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Behaviour and hypertension: a pathophysiological puzzle.

A B Weder1, M Takiyyuddin, M A Sekkarie

  • 1University of Michigan Hospitals, Department of Internal Medicine, Ann Arbor 48109-0356.

Journal of Hypertension. Supplement : Official Journal of the International Society of Hypertension
|February 1, 1989
PubMed
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This study found that neither clonidine nor atenolol, despite lowering baseline blood pressure, affected stress responses in patients with borderline hypertension. Therefore, stress reactivity may not be a direct cause of hypertension.

Area of Science:

  • Cardiovascular Physiology
  • Hypertension Research
  • Pharmacology

Background:

  • Borderline hypertension is associated with heightened sympathetic and reduced parasympathetic tone, personality traits, and stress hyperreactivity.
  • The 'hypertensive personality' theory suggests a persistent defense reaction increases sympathetic outflow and stress reactivity.
  • Previous research indicates blood pressure reactivity might be independent of average baseline blood pressure.

Purpose of the Study:

  • To investigate the effects of centrally-acting alpha 2-agonist clonidine and selective beta 1-blocker atenolol on blood pressure and stress responses.
  • To determine if pharmacological interventions targeting sympathetic tone influence reactivity to various stressors.

Main Methods:

  • A study comparing the effects of clonidine and atenolol in patients with borderline hypertension.

Related Experiment Videos

  • Assessment of baseline blood pressure and responses to mental arithmetic, isometric handgrip exercise, and cold pressor testing.
  • Main Results:

    • Both clonidine and atenolol demonstrated comparable antihypertensive effects on baseline blood pressure.
    • Neither medication altered the cardiovascular responses to mental stress, isometric exercise, or cold exposure.

    Conclusions:

    • Pharmacological agents that reduce baseline blood pressure do not necessarily modulate stress-induced cardiovascular reactivity.
    • Stress reactivity studies may offer limited insights into the underlying causes of human hypertension.