BLOOD PRESSURE EFECTS OF BEHAVIORAL STRESS AND SODIUM

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High blood pressure is a major risk factor for cardiovascular and cerebrovascular disease. Evidence from the animal laboratory indicates that behavioral stress combined with a high sodium intake can have synergistic effects on tonic blood pressure levels and cause hypertension. Understanding the physiological mechanisms and identifying the psychological characteristics associated with this loss of regulatory control over blood pressure could lead to the development and refinement of effective preventative interventions for hypertension, either dietary or behavioral, that are directed at those individuals who are most vulnerable to the synergistic blood pressure effects of behavioral stress and high sodium intake. The first study will examine neuroendocrine and other regulatory responses (e.g., changes in plasma electrolytes) to high sodium intake administered during the period preceding a stressful event (NaCl x STRESS). Medical students will be administered supplemental sodium chloride (600 mg/4.5 kg/day) or placebo tablets using a double-blind method during the 14 days prior to an examination (High Stress) and during a period of low academic demands (Low Stress). Cardiovascular, neuroendocrine, and emotional variables will be measured at rest (High and Low Stress) and in response to the examination (High Stress only). It is expected that activation of the pituitary adrenocortical system will play a more important role in mediating the NaCl x STRESS blood pressure elevations than activation of the sympathetic nervous system and that larger cardiovascular, neuroendocrine, and emotional responses to the examination, suggesting greater stress, will be associated with larger NaCl x STRESS blood pressure responses. The second study will determine whether BP and neuroendocrine responses to laboratory stressors and personality factors, such as hostility and suppressed anger, are associated with a larger NaCl x STRESS BP response. Prior to the High Stress sodium loading period, cardiovascular and neuroendocrine responses to mental arithmetic, social challenge, and studying exam-related material will be measured. It is expected that suppressed anger and greater CV and neuroendocrine reactivity to laboratory stressors will be associated with larger NaCl x STRESS blood pressure responses. The third study will determine whether a concurrent high potassium intake reduces the blood pressure elevating effects of NaCl x STRESS. Subjects will be randomly assigned to receive potassium supplemental sodium chloride tablets. It is expected that the concurrent high potassium intake will blunt the NaCl x STRESS blood pressure response.