Sympathoadrenal function in patients with paroxysmal hypertension

Abstract

The cause of paroxysmal hypertension in patients in who pheochromocytoma has been excluded (“pseudopheochromocytoma”) usually remains a mystery. We hypothesized that sympathoadrenal activation would explain these blood pressure (BP) disturbances. Plasma catecholamines and hemodynamics were examined in response to i.v. glucagon, isoproterenol, yohimbine, and trimethaphan in 8 patients with pseudopheochromocytoma and a comparison group of 9 normotensives and hypertensives. Adrenal medullary function was further examined by 18F-fluorodopamine positron emission tomography and measurements of plasma metanephrine, a metabolite of epinephrine produced within the adrenals. Patients with pseudopheochromocytoma had greater increases in BP after yohimbine and greater falls in BP in response to trimethaphan than controls. Exaggerated BP responses were associated with smaller changes in plasma norepinephrine. Heart rate responses to isoproterenol were also exaggerated. Patients had larger glucagon-induced increases in plasma epinephrine and a tendency to elevated baseline plasma levels of epinephrine, metanephrine, and cortisol compared to controls. Prominent adrenal uptake of 18F-fluorodopamine in some patients was consistent with adrenal medullary enlargement. In conclusion, increased release of norepinephrine by sympathetic nerves does not appear to contribute to the BP disturbances in most patients with pseudopheochromocytoma. Increased functional activity of the adrenal medulla and exaggerated adrenoceptor-mediated cardiovascular responses appear more likely causes of the paroxysmal hypertension.