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Operant conditioning, sodium loading, and experimental hypertension.

D E Anderson

    Journal of Cardiovascular Pharmacology
    |January 1, 1986
    PubMed
    Summary
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    High sodium intake combined with behavioral stress caused progressive hypertension in dogs. This sodium-dependent hypertension was linked to reduced heart rate and kidney function, resolving when stress and sodium were removed.

    Area of Science:

    • Cardiovascular Physiology
    • Behavioral Neuroscience
    • Renal Physiology

    Background:

    • Behavioral factors significantly influence cardiovascular regulation.
    • The interplay between sodium intake and stress in hypertension development requires further elucidation.
    • Understanding the physiological mechanisms of behavioral hypertension is crucial for public health.

    Purpose of the Study:

    • To investigate the development of hypertension in response to a combination of high sodium/potassium intake and avoidance conditioning.
    • To characterize the physiological changes associated with sodium-dependent behavioral hypertension.
    • To explore the potential role of the sympathetic nervous system, renin-angiotensin-aldosterone system, and pituitary-adrenal axis in this hypertensive model.

    Main Methods:

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    • Chronically instrumented, tethered dogs were subjected to avoidance conditioning tasks during periods of high sodium/potassium diet.
    • Arterial pressure, heart rate, glomerular filtration rate, and renal excretion of sodium, potassium, and urine volume were monitored.
    • Preliminary studies included administration of alpha adrenergic blocking drugs and renal denervation.
    • Activity of the renin-angiotensin-aldosterone system was assessed.

    Main Results:

    • Progressive increases in mean 24-hour arterial pressure were observed in dogs under high sodium/potassium intake and avoidance conditioning.
    • Arterial pressure did not increase in stressed dogs on a normal diet or in nonstressed, sodium-loaded dogs.
    • Development of hypertension was accompanied by bradycardia, decreased glomerular filtration rate, and altered renal excretion patterns.
    • Hypertension resolved upon cessation of avoidance schedules and saline infusion.
    • Evidence did not support increased sympathetic nervous system activity or renin-angiotensin-aldosterone system activity in mediating sodium retention.

    Conclusions:

    • Behavioral stress combined with high sodium intake can induce a form of hypertension in dogs.
    • The underlying mechanisms appear to involve complex interactions beyond sympathetic and renin-angiotensin-aldosterone systems.
    • Further investigation into the pituitary-adrenal axis is warranted to understand the pathophysiology of this behavioral hypertension model.