Blood pressure regulation in pheochromocytoma.

Abstract

SUMMARY Two sets of studies were performed in 13 patients with prored adrenal pheochromocytoma to test the hypothesis that the sympathetic nervous system (SNS) Is active and might contribute to the hypertensire state. Similar studies were performed in 15 additional patients considered to have essential hypertension. In the first set, 13 patients with pheochromocytoma were subjected to head-up tilt to assess the activity of the SNS. This maneuver decreased diastolic blood pressure in only two; heart rate increased appropriately in all except one. Changes in plasma noreplnephrine (NE) were variable and did not correlate with changes in blood pressure (BP) and heart rate (HR).In the second set, 10 patients with pheochromocytoma were given a single oral dose of clonldine (03 mg) to evaluate what role, if any, the SNS might contribute to the hypertensive state. Fifteen patients with essential hypertension were studied similarly for comparison. Clonidlne produced significant decreases in BP and HR but left plasma renln activity unchanged in both groups. In essential hypertension, the cardiovascular responses were accompanied by significant reductions in plasma NE. By contrast, plasma NE was unchanged in patients with pheochromocytoma, despite similar reductions in BP and HR. These results suggest that the sympathetic reflexes are intact in pbeochromocytoma, and that much of the hypertension associated with these tumors may be related to increased sympathetic activity. T HE hypertension that accompanies pheochromocytoma has generally been ascribed to the excessive circulating catecholamines released from the tumor. However, recent studies have demonstrated a marked discrepancy between the height of arterial pressure and the prevailing plasma catecholamine concentration; 1 in fact, some of these patients may have long periods of normotension despite high circulating catecholamines. Lack of correlation between blood pressure (BP) and plasma catecholamine levels has been attributed to varying responsiveness of the cardiovascular system dependent on several factors, including the rate of catecholamine inactivation (by uptake mechanisms and enzymatic degradation), the extent to which catecholamines diffuse and reach target cells, the inherent reactivity of vascular smooth muscle, and finally to receptor sensitivity.One possibility that has received little attention is the active participation of the sympathetic nervous system (SNS) in BP control; although it has been assumed that sympathetic activity could be depressed in pheochromocytoma by the high catecholamine levels, this possibility has not been critically assessed in man. We therefore planned two sets of studies to assess that hypothesis. In the first, we used head-up tilt to determine the activity of the SNS. In the second, we administered clonidine (a centrally-acting antihypertensive agent that inhibits neurally-mediated catecholamine release) to evaluate, from changes in heart rate (HR), BP, plasma norepinephrine (NE) and plasma renin activity (PRA), the role of ...

A reevaluation of the hemodynamics of pheochromocytoma.

“…- 13 It is noteworthy that, in the present study, a significant relation was found between diastolic blood pressure and plasma norepinephrine in pheochromocytoma. This correlation, however, was barely statistically significant (/?<0.05), and elimination of one patient would have reduced this relation to an insignificant level.…”

Rapid cyclic fluctuations of blood pressure associated with an adrenal pheochromocytoma.

“…It has been demonstrated that a neurogenic mechanism is active in patients with pheochromocytoma despite excessive levels of circulating catecholamines. 16 The reciprocal changes in pulse rate and blood pressure seen in our patient probably absolve an abnormal baroreceptor function as a mechanism for the cyclical hypertension.…”

Cerebral Infarction Along the Distribution of Perforating Arteries During Aneurysm Surgery in a Patient With Pheochromocytoma -Case Report-

“…10) In contrast, NE released locally from sympathetic nerve endings within the vasculature causes a 1 -adrenoceptor-mediated vasoconstriction, resulting in hypertension and depletion of blood volume. 3,10) Our patient experienced cerebral infarction twice during each aneurysm surgery, both times along the distribution of the perforating arteries. The maximum size of infarction during the initial and second operations was 14.4 mm and 19.3 mm in diameter, respectively.…”