The purpose of this study was to examine whether the hemodynamic and metabolic consequences of a physical (treadmill excercise) and behavioral (signaled shock-avoidance) stressor could be differentiated. To do this, direct continuous recordings of cardiac output, systolic and diastolic blood pressure, and discrete determinations of the arterial-mixed venous oxygen ((a-v)O2) content difference were analyzed in six dogs during exposure to three grades of treadmill exercise and when working on a shock-avoidance task. The results indicated that in five animals the relationship between cardiac output and the (a-v)O2 difference during shock-avoidance conditioning was significantly different from the corresponding pattern observed during exercise. In four animals the data suggested that avoidance conditioning, relative to exercise stress, elicited overperfusion. Behavioral stress also produced reliable elevations in diastolic and systolic blood pressure. These results suggest that, when compared to physical stress, behavioral stress can produce a dissociation of cardiovascular and metabolic processes in the presence of acute pressor responses.

The effects of two behavioral tasks, treadmill exercise and shock avoidance, on renal and cardiovascular function were examined in dogs during intravenous infusion of isotonic saline. Urine was collected with a bladder catheter. Control experiments established steady base lines of urine flow (V), sodium excretion (UNaV), glomerular filtration rate (GFR), free water clearance (CH2O), heart rate (HR), and arterial pressure (Pa). Exercise led to increased V, UNaV, GFR, HR, and Pa with no change in CH2O. Avoidance caused decreases in V and UNaV, increases in HR and Pa but no change in either GFR or CH2O. The hematocrit increased significantly during both tasks. Exercise and avoidance led to opposite urinary changes even when HR accelerations were identical. The natriuretic effect of exercise was the consequence of an increased filtered load, while the antinatriuretic effect of shock avoidance was apparently due to an increased rate of tubular reabsorption of filtrate. The results show that exercise and shock avoidance, while eliciting similar cardiovascular changes, lead to opposite adjustments in urine and sodium output.

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.

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.

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