本態性高血圧症患者および正常血圧者の Nifedipine 1回経口投与に対する交感神経ならびに内分泌応答のレニン群間比較

Behaviors of sympathetic and renin-angiotensin-aldosterone systems to an acute sublingual administration of nifedipine (10 mg) were studied in essential hypertensive (EHT) and normotensive (NT) groups. Basal values of plasma norepinephrine (NE) and plasma renin activity (PRA) were not consistent with mean blood pressure (BP), indicating no important role of NE and PRA values for determining BP level. Nifedipine reduced BP, and increased NE and PRA in both groups. Simultaneously, nifedipine produced a significant decrease of plasma aldosterone concentration (PAC) and plasma cortisol. High-renin EHT subgroup showed greater responses of BP, NE and PRA than normal- or low-renin subgroup but not in NT group. In high-, normal- and low-renin subgroups of both groups, the correlations between mean BP and △mean BP (r= -0.85, p<0.001; r= -0.89, p<0.001 and r= -0.77, p<0.001, respectively), △mean BP and △NE (r= -0.76, p<0.01; r= -0.71, p<0.05 and r= -0.57, NS, respectively) and △mean BP and △PRA (r= -0.87, p<0.001; r=0.59, NS and r= -0.05, NS, respectively) were observed. A significant relationship between basal PRA and △PRA was demonstrated in EHT group (r=0.77, p<0.001) but not in NT group (r=0.37, NS). These data indicate the presence of high vascular tone in high-renin EHT subgroup which is probably produced by an increased vascular responsiveness to sympathetic and/or to angiotensin II or by some other factors. It is suspected that juxtaglomerular cell response to vasodilator may be altered in patients with low-renin essential hypertension. The present study also suggests that nifedipine blocked aldosterone and cortisol secretion through Ca++ influx inhibition into the adrenal cortex

カテコールアミン心筋症を合併した褐色細胞腫の1症例

A 40-year-old female with the left adrenal pheochoromocytoma showed ECG abnormalities and the clinical features similar to acute myocardial infarction. Enzymological studies and UCG findings in the acute phase revealed the same pattern as those in acute myocardial infarction. After finding the existence of the left adrenal pheochromocytoma, the differential diagnosis between myocardial infarction and catecholamine cardiomyopathy as the cause of ECG, UCG and enzymological changes was tried to make. However, the differential diagnosis was not established during the preoperative period. The continued ECG abnormilities until the surgical removal of the tumor disappeared one week after the operation. Norepinephrine infusion test performed one and two weeks and 21 months after the operation could evoke the T wave change which disappeared soonly after norepinephrine infusion was stopped. Coronary angiography and 201Tl myocardial scintigraphy revealed the normal findings. These findings suggested that catecholamines released from pheochromocytoma was the cause of the myocardial damages and ECG abnormalities. The patient with catecholamine cardiomyopathy due to the adrenal pheochromocytoma whose ECG abnormalities continued until surgical treatment was reported