Adrenaline responsiveness in mild hypertension: no evidence for altered beta-adrenoceptor sensitivity.

The effects of circulating adrenaline on cardiovascular function were studied in 14 subjects (mean age, 36.5 years; range, 19-46 years) with mild hypertension and in 14 normotensive controls, matched for age and sex. Adrenaline was infused i.v. in step-wise increasing doses (0.1, 0.2, 0.4, and 0.8 nmol/kg/min). Cardiovascular responses were evaluated by echocardiography and noninvasive blood pressure measurements. Noradrenaline, adrenaline, potassium, and cyclic adenosine monophosphate (cAMP) were determined in venous plasma. Systolic and diastolic blood pressure responses to adrenaline were similar in both groups. Adrenaline increased myocardial contractility and stroke volume, but less so in the hypertensive patients. Cardiac output was increased in the hypertensive patients at rest, but the signs of increased myocardial contractility disappeared during adrenaline infusion, most likely because of a reduced myocardial compliance. Increased heart rate and systemic vascular resistances were displayed by the hypertensive patients at all adrenaline concentrations studied, but the responses were similar in both groups. The adrenaline-induced decreases in potassium and increases in cAMP were also similar in both groups. The increases in myocardial contractility and in heart rate are compatible with an increased arousal in mild hypertension at rest. Mild hypertension does not appear to be associated with alterations of beta2-adrenoceptor sensitivity, and the findings do not support that adrenaline is involved in the pathogenesis of primary hypertension.