Biomedical subjects

R Ozono

Publications and source records attributed to R Ozono.

At least 37 records · Page 2Linked to original sources

PubMed1998

Immunolocalization of subtype 2 angiotensin II (AT2) receptor protein in rat heart.

Angiotensin II exerts its effects on cardiovascular function and water and sodium homeostasis by interacting with plasma membrane receptors on target organs. The existence of subtype 2 angiotensin II (AT2) receptors in the rat heart has been demonstrated by ligand binding and reverse transcription-polymerase chain reaction. In the present study, the expression and localization of AT2 receptor protein in the rat heart was investigated using an antipeptide polyclonal antibody against the native rat AT2 receptor by light microscopic immunocytochemistry and Western blot analysis. In frozen tissue sections, positive immunostaining was observed in the myocardium and coronary vessels throughout the ventricle and atrium of neonatal and young rat hearts. Coronary vessels of the neonatal heart were more intensely stained compared with the surrounding myocardium. Positive immunoreactivity in the coronary vessels of young rats was localized to vascular endothelium but not in the smooth muscle cells. Preadsorption controls were all negative. Western blot analysis showed that the AT2 receptor protein (approximately 44 kDa) was detectable from the AT2 receptor-transfected COS-7 cells and neonatal rat cardiac myocytes but not from fibroblasts or young rat aortic smooth muscle cells. The neonatal rat heart expressed significantly more AT2 receptors than young rat heart. These data provide the first direct evidence for the expression and localization of AT2 receptor protein in the rat heart.

Angiotensin II↗

PubMed1997

Change in blood pressure during altered sodium intake is not associated with calciotropic hormone level.

1. We evaluated the effects of the dietary restriction of sodium chloride on blood pressure and systemic calcium metabolism in 19 in-patients with essential hypertension (11 men and 8 women, mean age 49.9 +/- 12.1 years). 2. All patients received a high-sodium diet (250 mmol/day) for 1 week, followed by a low-sodium diet (10 mmol/day) for another week. Intake of potassium (100 mmol/day) and of calcium (15 mmol/day) were kept constant throughout the study. 3. Sodium restriction significantly reduced the mean blood pressure (from 114.0 +/- 1.9 to 105.0 +/- 13.7 mmHg, P < 0.01). Urinary calcium excretion was significantly reduced (from 5.1 +/- 2.4 to 2.2 +/- 1.0 mmol/day, P < 0.01). 4. The change in mean blood pressure after sodium restriction was not correlated with a change in any parameter of calcium metabolism [whole blood ionized calcium, plasma intact parathyroid hormone, or 1,25-(OH)2 vitamin D3]. 5. Plasma renin activity during a regular sodium diet, an index of renin status, was significantly and inversely correlated with the change in blood pressure during sodium restriction, but not with any change in the parameters of calcium metabolism. 6. We conclude that sodium restriction reduces blood pressure and decreases urinary calcium excretion. However, we observed no significant role of extracellular calcium concentration or of calciotropic hormone concentration in the mechanism of sodium sensitivity.

Adult↗

PubMed1997

Relationship between insulin resistance and endothelium-dependent vascular relaxation in patients with essential hypertension.

The infusion of L-arginine induces the production of nitric oxide and stimulates the immediate secretion of insulin. To examine the relationship between insulin resistance and endothelium-dependent vascular relaxation in patients with essential hypertension, we evaluated the renal and insulin responses to L-arginine, 500 mg/kg infused intravenously over 30 minutes, in 23 patients with mild essential hypertension who were neither obese nor diabetic and in 20 normotensive control subjects. We found no difference between the two groups in blood glucose or insulin in the fasting condition. The renovascular relaxation induced by L-arginine was significantly less in patients with essential hypertension than in normotensive control subjects. The increase in plasma cyclic GMP in response to L-arginine was lower in hypertensive patients than in normotensive subjects. Although the serum concentrations of glucose in response to L-arginine were similar in the two groups, the serum insulin response of the essential hypertensives was significantly higher than that of the normotensive subjects. In all subjects, the peak cyclic GMP response to L-arginine was significantly correlated with the peak delta glucose/ delta insulin ratio response to L-arginine (r = .69, P < .001). Findings suggested that an impairment of endothelium-dependent renal vascular relaxation and a reduced sensitivity to insulin are present in patients with essential hypertension. A link may be present between the abnormality of the L-arginine/nitric oxide/cyclic GMP pathway and insulin resistance in patients with essential hypertension.

Arginine↗

PubMed1997

Dopamine D1A receptors and renin release in rat juxtaglomerular cells.

Two dopamine D1-like receptors have been cloned from mammals, the D1 and D5 receptors, also known as D1A and D1B receptors, respectively, in rodents. Although D1-like receptors are known to stimulate renin release, the receptor subtype mediating this action has not been determined. We investigated D1 receptor subtype expression in rat juxtaglomerular cells obtained after enzymatic dispersion of kidney cortex and differential centrifugation. Juxtaglomerular cells in primary culture were immunocytochemically 85% to 95% renin positive. These cells expressed the D1A but not the D1B receptor (mRNA and protein). D1-like receptor function was demonstrated by a concentration-dependent stimulation of cAMP production by dopamine (n = 5-9 per group). Fenoldopam, a D1-like receptor agonist, also caused a concentration-dependent increase in cAMP production and renin secretion that was blocked by the selective D1-like receptor antagonist SCH23390 (n = 4-13 per group). Although the D1 ligands do not distinguish between the cloned D1-like receptors, the actions of fenoldopam were due to occupancy of the D1A receptor: (1) the D1B receptor, the only other mammalian D1-like receptor, is not expressed in juxtaglomerular cells; (2) antisense but not sense D1A oligonucleotides completely blocked the stimulatory effect of fenoldopam on cAMP production and renin secretion. We conclude that there is selective dopamine receptor gene expression in juxtaglomerular cells; the dopamine receptor subtype linked to the stimulation of cAMP and renin secretion in juxtaglomerular cells is the D1A subtype.

Animals↗

PubMed1997

Nocturnal decline in blood pressure is attenuated by NaCl loading in salt-sensitive patients with essential hypertension: noninvasive 24-hour ambulatory blood pressure monitoring.

We investigated the effect of NaCl on the circadian blood pressure rhythm in patients with essential hypertension classified according to the presence or absence of salt sensitivity. We obtained 24-hour noninvasive ambulatory blood pressure measurements in 64 Japanese patients with mild to moderate essential hypertension who ate a low NaCl diet (50 mmol/d) for 1 week, followed by a high NaCl diet (340 mmol/d) for 1 week. Twenty-six patients whose mean blood pressure was increased more than 10% by NaCl loading were classified as salt sensitive. The remaining 38 patients were classified as salt resistant. The nocturnal decline in mean blood pressure was significantly smaller in salt-sensitive patients (8.3+/-1.0%) than in salt-resistant patients (11.5+/-0.9%) (P<.05) during a high NaCl diet but was similar in both groups during a low NaCl diet. There was no significant difference in the prevalence of the non-dipper pattern between groups on a low NaCl diet, but the prevalence of the non-dipper pattern was significantly higher in salt-sensitive patients than in salt-resistant patients on a high NaCl diet (0.57 versus 0.26, chi2=6.4; P=.02; odds ratio, 3.82). These findings suggest that the NaCl loading blunted the nocturnal decline in blood pressure in salt-sensitive patients but not in salt-resistant patients.

Blood Pressure↗

PubMed1997

Aging and severity of hypertension attenuate endothelium-dependent renal vascular relaxation in humans.

Endothelial dysfunction may be related to cardiovascular risk factors, such as aging, hypertension, and atherosclerosis. We investigated whether aging and hypertension independently alter endothelial function in the renal circulation in humans in the absence of abnormalities in lipid and glucose metabolism. L-Arginine (500 mg/kg over 30 minutes) was intravenously administered to 33 patients with essential hypertension and 35 normotensive subjects. The L-arginine-induced increases in renal plasma flow (10.1+/-0.8% versus 15.8+/-0.9%, P<.05) and plasma cGMP (53+/-4% versus 82+/-5%, P<.05) were significantly smaller in patients with essential hypertension than in the normotensive subjects. Multivariate stepwise regression analysis showed that age (P<.0002) and the mean blood pressure (P<.0001) were independently and negatively correlated with the renal plasma flow response to L-arginine. Age (P<.002), mean blood pressure (P<.0001), and male sex (P<.05) were independently correlated with the L-arginine-induced increase in plasma cGMP. The peak change in plasma cGMP was significantly correlated with the L-arginine-induced increase in renal plasma flow (r=.63, P<.001). These findings suggest that aging and hypertension may independently impair endothelium-dependent renovascular dilation and that this effect may be caused at least in part by a decrease in nitric oxide production.

Adult↗

PubMed1997

Localization of the dopamine D1 receptor protein in the human heart and kidney.

The dopamine D1 receptor has recently been identified in the rat heart and kidney. In the present study, using Western blot analysis and light microscopic immunohistochemistry, we examined D1 receptor protein expression in the human kidney and heart. Antipeptide polyclonal rabbit antiserum was raised against the third extracellular domain of the native receptor and affinity-purified using a protein-A column. Selectivity of the antiserum was validated by recognition of the D1 receptor expressed in stably transfected LTK- cells and Sf-9 cells. The immunohistochemical staining for D1 receptor protein was distributed throughout the atrium and ventricular myocardium and in the coronary vessels. In the kidney, positive immunoreactive signal was detected in the proximal and distal tubules, the collecting ducts, and the large intrarenal vasculature, whereas staining was absent in the juxtaglomerular (JG) cells and the glomeruli. D1 receptor antiserum preadsorbed against the immunizing peptide did not produce significant staining. In Western blot analysis, a single 55-kD band was detected for the D1 receptor in membranes from the D1 receptor transfected Sf-9 cells but not in nontransfected cells. In the heart and kidney, we detected a 55-kD band as well as an additional 40-kD band, which may reflect partial degradation of the receptor protein. These results provide the first evidence for the localization of the dopamine D1 receptor protein in the human heart and kidney. The similar distribution of this subtype receptor in the human heart and kidney to that in the rat supports the possible (patho)physiological significance of the peripheral dopamine system in humans.

Aged↗

PubMed1997

Expression of the subtype 2 angiotensin (AT2) receptor protein in rat kidney.

In situ hybridization studies have suggested that the subtype 2 angiotensin (AT2) receptor gene is expressed in fetal and newborn rat kidney but is undetectable in the adult animals. In the present study, we investigated the expression of AT2 receptor protein in the fetal (days 14 and 19 of fetal life), newborn (day 1 postpartum), and adult (4-week-old and 3-month-old) rat kidney. Polyclonal anti-peptide antiserum was raised against the amino terminus of the native AT2 receptor. The selectivity of the antiserum was validated by recognition of the AT2 receptor in a stably transfected COS-7 cell line by Western blot and immunocytochemical analysis. As a positive control, the AT2 receptor signal was detected strongly in the adrenal gland. Positive immunohistochemical staining was observed in the mesenchymal cells and ureteric buds of the 14-day fetal kidney and in the glomeruli, tubules, and vessels in the 19-day fetal and newborn kidney. Glomeruli expressing the AT2 receptor were localized mainly in the outer layer of the renal cortex. In the young (4-week-old) and mature (3-month-old) adult rat on normal sodium intake, renal AT2 receptor immunoreactivity was present in glomeruli but substantially diminished compared with that of newborn rats. In both young and mature adult rats, dietary sodium depletion increased the renal AT2 receptor signal, mainly in the glomeruli and interstitial cells. Preimmune and preadsorption controls were negative. Western blot analysis detected a single 44-kD band in the fetal and newborn rat kidney and in the young and mature adult rat kidney. Dietary sodium depletion increased the density of the AT2 receptor band in mature adult rat kidneys. These data provide evidence that the AT2 receptor protein is expressed in the fetal and newborn rat kidney, diminishes in adult life, and is reexpressed in the adult in response to sodium depletion.

Adrenal Glands↗

PubMed1997

[Evaluation of angiotensin I converting enzyme gene polymorphism in patients with essential hypertension and coronary artery disease].

We investigated the role of the insertion (I)/deletion(D) polymorphism in the angiotensin I converting enzyme (ACE) gene in the cardiovascular diseases. First, we studied 520 patients who had undergone coronary angiography: including 220 patients with acute myocardial infarction, 98 patients with effort angina pectoris (> 75% stenosis), 83 patients with vasospastic angina and 119 controls with normal coronary artery. There was no difference in the frequency of ACE gene I/D allele or genotype II, ID and DD among the four groups. Second, we studied the correlation between ACE gene I/D polymorphism and the clinical characteristics in patients with essential hypertension. The distribution of I/D allele and genotype were similar in 140 essential hypertensives and 83 normal controls. In patients with DD genotype, age at onset of hypertension was lower and left ventricular mass index was greater than those in patients with ID and II, although blood pressure levels and the severity of damage to other organs-were similar in the three groups. Further, 66 patients with essential hypertension were classified into 35 salt-sensitive and 31 salt-resistant patients according to changes in mean blood pressure during a week of low salt diet followed by a week of high salt diet. The frequency of I allele was significantly higher in the salt-sensitive group than in the salt-resistant group. In conclusion, ACE gene I/D polymorphism is not associated with coronary artery diseases. In patients with essential hypertension, the D allele was associated with early onset and left ventricular hypertrophy, while I allele was associated with salt sensitivity.

Age of Onset↗

PubMed1996

Expression of the subtype 1A dopamine receptor in the rat heart.

The subtype 1A dopamine receptor (D1A) has recently been detected in the rat kidney. In the present study using light microscopic immunohistochemistry, electron microscopic immunocytochemistry, and in situ amplification of mRNA, we demonstrate the D1A receptor in Sprague-Dawley and Wistar Kyoto rat hearts. For immunohistochemistry and immunocytochemistry, anti-peptide polyclonal antibodies were directed toward amino acid sequences of the third extracellular and intracellular domains of the native receptor. Selectivity was validated by recognition of the D1A receptor expressed in stably transfected LTK- cells. D1A receptor mRNA was detected with a novel transcription-based isothermal in situ amplification system as well as with reverse transcription-polymerase chain reaction. D1A receptor protein was distributed throughout the atrium and ventricular myocardium. Preimmune and preabsorption controls were negative. Electron microscopic immunocytochemistry using the protein A gold method demonstrated the D1A receptor along the cellular membranes of coronary smooth muscle cells and ventricular myocytes and in the myosin thick filaments and M-lines. D1A receptor mRNA was present in coronary vessels and myocardium in amplified but not in unamplified sections. Western blot analysis showed specific D1A bands in transfected LTK- cells and the atrium but not in nontransfected LTK- cells and the ventricle. The selective D1-like receptor agonist SKF38393 stimulated adenylyl cyclase in ventricular myocardial plasma membranes in a dose-related fashion, and the response was abolished by the selective D1-like receptor antagonist SCH23390. These results demonstrate that the D1A receptor gene and protein are expressed in normal rat heart. The physiological and pathophysiological roles and predominant cell signaling mechanism or mechanisms of this receptor remain to be determined.

Animals↗

PubMed1996

Modulation of target tissue response to angiotensin II and sodium sensitivity in Japanese patients with essential hypertension.

"Non-modulators" are essential hypertensive patients who fail to modulate an adrenal response, renovascular response, or both, to angiotensin II (Ang II). The aim of the present study was to characterize "non-modulators" among Japanese patients with normal-renin essential hypertension and to determine whether non-modulation is related to sodium sensitivity of blood pressure. The increase in plasma aldosterone concentration (PAC response) and the decrease in renal plasma flow (RPF response) in response to Ang II infusion (3 ng/kg/min) were assessed in 15 Japanese patients with essential hypertension who received a high sodium diet (250 mEq/d) followed by a low sodium diet (10 mEq/d). The subjects were divided into two groups (6 modulators and 9 non-modulators) based on their ability to modulate the PAC response during sodium restriction. There was no significant difference between modulators and non-modulators in electrolyte balance or in plasma Ang II levels on either diet. Changes in the PAC response during sodium restriction were significantly correlated with the change in mean blood pressure during sodium restriction (r = -0.67, p < 0.01), while changes in the RPF response were not. RPF responses in both groups decreased during sodium restriction, although an effect on the RPF response in non-modulators was unexpected. These results suggest that non-modulators do exist among Japanese patients, but that this defect does not involve both the adrenal gland and the kidney. Apparently, only non-modulation of the adrenal response is involved in the mechanism of sodium sensitivity.

Adult↗

PubMed1995

Dietary salt decreases cytosolic calcium in platelets from Dahl salt-sensitive rats.

To determine whether abnormal cellular Ca2+ handling is involved in salt-induced hypertension of Dahl salt-sensitive rats (DS), we investigated Ca2+ handling in fura 2-loaded platelets of DS and Dahl salt-resistant rats (DR) fed a high-NaCl (8%) or a low-NacL (0.3%) diet for 4 wk from 5 wk of age. At 5 wk of age, blood pressure, resting cytosolic Ca2+ concentration ([Ca2+]i), the thrombin-evoked increase in [Ca2+]i and the size of internal Ca2+ stores of DS were comparable with those of DR. After 4 wk on the diets, resting [Ca2+]i of DS on high-NaCl diet was lower than that of DS on low-NaCl diet, and there was no effect of high salt intake on resting [Ca2+]i in DR. In DS, high salt intake attenuated the [Ca2+]i response to thrombin in the presence of external Ca2+. In contrast, the [Ca2+]i response to thrombin in the absence of external Ca2+ was enhanced by high salt intake in DS. The size of internal Ca2+ stores was increased by high salt intake in DS but not in DR. These data suggest that it is not obligatory for hypertension to be accompanied by an increase in platelet [Ca2+]i.

Animals↗

PubMed1995

Effects of L-arginine infusion on renal hemodynamics in patients with mild essential hypertension.

Previous studies have shown that endothelium-derived relaxing factor/nitric oxide plays an important role in the regulation of systemic and renal hemodynamics. The purpose of the present study was to determine whether endothelium-dependent renovascular relaxation was impaired in patients with mild essential hypertension who had normal renal plasma flow and glomerular filtration rate. We evaluated the effects of intravenous administration of L-arginine on blood pressure and renal hemodynamics in 13 patients with mild essential hypertension and 15 normotensive control subjects. L-Arginine infusion (500 mg/kg over 30 minutes) reduced mean blood pressure (from 82.5 +/- 2.5 to 76.3 +/- 2.6 mm Hg in hypertensive patients and from 106.1 +/- 3.0 to 97.5 +/- 2.9 mm Hg in control subjects; P < .001) and renovascular resistance (from 0.084 +/- 0.009 to 0.067 +/- 0.009 mm Hg.mL-1.min-1.[1.48 m2]-1 and from 0.105 +/- 0.010 to 0.093 +/- 0.011 mm Hg.mL-1.min-1.[1.48 m2]-1, respectively; P < .001). L-Arginine infusion increased renal plasma flow (from 602 +/- 36 to 698 +/- 40 mL.min-1.[1.48 m2]-1, P < .05) in normotensive subjects but not in hypertensive subjects, and glomerular filtration rate was unaffected in both groups. Although the L-arginine-induced reduction in mean blood pressure was similar in both groups, the decline in renovascular resistance was smaller in hypertensive subjects. The response of renal plasma flow was also smaller in hypertensive subjects. These findings suggest that dysfunction of the L-arginine-nitric oxide pathway exists in the renal circulation even in mild essential hypertension with normal renal plasma flow and glomerular filtration rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1995

Systemic magnesium deficiency disclosed by magnesium loading test in patients with essential hypertension.

The present study was designed to determine whether magnesium (Mg) deficiency is present in patients with essential hypertension. We measured the retention of an intravenously administered Mg load (0.2 mmol/kg MgSO4 over 4 h), and serum and erythrocyte Mg concentrations in 17 inpatients with essential hypertension and in 15 normotensive controls. There was no significant difference between the two groups in erythrocyte Mg concentration (normotensives vs., hypertensives: 2.0 +/- 0.5 vs. 2.1 +/- 0.4 mmol/l cells), serum Mg concentration (normotensives vs. hypertensive: 2.1 +/- 0.2 vs. 2.1 +/- 0.2 mg/dl), or in urinary Mg excretion (normotensives vs. hypertensives: 65.8 +/- 25.5 vs. 73.7 +/- 26.7 mg/day). However, Mg retention was significantly higher in hypertensives than in normotensives (normotensives vs. hypertensives: 31.8 +/- 12.1 vs. 41.9 +/- 13.3%). These results suggest that a systemic Mg deficiency, which is undectectable by serum or erythrocyte Mg determination, may exist in patients with essential hypertension.

Adult↗

PubMed1994

Lack of effect of ouabain on calcium homeostasis in rat platelets: comparative study with human platelets.

The precise mechanisms of Ca2+ handling in rat platelets are not fully understood. We sought to determine whether rat platelets possess a Na(+)-Ca2+ exchanger. First, we investigated the time course of the effect of ouabain (10(-4) M) on cytosolic sodium concentration ([Na+]i) and Ca2+ homeostasis in platelets from Wistar rats in comparison with those from humans. Ouabain increased platelet [Na+]i in both rat and human platelets. Whereas ouabain induced a time-dependent increase in basal and thrombin-stimulated (0.3 units/ml) cytosolic calcium concentration ([Ca2+]i) in human platelets, no change was found in rat platelets. Furthermore, 90-min pretreatment of rat platelets with ouabain did not affect the [Ca2+]i response to thrombin (0.1-1.0 units/ml) or a maximal dose of ionomycin (5 microM). Also the decline in [Ca2+]i after the peak response evoked by these agonists in the absence of extracellular Ca2+ was not changed by ouabain pretreatment. Similarly, replacement of extracellular Na+ had no influence on any of these determinations. Thus decreasing the plasma membrane Na+ gradient did not affect basal [Ca2+]i, thrombin-induced mobilization of Ca2+ from intracellular stores, internal Ca2+ discharge capacity, or Ca2+ extrusion from cytosol of rat platelets. In contrast to human platelets, a Na(+)-Ca2+ exchange mechanism does not appear to play a significant role in Ca2+ homeostasis of rat platelets.

Animals↗

PubMed1994

Lack of increase in platelet Ca2+ and Na+ in deoxycorticosterone acetate-salt hypertensive rats.

We have previously characterized abnormal Ca2+ handling in platelets of spontaneously hypertensive rats (SHRs). In this study, we investigated whether cellular Ca2+ metabolism and/or Na+ concentration is altered in platelets of deoxycorticosterone acetate-salt hypertensive rats (DOCA rats). The resting cytosolic Ca2+ concentration ([Ca2+]i) in platelets was significantly lower in DOCA rats than controls (54.5 +/- 1.4 vs. 61.2 +/- 2.3 nmol/l). The amplitude of the [Ca2+]i transient induced by thrombin was significantly increased in the absence, but not the presence, of external Ca2+ in DOCA rats compared with control rats. The [Ca2+]i response to 5 mumol/l ionomycin in the Ca(2+)-free buffer was greater in DOCA rats than in controls (546 +/- 23 vs. 470 +/- 18 nmol/l), indicating larger intracellular Ca2+ stores. The rate of recovery of [Ca2+]i after the peak response to thrombin was decreased in DOCA rats (79% at 0.1 U/ml and 91% at 1.0 U/ml thrombin of control rats). Cytosolic Na+ concentration ([Na+]i) in platelets was similar in DOCA and control rats. Altered Ca2+ levels are not correlated with [Na+]i in this salt-sensitive hypertensive model. Therefore, an increased [Ca2+]i is not an obligatory phenomenon in hypertension.

Animals↗

PubMed1994

Effects of age and sex on sodium chloride sensitivity: association with plasma renin activity.

The mechanism by which excessive NaCl intake raises blood pressure has not been fully clarified. The present study was undertaken in 87 Japanese inpatients with essential hypertension to investigate the interrelation among effects of age, sex and the renin-angiotensin system on NaCl sensitivity. After ingesting a regular NaCl diet (170 mmol/day) for one week, subjects were placed sequentially on a week of low NaCl diet (50 mmol/day) and a week of high NaCl diet (340 mmol/day). NaCl sensitivity defined as the difference in mean blood pressure between the low and high NaCl diets did not differ between genders. NaCl sensitivity was positively correlated with age and the change in PRA. The fall in PRA after NaCl loading was significantly smaller in women than in men. By multiple regression analysis, age and the change in PRA independently contributed to the change in mean blood pressure. Furthermore, the interaction between sex and the change in PRA was selected as a statistically significant variable. In conclusion, NaCl sensitivity of blood pressure is independently associated with age and the inadequate suppression of the renin-angiotensin system. Because the contribution of the change in PRA to NaCl sensitivity was greater in women than in men, the mechanism of blood pressure elevation after NaCl loading may differ between genders.

Age Factors↗

PubMed1993

[The prediction of blood pressure after adrenalectomy in primary aldosteronism].

In 30-40% of patients with primary aldosteronism owing to adenoma, hypertension is not relieved even though a hyper-functioning adenoma has been completely removed. The purpose of this study is to determine whether the prognosis of hypertension can be evaluated pre-operatively in patients with primary aldosteronism. Thirteen patients (6 men, 7 women; 47 +/- 9 years old) with primary aldosteronism were studied and adrenalectomy was performed in all cases. The success of the operation was confirmed by the normalization of plasma renin activity (PRA), plasma aldosterone concentration (PAC) and serum potassium. Eight patients, 3 men and 5 women, whose blood pressure (BP) was reduced to below 140mmHg systolic and 90mmHg diastolic at one year after the operation were classified as "group N" and the other 5 cases, 3 men and 2 women, remained hypertensive and were classified as "group H". There were no significant differences in the age of the patients, duration of hypertension, pretreatment mean BP and severity of hypertension between the two groups. Thus, it is doubtful that the lack of improvement of hypertension is due to the irreversible damage of the small arteries. Although pretreatment BP was similar in the two groups, systolic BP after the administration of 200mg per day of spironolactone for one week was significantly reduced in group N, but not in group H. Moreover, a significant correlation was found between mean BP after treatment with spironolactone and post-operative mean BP in all subjects. Pretreatment PRA was significantly lower in group H.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗