motor preparation aspects of cardiovascular reactivity to psychological challenge.

Neural control of the circulation has evolved in such a way that behavioral responses to psychological stress may be accompanied by a dramatic activation of the cardiovascular system. This study was designed to address the hypothesis that such instances of cardiovascular mobilization reflect a functional motor preparation response. Twenty-four healthy young men participated in reaction time (RT) tasks which involved responding by squeezing a handgrip dynamometer. Motor preparation demands were manipulated by varying the temporal predictability of response requirements as well as the physical effort involved in responding, while controlling for other factors previously established to influence cardiovascular reactivity to psychologically challenging tasks. Physiological response measurements included heart rate, blood pressure and oxygen consumption. Increases in heart rate and systolic blood pressure during the RT tasks showed a general pattern which was consistent with the predictions of the motor preparation hypothesis, with the greatest elevations occurring in association with low temporal predictability and high physical effort. The possibility is discussed that factors such as incentives and elements of uncertainty may influence cardiovascular reactivity by accentuating behavioral arousal, of which motor preparation may be an inextricable component.

Effects of race and marginally elevated blood pressure on responses to stress.

A total of 228 men, aged 18 to 22 years (109 black and 119 white), underwent monitoring of heart rate (HR) and systolic (SBP) and diastolic blood pressure (DBP) responses during several stressor conditions and a 30-minute posttask rest period. Stressors included the cold pressor test and three reaction-time tasks: noncompetitive, competitive, and competitive plus money incentive. Substantial within-subject variations in blood pressure and heart rate were induced, varying from 119/70 to 148/94 mm Hg and from 63 to 91 beats/min on the average. Men (25 black and 39 white) with marginal SBP elevations during initial casual determinations had higher SBP under all conditions compared with men whose casual SBP levels were normal, and they also showed greater elevations over baseline levels in heart rate, SBP, and DBP during the stressors and the initial casual determination. Black and white subjects did not differ in their blood pressures at baseline or during the initial casual determinations, although blacks had slightly lower heart rates. Blacks did show greater SBP elevations over baseline levels than whites during the stressors, primarily because the blacks with marginally elevated SBP showed substantially greater stress-induced increases than whites with marginally elevated SBP. This enhanced pressor response to stress in blacks with marginal blood pressure elevations may be due to higher vascular resistance during enhanced sympathetic activity and could contribute to the higher incidence of hypertension among blacks.

Stability of cardiovascular reactivity to laboratory stressors: a 2 1/2 yr follow-up.

The temporal stability of cardiovascular reactivity to laboratory stressors over a 2 1/2 yr period was studied. Subjects who had earlier received a cold pressor and a shock avoidance reaction time task were brought back for retesting using almost identical tasks. Cardiovascular variables that were common to both sessions included heart rate, systolic and diastolic blood pressure, and pre-ejection period. Correlations were computed to examine the association of responses across both sessions for the four cardiovascular variables during rest and the two tasks. Correlations of both heart rate and systolic blood pressure were high for all tasks and rest, whereas inconsistent correlations were found for diastolic pressure and pre-ejection period. Inconsistencies in diastolic pressure are speculated to be due to individual differences in beta-adrenergic response, whereas lack of consistent pre-ejection period associations may be due to differences in methodology. The results generally support the assumption of stability of cardiovascular reactivity.

Vasopressin and urine flow rate responses to stress in conscious dogs.

Behavioral stress increases arterial pressure while decreasing urine flow rate; the urine flow rate response can be abolished by surgical renal denervation. In this study, the effects of infusion of alpha-adrenoceptor antagonists (intravenous phenoxybenzamine or prazosin) on the antidiuretic and plasma vasopressin responses to stress were examined. Without alpha-adrenoceptor blockade, 20 min of stress increased arterial pressure and decreased urine flow rate, but no change in urine osmolality or plasma vasopressin concentration occurred. Arterial pressure and urine flow rate returned to base-line level during a 20-min recovery period. With alpha-adrenoceptor blockade, which prevented the arterial pressure response to stress, urine flow rate still decreased during stress, but urine osmolality and plasma vasopressin concentration increased. The decrease in urine flow rate and increase in urine osmolality and plasma vasopressin concentration persisted into the first 20-min recovery period but returned to base-line level during a second 20-min recovery period. We conclude that the antidiuretic response to behavioral stress in conscious dogs with saline infusion alone is not mediated via a change in vasopressin release. In contrast, the antidiuretic response to behavioral stress with alpha-adrenoceptor antagonist infusion may be mediated via an increased release of vasopressin.

Central beta adrenoceptor mediation of the antinatriuretic response to behavioral stress in conscious dogs.

This study examined the renal excretory response to behavioral stress (aversive conditioning) in conscious dogs during infusion of beta adrenoceptor antagonists that either readily cross, or that do not readily cross the blood-brain barrier. With saline infusion alone (n = 7), behavioral stress decreased sodium excretion (-47 +/- 7% from 345 microEq/min) and urine flow rate (-48 +/- 5% from 2.1 ml/min). In the same dogs, infusion of propranolol, which readily crosses the blood-brain barrier, abolished the sodium excretion and urine flow rate responses to behavioral stress (-2 +/- 6% from 527 microEq/min and -5 +/- 3% from 3.0 ml/min, respectively). In a different group of dogs (n = 5), infusion of timolol or oxprenolol, antagonists that cross the blood-brain barrier less readily than propranolol, did not abolish the excretory response to behavioral stress. Behavioral stress decreased sodium excretion and urine flow rate during timolol infusion (-38 +/- 6% from 452 microEq/min and -36 +/- 6% from 2.4 ml/min, respectively) and oxprenolol infusion (-25 +/- 9% from 328 microEq/min and -19 +/- 8% from 1.8 ml/min, respectively). With saline infusion alone in these same dogs, behavioral stress decreased sodium excretion (-48 +/- 7% from 316 microEq/min) and urine flow rate (-40 +/- 7% from 1.7 ml/min). Mean arterial pressure increased similarly among all conditions in this study. Since the three antagonists accumulate to a high degree in the kidney, but only propranolol abolished the excretory response to behavioral stress, renal beta adrenoceptors did not appear to mediate the excretory response.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II in the renal excretory response to behavioral stress in conscious dogs.

The effects of inhibition of the renin-angiotensin system on the decreased renal excretion of sodium and water resulting from behavioral stress (shock avoidance) were examined in conscious saline-infused (4-5 ml/min) dogs. During saline infusion alone in six dogs, avoidance decreased sodium excretion (64% from 329 mueq/min) and urine flow (63% from 1.9 ml/min). During converting enzyme inhibition with captopril in the same dogs, the decreases in sodium excretion (35% from 464 mueq/min) and urine flow (35% from 2.6 ml/min) during avoidance were attenuated. Similarly, in six other dogs, avoidance decreased sodium excretion (41% from 361 mueq/min) and urine flow (43% from 2.1 ml/min) with saline infusion alone. During angiotension II (ANG II) receptor antagonism with saralasin, decreases in sodium excretion (29% from 417 mueq/min) and urine flow (27% from 2.2 ml/min) were attenuated. These mean changes in excretion during inhibition of the renin-angiotensin system were significantly (P less than 0.05) less than during saline alone. Whereas decreases in fractional sodium and water excretion were attenuated by renin-angiotensin inhibition, decreases in glomerular filtration rate and effective renal blood flow and increases in mean arterial pressure were not affected. These results indicate that ANG II contributes to the renal excretory response to avoidance.

Neural control of renal excretory function during behavioral stress in conscious dogs.

The renal and neural mechanisms underlying the excretory response to behavioral stress (aversive conditioning) were examined in 30 conscious dogs. Twenty-one dogs decreased urine flow more than 20% during stress, whereas 9 dogs showed less than a 10% decrease. In 11 of the 21 renal-reactive dogs, decreases in urine flow (42%) and sodium excretion (45%) were associated with unchanged glomerular filtration (-1.5%; GFR; inulin clearance) and effective renal blood flow (-4%; RBF; p-aminohippurate clearance). In the other 10 renal-reactive dogs, similar declines in urine flow (54%) and sodium excretion (52%) occurred with decreases in GFR (24%) and RBF (27%). Among all 30 dogs, greater increases in cardiovascular activity during stress were associated with greater decreases in renal excretion. Surgical renal denervation abolished the excretory response to stress in 4 of 5 dogs. These findings suggest that excretory responses in most dogs are mediated 1) primarily via increased tubular reabsorption rather than decreased GFR, 2) via central integration with cardiovascular responses, and 3) via the renal nerves.