Behavioral stress combined with high sodium intake induces hypertension in an experimental dog model, independent of sympathetic or renin-angiotensin-aldosterone system activation.
Combined stress and high-sodium intake may promote hypertension in dogs; leaves open translation to human disease and mechanisms.
Chronically instrumented, tethered dogs were presented with brief but recurrent avoidance conditioning tasks over periods of days of high sodium/potassium intake. Under these conditions, mean 24-h arterial pressure levels increased progressively. By contrast, arterial pressure did not rise in stressed dogs on a normal sodium/potassium diet, or in sodium-loaded, nonstressed dogs. The development of the sodium-dependent behavioral hypertension was accompanied by progressive bradycardia, decrease in glomerular filtration rate and decreased renal excretion of sodium during the first few days, but increased output of urine volume. Termination of the avoidance schedules and saline infusion was associated with a return to normotensive pressure levels. The results of preliminary studies involving use of alpha adrenergic blocking drugs or renal denervation do not support the view that the sodium retention was mediated by increased sympathetic nervous system activity. Additionally, activity of the renin-angiotensin-aldosterone system was decreased in these hypertensive dogs. Studies of the pituitary-adrenal axis may elucidate the physiological mechanism responsible for this form of behavioral hypertension.
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David E. Anderson (1986) studied this question.
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