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Biomedical subjects

S Takishita

Publications and source records attributed to S Takishita.

At least 19 recordsLinked to original sources

Effect of the Hanshin-Awaji earthquake on home blood pressure in patients with essential hypertension.

At 5:46 AM on January 17, 1995, the Hanshin-Awaji district of Japan was struck by a major earthquake. We investigated changes in home blood pressure (BP) of 36 hypertensive patients before and after the earthquake. In the 16 patients who lived within 50 km from the epicenter, the home Bp on the day of the earthquake was significantly higher than that just before the earthquake (+11/+6 mm Hg; P < .01 for systolic BP and P < .05 for diastolic BP). It remained higher throughout the first week after the earthquake, then gradually returned to the baseline level within 4 weeks. The home BP did not change significantly in the 20 patients who lived farther than 50 km from the epicenter. The earthquake-induced stress increased the BP in these hypertensive patients; however, its pressor effect was not persistent.

Aged

Effect of exercise on plasma adrenomedullin and natriuretic peptide levels in myocardial infarction.

1. We investigated the effect of exercise on plasma adrenomedullin, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) concentrations and studied the relationship between these peptides and haemodynamic parameters in nine patients with old myocardial infarction (MI) and in eight normal subjects. 2. The exercise protocol consisted of two fixed work loads (40 and 80 W) for 4 min each and venous blood samples were taken at rest, during each exercise stage and after exercise while monitoring the mean arterial pressure (MAP) and heart rate (HR). In MI, pulmonary arterial pressure (PAP), pulmonary capillary wedge pressure (PCWP), left ventricular end-diastolic pressure (LVEDP) and cardiac output (CO) were measured throughout exercise. 3. Adrenomedullin levels did not significantly increase with exercise. Adrenomedullin levels correlated with PAP and PCWP at rest (P < 0.05). Atrial natriuretic peptide levels correlated with PAP, PCWP and LVEDP throughout exercise (P < 0.05) but, on multiple regression analysis, PCWP correlated only with ANP (P < 0.01). Brain natriuretic peptide levels correlated with LVEDP throughout exercise (P < 0.01) and its increment correlated closely with basal BNP levels at rest (P < 0.01). 4. These results suggest that adrenomedullin does not respond to the acute haemodynamic changes of exercise, whereas ANP responds to it and PCWP is the major stimulus factor. Brain natriuretic peptide responds to exercise in proportion to the basal synthesis of BNP in patients with left ventricular dysfunction and LVEDP may play a role in increasing BNP during exercise.

Adrenomedullin

Different secretion patterns of adrenomedullin, brain natriuretic peptide, and atrial natriuretic peptide during exercise in hypertensive and normotensive subjects.

The purpose of this study was to investigate the effect of exercise on plasma concentrations of adrenomedullin, brain natriuretic peptide (BNP), and atrial natriuretic peptide (ANP) in patients with essential hypertension (n = 15) and in normotensive controls (n = 10). Exercise consisted of two fixed workloads, 40 and 80 watts of work load using a supine bicycle ergometer. Plasma levels of all three peptides at rest were significantly higher in hypertensives than in controls. Plasma concentrations of ANP increased with exercise in both groups and had greater increments in hypertensive patients than in normotensives. Plasma concentrations of BNP increased only in patients with hypertension and the levels of increase correlated with basal plasma BNP levels (r = 0.94, p < 0.001) and with left ventricular mass (r = 0.62, p < 0.01) determined by echocardiography. In contrast, plasma adrenomedullin did not change with exercise in either group. These results suggest that secretion patterns of these peptides are regulated by different mechanisms and that the amount and kind of peptides mobilized by exercise may depend on the underlying diseases or pathophysiologic condition.

Adrenomedullin

Seasonal variations in office, home and 24 h ambulatory blood pressure in patients with essential hypertension.

OBJECTIVE: To study the influence of seasons on blood pressure in ordinary circumstances. DESIGN AND METHODS: We examined seasonal variations of home and 24 h ambulatory and office blood pressures in outpatients with essential hypertension. Office, home and ambulatory blood pressures of 50 outpatients with essential hypertension were recorded in 1993. The subjects were 26 women and 24 men, aged 59.3 +/- 1.1 years (mean +/- SEM). Office blood pressure was measured monthly by physicians. Home blood pressure was measured every day by the patients in the morning and evening. Ambulatory blood pressure was recorded every 30 min in summer and in winter. The order of ambulatory blood pressure monitoring was randomized. The daytime and night-time blood pressures were calculated according to the true waking and sleeping times of the individual patients. RESULTS: Both office and home blood pressures showed significant seasonal variations. The winter-summer differences in office and home blood pressures were 4.7 +/- 1.3/ 3.3 +/- 0.9 and 5.9 +/- 1.1/2.7 +/- 0.6 mmHg, respectively. They were not influenced by the presence of antihypertensive agents. The winter-summer difference was also significant for daytime ambulatory blood pressure (3.5 +/- 1.4/ 2.5 +/- 0.8 mmHg), but not for night-time ambulatory blood pressure (-2.9 +/- 1.7/-1.2 +/- 1.0 mmHg) or average 24 h blood pressure (1.5 +/- 1.3/1.2 +/- 0.7 mmHg). There were no significant differences in the waking and sleeping times between the two seasons. CONCLUSIONS: Office, home and daytime ambulatory blood pressure levels were higher in winter than they were in summer in patients with essential hypertension. However, the seasonal variations in average 24 h blood pressure may be small because of the lack of changes in night-time blood pressure.

Adult

Blood pressure and its regulation in spontaneously hypertensive rats bred on the lowest sodium diet for normal growth.

To investigate the effects of dietary sodium restriction from conception to adulthood on blood pressure and its regulatory mechanisms, male offspring were derived from inbreeding in spontaneously hypertensive rats fed a diet containing sodium of 175 mumol/g food (control) or 22 mumol/g (low sodium), which is the least sodium content for normal growth. While urinary sodium excretion was markedly less, the low sodium diet did not inhibit body growth and failed to blunt the development of hypertension. Neither plasma catecholamine concentration nor depressor response to hexamethonium was different between the two groups at any age examined (8, 12, and 20 weeks). Plasma renin concentration was not elevated, whereas urinary excretion of aldosterone was increased at any age in the low sodium group compared with that in the control group. Other sets of rats were fed a diet containing sodium of 175 mumol/g plus mefruside (a diuretic) of 0.001% in the same manner as in the other two groups. Urinary sodium excretion per creatinine was higher than in the other groups. The diuretic treatment inhibited body growth and suppressed adult blood pressure. While the sympathetic function was not affected, both plasma renin concentration and urinary excretion of aldosterone were elevated. These results indicate that dietary sodium restriction with the least sodium for normal growth from conception cannot blunt either the sympathetic nervous function or the development of hypertension in spontaneously hypertensive rats. Aldosterone appears to play an important role in maintaining sodium homeostasis under the dietary sodium restriction.

Aldosterone

Different effects of alcohol and salt on 24-hour blood pressure and heart rate in hypertensive patients.

To compare the influences of alcohol and salt intake on 24-h blood pressure (BP), we studied short-term effects of repeated alcohol ingestion and dietary salt intake in hypertensive patients. Thirty-two Japanese men with mild to moderate essential hypertension (54 +/- 1 years old, mean +/- SE) were examined. Sixteen patients were given alcohol (1 ml/kg) with dinner for 7 d after a 7-d control period with an isocaloric beverage. Another group consisting of 16 age- and weight-matched patients consumed a low-sodium diet (25 mmol/d) for 7 d, followed by a high-sodium diet (250 mmol/d) for 7 d. Twenty-four-hour BP was measured at the end of each period. Average 24-h BP in the alcohol period (137 +/- 4/83 +/- 2 mmHg) was similar to that in the control period (138 +/- 4/84 +/- 2 mmHg). However, BP in the alcohol period was significantly lower in the evening, but significantly higher in the morning than that in the control period. Heart rate increased for several hours after alcohol ingestion, resulting in a significant increase in 24-h heart rate (67 +/- 2 vs. 64 +/- 2 beats/min). Average 24-h BP was higher in the high salt period (144 +/- 4/89 +/- 4 mmHg) than in the low salt period (135 +/- 3/85 +/- 3 mmHg, p < 0.05). The pressor effect of high salt intake was sustained throughout the day and was associated with a decrease in 24-h heart rate (60 +/- 2 vs. 66 +/- 2 beats/min). In conclusion, short-term repeated intake of alcohol may have little effect on average 24-h BP while it causes an evening fall and a morning rise in BP, and high salt intake raises BP throughout the day. Alcohol consumption increases and salt loading decreases 24-h heart rate.

Adult

Mild mental stress increases insulin sensitivity in healthy young men.

We examined if mental stress alters insulin sensitivity and renal sodium handling in 11 normotensive young men. Following a 60-minute period of equilibration, we performed euglycemic hyperinsulinemic glucose clamp for 150 minutes. The clamp period was divided into three phases; control phase for 90 minutes (I), mental arithmetic phase for 30 minutes (II), and recovery phase for 30 minutes (III). Blood pressure, heart rate and glucose disposal rate (M value) significantly elevated during phase II of the stress study. In a time control study, in which mental arithmetic was not loaded during phase II, blood pressure was kept constant and the changes in M value from phase I to phase II were significantly smaller than those in the stress study. In both studies, fractional excretion of sodium did not significantly change throughout the study period. Thus, insulin sensitivity concerning glucose metabolism increased in response to mild mental stress. However, the effect of insulin on sodium handling was not altered by the stress.

Adult

Pressor and depressor hormones during alcohol-induced blood pressure reduction in hypertensive patients.

Alcohol acutely causes vasodilation and hypotension in Orientals. To study the mechanisms responsible for the alcohol-induced blood pressure (BP) reduction, we examined levels of various vasoactive hormones after a single intake of alcohol in twelve Japanese men with mild hypertension. On the alcohol intake day, they consumed 1 ml/kg of alcohol with an evening meal, while on the control day they took an isocaloric control drink. BP and vasoactive hormone levels were determined before and 2 h after intake of the alcohol or the control drink. BP after alcohol ingestion was significantly lower than that before drinking or on the control day. This alcohol-induced hypotension was associated with significant increases in heart rate, plasma catecholamines and plasma renin activity (PRA). The changes in heart rate and plasma noradrenaline were inversely related to the changes in BP. Plasma levels of vasopressin and insulin were lower in the alcohol period than in the control period, but these changes were not correlated with the changes in BP. Levels of aldosterone, cortisol, atrial natriuretic peptide, prostaglandin (PG) E2, 6-keto-PGF1 alpha, beta-endorphin, and cyclic GMP were not significantly different between the alcohol and the control periods. These results suggest that changes in pressor hormones may not contribute to the acute hypotensive effect of alcohol, and that the sympathetic nervous system is activated by the BP reduction. The levels of the depressor hormones measured also appear to play no role in alcohol-induced hypotension.

Adult

Modulation of baroreflex function by angiotensin II endogenous to the caudal ventrolateral medulla.

Neurons in the ventrolateral medulla (VLM) mainly determine the tonic sympathetic activity. The caudal VLM (CVLM) relays baroreflex signals to the rostral VLM. We have reported that endogenous angiotensin II (ANG II) contributes to the ongoing activity of the VLM neurons. In the present study, we examined if ANG II endogenous to the CVLM modulates the baroreflex function in anesthetized normotensive Sprague-Dawley rats. Changes in renal sympathetic nerve activity (RSNA) in response to changes in mean arterial pressure (MAP) induced by i.v. infusion of phenylephrine and nitroglycerin were recorded before and after bilateral microinjection of [Sar1, Thr8]-ANG II, an ANG II antagonist, into the CVLM. The ANG II antagonist injection into the CVLM significantly increased MAP and RSNA by 17.6 +/- 8.0 mmHg (mean +/- S.D.) and 36.3 +/- 18.1%, respectively. It also significantly increased the baroreflex sensitivity (BS) from -0.49 +/- 0.38 to -0.74 +/- 0.37%/mmHg during nitroglycerin infusion. In contrast, the BS examined by phenylephrine infusion was not altered by the pretreatment with ANG II antagonist. Injection of artificial CSF affected neither the baseline values of MAP and RSNA nor the BS. These results suggest that ANG II endogenous to the CVLM exert a modulating role in baroreflex control of RSNA.

Adrenergic Fibers

Brain angiotensin II contributes to the development of hypertension in Dahl-Iwai salt-sensitive rats.

OBJECTIVE: To examine the role of brain angiotensin II in the development of salt-induced hypertension in Dahl-Iwai salt-sensitive (DIS) rats. METHODS: Male DIS and Dahl-Iwai salt-resistant (DIR) rats aged 5 or 6 weeks were implanted with an intracerebroventricular cannula, and either chronic intracerebroventricular infusion of 5 micrograms/day CV-11974, a non-peptide type-1 angiotensin II receptor antagonist or artificial cerebrospinal fluid (aCSF) was started. The rats were fed a diet containing 8% sodium chloride. RESULTS: On day 11 or 12 of chronic infusion, DIS rats given CV-11974 intracerebroventricularly exhibited a significantly lower mean arterial pressure than DIS rats given aCSF intracerebroventricularly or intravenous infusion of CV-11974. In DIR rats, intracerebroventricular infusion of CV-11974 did not alter the mean arterial pressure. Sodium and water balances were similar in all of the groups. Plasma vasopressin and noradrenaline levels did not differ among the groups, although the plasma renin concentration was significantly lower in DIS rats given aCSF intracerebroventricularly. Arterial baroreflex control of heart rate and pressor response to intravenous injection of phenylephrine were not altered in rats given CV-11974 intracerebroventricularly. CONCLUSION: The integrity of the brain renin-angiotensin system is necessary for the development of salt-induced hypertension in DIS rats.

Angiotensin II

Alterations of alpha 1-adrenergic receptor densities in right and left ventricles of spontaneously hypertensive rats.

To clarify whether alpha 1-adrenergic receptors contribute to cardiac hypertrophy, we examined alpha 1-adrenergic receptor densities in the right and left ventricles of 5- and 20-week-old spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY) using [3H]prazosin. Also, we analyzed a pharmacologically distinct subtype of alpha 1-adrenergic receptors by pretreatment with chloroethylclonidine. The ratio of right ventricular weight to body weight as well as left ventricular weight to body weight was higher in SHR than in WKY at 5 weeks of age. At 20 weeks of age, only the left ventricular weight to body weight ratio was higher in SHR. At 5 weeks of age, the right and left ventricular alpha 1-adrenergic receptor densities in SHR were greater than those in WKY (LV 1760 vs. 1275, RV 2543 vs. 1521 fmol/mg protein). At 20 weeks of age, only right ventricular alpha 1-adrenergic receptor density remained higher in SHR (1425 vs. 885 fmol/mg protein). The percentage of pharmacologically distinct alpha 1A receptor was higher in the right ventricle of SHR than in that of WKY at 5 weeks of age (25% vs. 18%). There were no significant differences in the dissociation constants among the alpha 1-adrenergic receptor assays. These findings suggest that an increase in alpha 1-adrenergic receptors might be involved in cardiac hypertrophy in the early phase of hypertension in SHR.

Adrenergic alpha-Antagonists

Alpha 2-adrenoceptors in brain and kidney during development of hypertension in Dahl-Iwai salt-sensitive rats.

BACKGROUND: Both renal and extrarenal factors have been considered to contribute to the development of hypertension in Dahl salt-sensitive rats, but contents of both factors have not been established precisely. AIM: To clarify the role of those factors in the sympathetic nervous system, we examined the regulation of alpha2-adrenoceptors in the lower brainstem and the renal tubular basolateral membranes simultaneously during the development of salt-induced hypertension in Dahl-Iwai salt-sensitive rats. METHODS: Dahl-Iwai salt-sensitive or resistant rats were fed a high (8.0% NaCl)- or low (0.3%)- salt diet from 4 to 6 or 10 weeks of age. At 4, 6 and 10 weeks of age, the plasma membranes of the lower brainstem and the renal tubular basolateral membranes were obtained simultaneously and alpha 2-adrenoceptors were quantified by a radioligand binding assay using 3H-rauwolscine. RESULTS: In the salt-sensitive rats, systolic blood pressure was significantly higher in those fed a high-salt diet than in those fed a low-salt diet. In the salt-resistant rats, both the high- and the low-salt groups showed similar blood pressure levels. At 6 weeks of age, alpha 2-receptor densities of the salt-sensitive rats fed a high-salt diet were lower in the lower brainstem and higher in the renal basolateral membranes than those fed a low-salt diet. In contrast, in the salt-resistant rats, both the high- and the low-salt groups had similar densities. At 10 weeks of age, the difference between the high- and the low-salt groups in the salt-sensitive rats disappeared in both the brainstem and the renal basolateral membranes. CONCLUSIONS: Alpha 2-adrenoceptor regulation in the brainstem and the renal basolateral membranes differs between Dahl-Iwai salt-sensitive and salt-resistant rats. The modulation of alpha 2-adrenoceptors by a high salt intake may be essential particularly in the early phase of the development of salt-induced hypertension.

Animals

Neural effects on renal blood flow during acute hypotension vary with antihypertensive drugs.

To examine the neural effects of antihypertensive drugs on renal blood flow, we measured blood flow and renal sympathetic nerve activity simultaneously in conscious spontaneously hypertensive rats aged 13 to 15 weeks. One to two days after surgery, intravenous administration of manidipine (calcium antagonist, n = 10), doxazosin (alpha 1-adrenergic receptor antagonist, n = 9), and clonidine (n = 7) lowered mean arterial pressure by at least 20% from baseline levels. Manidipine initiated a reduction of renal blood flow when mean pressure decreased by 20 +/- 2 mm Hg. At the maximal decrease in renal blood flow (mean pressure, -33 +/- 2 mm Hg), percent decrease in flow (-27 +/- 2%) significantly correlated with percent increase in renal nerve activity (+205 +/- 40%, r = -.878). Doxazosin began to decrease renal blood flow at a level of arterial pressure similar to that in manidipine treatment, whereas the maximal decrease in flow (-19 +/- 2%; mean pressure, -33 +/- 2 mm Hg; nerve activity, +225 +/- 44%) was significantly less than that in manidipine treatment. Although clonidine decreased arterial pressure and renal nerve activity, renal blood flow did not decrease even at the maximal decrease in mean pressure of 29 +/- 1 mm Hg. The addition of clonidine to manidipine treatment suppressed reflexly enhanced renal nerve activity and restored blood flow to the pretreatment level despite pronounced hypotension. These results clearly demonstrate that antihypertensive drugs with blocking action on renal nerve activity are capable of maintaining renal blood flow and that those associated with reflex-induced enhancement of nerve activity exert deteriorating effects on renal blood flow. Furthermore, a decrease in renal blood flow induced by calcium antagonists is mainly attributed to reflexly enhanced renal nerve activity.

Animals

Short-term effects of angiotensin II blockade on renal blood flow and sympathetic activity in awake rats.

To investigate the effects of an angiotensin II type 1 receptor antagonist (CV-11974) on renal blood flow and renal sympathetic nerve activity compared with a calcium antagonist (nicardipine), we measured both parameters in conscious spontaneously hypertensive rats aged 13 to 15 weeks. One to 2 days after surgery, CV-11974 (n = 9) and nicardipine (n = 8) were intravenously administered to decrease arterial pressure in a similar time course and degree of hypotension. CV-11974 increased renal blood flow by 23 +/- 4% at the maximal fall in mean arterial pressure (-32 +/- 1 mm Hg), and renal nerve activity increased by 70 +/- 7%. The maximal increase in renal blood flow (+27 +/- 4%) was observed when mean pressure was reduced by approximately 20 mm Hg. The maximal reduction of renal vascular resistance (-33 +/- 3%) correlated significantly with pretreatment levels of plasma renin concentration (r = -.792). In contrast, nicardipine produced a progressive reduction of renal blood flow and marked increases in heart rate and renal nerve activity. Increases in heart rate and nerve activity were greater than those with CV-11974 treatment (P < .001). At the maximal fall in mean pressure (-32 +/- 1 mm Hg), renal blood flow decreased by 23 +/- 4%, which was significantly correlated with percent changes in renal nerve activity (+150 +/- 11%, r = -.744). Renal denervation in another set of rats (n = 6) improved renal blood flow and renal vascular resistance responses to nicardipine.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin Receptor Antagonists

Carbamazepine-induced hyponatremia in a patient with partial central diabetes insipidus.

A 51-year-old Japanese man was referred for the evaluation of persistent hyponatremia. The serum sodium level remained around 120 mmol/l despite mild water restriction. His past history included chronic alcoholism, myocardial infarction and lumbar disc herniation. Carbamazepine (200 mg, b.i.d.) has been used for more than 8 years for low back pain. Serum sodium returned to normal after carbamazepine was stopped, and rechallenge produced acute symptomatic hyponatremia (117 mmol/l) on day 2 after a total dose of 600 mg. Hepatic, renal and endocrine function were within normal limits, and the response to a water load (20 ml/kg) was also normal. Partial central diabetes insipidus was diagnosed by his response to water restriction and nasal desmopressin administration. Polyuria and hypernatremia were not evident in this case, probably due to a combination of low solute intake and low, but not deficient, levels of plasma ADH. This case demonstrates that carbamazepine may cause acute hyponatremia even in central diabetes insipidus, probably by sensitizing the distal renal tubules.

Carbamazepine

Arterial pressure and its regulation in rats bred successively on low sodium diet.

To investigate the effects of long-term sodium restriction on mechanisms regulating cardiovascular function, Wistar rats at weaning (F0) were placed on a normal (0.4%) or low (0.05%) sodium diet. The first (F1) and second (F2) generations were derived from inbreeding within each group. The resting mean arterial pressure did not differ between the diet groups of F0 or F1 rats, but it was significantly lower in F2 rats on the low sodium diet. Plasma renin concentration was similar in the two groups in each generation, and the F2 rats on both diets responded to [Sar1, Ala8] angiotensin II with the same degree of decrease in arterial pressure. Plasma norepinephrine was not influenced by sodium intake in the F0 or F1 rats, but was significantly lower in F2 rats on the low sodium diet. The depressor response to hexamethonium was similar in the two F1 groups, while low sodium F2 rats exhibited a lesser response. These results suggest that rats bred successively on a low sodium diet have a suppressed sympathetic nerve function with no enhancement of the renin-angiotensin system, which in turn results in a lower arterial pressure.

Animals

Renin responses in patients with orthostatic hypotension: case reports.

In orthostatic hypotensive patients renin is reported to increase in response to head-up tilt unless the lesion involves postganglionic sympathetic efferent nerves. The authors examined responses of plasma renin activity (PRA) to acute blood pressure reduction in 4 patients with orthostatic hypotension. When the coexistence of normal plasma norepinephrine (PNE) and normal or high-normal pressor response to alpha stimulant is considered to be a sign of preserved function of postganglionic fibers, 2 of the patients had sympathetic lesions mainly confined to central and/or preganglionic fibers. They were diagnosed as having multiple system atrophy (MSA). The other 2 were diagnosed as having idiopathic orthostatic hypotension with possible postganglionic lesions. Although 1 MSA patient showed an increase in PRA from 2.0 to 4.7 ng/mL/hr in response to the tilt, the other MSA patient showed no PRA response to the tilt. The head-up tilt did not provoke an apparent PRA response in patients with idiopathic orthostatic hypotension. The authors infused sodium nitroprusside (SNP) in the 3 patients whose PRA did not respond to the head-up tilt. The infusion decreased blood pressure by 40 mmHg or more, but PRA responses were inappropriately small or suppressed. In all cases, PNE did not respond at all to the head-up tilt and to the infusion of SNP. These findings suggest that possible preservation of postganglionic fibers does not necessarily indicate an intact responsiveness of PRA. The PRA profiling may not be an accurate predictor for the site of the fiber degeneration in orthostatic hypotension.

Aged

[Evaluation of the localizing procedures of primary aldosteronism].

The validity of preoperative localizing procedures was studied in 36 patients with primary aldosteronism due to adrenal adenoma, all of whom were confirmed surgically. Adrenalectomy resulted in normalization of blood pressure and serum potassium. Furthermore, we reviewed the correlation between mass size and some clinical parameters as well as the accuracy of localization procedures. Adopted localization procedures included imaging techniques such as abdominal ultrasonography, computed tomography (CT), adrenal scintiscan, magnetic resonance imaging (MRI) and adrenal venography, and as a functional diagnostic procedure, adrenal venous sampling. Among imaging procedures, CT was the most effective to detect adrenal mass with as high accuracy as 88%, adrenal venography following with 83%. The correct localization was obtained in 60% by adrenal scintiscan and only 39% by ultrasonography. Although MRI was performed only in 2 cases, the smallest adenoma could be detected only by MRI, suggesting that MRI might be useful to detect microadenoma by increased signal intensity. Although adrenal scintiscan had been considered to be useful because of its functional diagnostic characteristics, the correct localization was as low accuracy as 60%, which was not improved by the administration of dexamethasone. To assess the accuracy of lateralization for adrenal venous sampling, we calculated the ratio of aldosterone concentration in adrenal vein to inferior vena cava. When the ratio was more than 10 or less than 1, the correct localization was made.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen