dinoprost and Pheochromocytoma

Authors assessed correlation between venous blood catecholamines and prostaglandins concentrations before and after inhibition of sympathetic activity by clonidine in patients with primary hypertension or pheochromocytoma. 30 patients with essential uncomplicated hypertension and 11 with pheochromocytoma underwent the study. The control group consisted of 6 healthy volunteers. Serum norepinephrine (NA), epinephrine (A), prostaglandins: PGE2 PGF2 alpha and prostacyclin metabolite -6-keto-PGF1 alpha were determined before and 3 hours after oral administration of 0.3 mg clonidine. Negative correlation was stated between basic serum norepinephrine and 6-keto-PGF1 alpha concentrations in patients with pheochromocytoma, which could indicate prostacyclin metabolism disorders during persistent hypercatecholaminemia . There was no correlation between catecholamines and prostaglandins during the inhibition of sympathetic activity in patients with pheochromocytoma as well as essential hypertension. The positive correlation was observed between changes in serum NA and PGF2 alpha levels in patients with borderline hypertension. Thus, one may suppose, that correlation between na excretion and vasoconstrictive PGF2 proved in acute experiments, becomes evident within the early stage of hypertension also during sympathetic activity inhibition.

Topics: Adrenal Gland Neoplasms; Adult; Clonidine; Dinoprost; Dinoprostone; Epinephrine; Humans; Hypertension; Middle Aged; Norepinephrine; Pheochromocytoma

In order to relate urinary prostaglandin excretion in pheochromocytoma (Ph) to the pattern of noradrenaline (NA), adrenaline (A) and dopamine (D), 14 patients with this disease were investigated during normal sodium intake. 20 healthy volunteers served as controls (C). Urinary PGs were determined by RIA; NA, A and D were measured fluorometrically. In patients with elevated excretion of NA + A (n=3), NA alone (n=6) and D (n=5), urinary PGE2 was significantly (p less than 0.01) diminished respectively 367,4 +/- 143,6; 445 +/- 104; 440,4 +/- 125,2 pmol/24h in comparison to C/1075 +/- 165,4 pmol/24 h. On the other hand urinary excretion of PGF2 alpha was distinctly increased in patients with elevated NA + A, normal NA + A and elevated D respectively 6375 +/- 1697, 1035 +/- 217,8, 5070 + 1225 pmol/24 h and decreased in patients with elevated A 989 +/- 217,5 pmol/24 h in comparison to C/1886 +/- 255,7 pmol/24 h. It is concluded, that in patients with Ph PGs excretion is related to the pattern of catecholamines excretion. Low PGE2 excretion in most patients with Ph suggests that the physiological interrelationship between catecholamines and PGs is disturbed in this disease. High PGF2 alpha excretion may reflect enhanced activity of 9-ketoreductase PGE2 probably caused by an excess of catecholamines.

Topics: Adrenal Gland Neoplasms; Adult; Catecholamines; Dinoprost; Dinoprostone; Dopamine; Epinephrine; Female; Humans; Male; Middle Aged; Norepinephrine; Pheochromocytoma; Prostaglandins E; Prostaglandins F