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PubMed2001

Genetic alterations in patients with primary aldosteronism.

The syndrome of primary aldosteronism is characterized by hypertension with excessive production of aldosterone, potassium loss, and suppression of the renin-angiotensin system. The most common clinical subtypes of primary aldosteronism are aldosterone-producing adrenocortical adenoma (APA) and bilateral adrenal cortical hyperplasia (idiopathic hyperaldosteronism, or IHA). It has been reported that renin suppression and aldosterone levels are lower and hypokalemia milder in patients with IHA than in patients with APA. In the present study, we investigated the genetic analysis of aldosterone synthase gene, CYP11B2 in patients with primary aldosteronism and review the recent studies. The chimeric CYP11B1/CYP11B2 gene, which is a candidate gene for glucocorticoid-remediable hyperaldosteronism, was not found in either the DNA from aldosteronoma or in the genomic DNA from patients with APA or IHA. Mutations in the CYP21 or CYP11B1 gene were not present in patients with APA. No mutations in the coding region of the CYP11B2 gene were found in patients with IHA or APA. The level of CYP11B2 messenger RNA (mRNA) was much higher in the aldosteronoma portion than in nonadenomatous portion. The overexpression of CYP11B2 mRNA seen in the mononuclear leukocytes of patients with IHA suggests that unidentified aldosterone-stimulating factors or abnormalities of the CYP11B2 promoter region may cause the overproduction of aldosterone characteristic of IHA. The variants of the CYP11B2 gene may also contribute to dysregulation of aldosterone synthesis and lead to susceptibility to IHA.

Cytochrome P-450 CYP11B2↗
PubMed2004

Prospective study on the prevalence of secondary hypertension among hypertensive patients visiting a general outpatient clinic in Japan.

Secondary hypertension (SH) including endocrine hypertension has been reported to be uncommon. We estimated the prevalence of SH among hypertensive patients. We prospectively studied 1,020 hypertensive patients. As an initial screening, we measured plasma aldosterone concentration, plasma renin activity, serum cortisol concentration and plasma catecholamine concentration and conducted abdominal ultrasonography (US). As a secondary screening, we performed furosemide plus upright test, captopril renography, dexamethasone suppression test, 24-h urine catecholamine measurement and abdominal CT. Finally, primary aldosteronism with the exception of idiopathic hyperaldosteronism, pheochromocytoma, and Cushing's syndrome were diagnosed by histopathological examination of surgical specimens. Idiopathic hyperaldosteronism was clinically diagnosed by adrenocorticotrophic hormone (ACTH)-stimulated adrenal venous sampling and renovascular hypertension by renal arteriography. There were 61 patients with primary aldosteronism, 5 with renovascular hypertension, 11 with Cushing's syndrome, 10 with preclinical Cushing's syndrome and 6 with pheochromocytoma, and the prevalence of SH was 9.1% among 1,020 hypertensive patients. In 76 (82%) of 93 patients with SH, hypertension was cured or improved after unilateral adrenalectomy, transsphenoidal pituitary adenectomy or percutaneous transluminal angioplasty. With the exception of US and CT, all initial and secondary screening tests were found to be sensitive and specific for differentiating SH from essential hypertension (EH). In conclusion, the measurement of various hormone concentrations was very sensitive for ruling out SH--a condition for which, in the present study, there were few specific signs or symptoms--while CT and US examinations were not always useful for differentiating SH from EH. The prevalence of curable SH among hypertensive subjects was higher in this study, which was conducted by our simple method of screening tests, than in previous reports. Hypertensive patients should be screened for SH and the underlying disease treated appropriately to avoid long-term use of antihypertensive drugs and risks of atherosclerotic complications.

Adrenal Gland Diseases↗
PubMed2004

Aldosterone excretion among subjects with resistant hypertension and symptoms of sleep apnea.

OBJECTIVE: The severity of obstructive sleep apnea (OSA) correlates with the difficulty of controlling BP. The mechanism, however, by which sleep apnea contributes to the development of resistant hypertension remains obscure. Having observed a high prevalence of OSA among hypertensive subjects with primary hyperaldosteronism, we hypothesized a possible association between sleep apnea and aldosterone excretion. DESIGN: In consecutive subjects referred to a university clinic for resistant hypertension, we prospectively determined plasma renin activity (PRA), plasma aldosterone concentration (PAC), and 24-h urinary aldosterone excretion during high dietary salt ingestion. In addition, all subjects completed the Berlin Questionnaire, a survey designed to identify subjects at risk of having sleep apnea. Primary hyperaldosteronism (PA) was defined as a PRA < 1.0 ng/mL/h and 24-h urinary aldosterone excretion > 12 micro g during high urinary sodium excretion (> 200 mEq/24 h). RESULTS: Of the 114 subjects evaluated, 72 subjects had a high probability and 42 subjects had a low probability of having sleep apnea based on their responses to the Berlin Questionnaire. Subjects at high risk for sleep apnea were almost two times more likely to have PA diagnosed (36 vs 19%, p < 0.05), tended to have lower PRA (1.2 +/- 1.8 ng/mL/h vs 1.9 +/- 4.1 ng/mL/h), and had significantly greater 24-h urinary aldosterone excretion (13.6 +/- 9.6 micro g vs 9.8 +/- 7.6 micro g, p < 0.05) compared to subjects at low risk of sleep apnea. CONCLUSION: These data provide evidence of increased aldosterone excretion in subjects with resistant hypertension and symptoms of sleep apnea. While the causality of this association is unknown, it is hypothesized that sleep apnea contributes to the development of resistant hypertension by stimulating aldosterone excretion.

Aldosterone↗
PubMed1982

[The effect of trilostane, a new inhibitor of adrenal steroid biosynthesis, on blood pressure, plasma aldosterone and other steroid hormones, serum potassium and plasma renin activity in primary aldosteronism (author's transl)].

Six patients with primary aldosteronism (PA), one with idiopathic hyperaldosteronism (IHA), one with glucocorticoid responsible hyperaldosteronism (GRHA) and eight with essential hypertension (EH) were treated with trilostane (MWD-1822) (4 alpha, 5-epoxy-17 beta-hydroxy-3-oxo-5 alpha-androstane-2 alpha-carbonitrile), an inhibitor of adrenal steroid biosynthesis, for 9-47 days with a daily dose of 30-960 mg. Blood pressure decreased slightly and gradually from 30 min. to 360 min, plasma aldosterone (PAC) and cortisol concentration (F) decreased, and plasma dehydroepiandrosterone concentration (DHEA) increased 120 min. after the administration of a single dose of 120 mg of trilostane. In the patients with PA, IHA and GRHA on long term therapy with trilostane, blood pressure decreased, PAC and F were depleted, serum improved within normal limits and DHEA increased, but plasma progesterone concentration (Prog.) changed variously and plasma renin activity (PRA) remained suppressed. In the patients with EH, systolic pressure decreased in 5 out of 8 (under - 20 mmHg), and diastolic pressure decreased in 3 out of 8 (under - 10 mmHg), DHEA increased in all, but the changes in serum potassium, PAC, F, Prog. and PRA were various. There was no remarkable reaction after the administration of trilostane. It is concluded that trilostane is an effective inhibitor of 3-hydroxysteroid dehydrogenase in vivo and that it is useful in the treatment of primary aldosteronism and other hypertension due to hyperproduction of aldosterone.

Adult↗
PubMed1983

[Acute antihypertensive effect of captopril in hypertensive patients: with special reference to kallikrein-kinin system].

In order to clarify the role of the kallikrein-kinin system in the hypotensive mechanisms of converting-enzyme inhibition, captopril was administered in a single oral dose of 50 mg to 17 hypertensive patients, of whom 14 had essential hypertension, one had chronic renal failure, one had primary aldosteronism, and one had glucocorticoid responsive hyperaldosteronism. Captopril lowered blood pressure remarkably in either low-renin or normal-, and high-renin hypertensives, however, there was no significant relationship between the fall in blood pressure and pretreatment levels of plasma renin activity (PRA) in any of the patients any time after the administration. PRA was significantly increased in normal- and high-renin hypertensives but not in low-renin patients. Plasma aldosterone concentration (PAC) was decreased significantly in normal- and high-renin patients, while no significant change in PAC was observed in patients with low-renin activity. Captopril elevated plasma bradykinin concentration (PBK) from a control value of 12.5 +/- 4.1 (mean +/- s.d.) to 20.3 +/- 7.7 pg/ml (p less than 0.001) at 30 min, and there was a significant correlation between changes in PBK and changes in mean blood pressure 120 min after the administration in all the patients (r = 0.741, p less than 0.01, n = 17). In one patient with primary aldosteronism, PBK increased from a baseline of 10.0 to a maximum value of 19.0 pg/ml, corresponding to the rapid fall in blood pressure. Also, in one patient with glucocorticoid responsive hyperaldosteronism, captopril increased PBK from a control of 14.1 to 27.9 pg/ml at 30 min, corresponding to the marked fall in blood pressure from 170/106 to 136/90 mmHg. From these findings, it is suggested that the accumulation of kinins following captopril administration plays a major role in the short-term reduction of blood pressure in hypertensive patients, especially in those with low renin-angiotensin activity.

Adult↗
PubMed1989

A case of normotensive primary aldosteronism with hypopituitarism, epilepsy, and medullary sponge kidney.

A 55-year-old man with normotensive primary aldosteronism, hypopituitarism, epilepsy, and medullary sponge kidney is reported. Seventeen years before admission, he had been noted to have hypokalemia associated with high potassium clearance, suppressed plasma renin activity, metabolic alkalosis, and normal blood pressure as well as low urinary excretion of 17-hydroxycorticosteroids. He kept normotensive in spite of hyperaldosteronism until nine months after the initiation of replacement therapy with glucocorticoid and thyroxine for hypopituitarism, when he became hypertensive. Hypopituitarism seemed to play a role in keeping a normal blood pressure despite long-standing hyperaldosteronism.

Adrenal Glands↗
PubMed1993

Circadian blood pressure variations in endocrine disorders.

Circadian rhythm of blood pressure and of heart rate was studied in patients with hyperthyroidism (n = 10), pheochromocytoma (n = 8), primary hyperaldosteronism (n = 7), and in a control group of essential hypertensive patients (n = 18) and of normotensive healthy subjects (n = 11). 24-hour blood pressure was monitored non-invasively using SpaceLabs (SL 90207) with 8-min intervals in the daytime (8 a.m. to 10 p.m.) and 30-min intervals during night-time (10 p.m. to 8 a.m.). To characterize circadian blood pressure rhythm the difference between the mean blood pressure during daytime and that during night-time was calculated. In patients with hyperthyroidism the day-night difference of the systolic and diastolic blood pressure and of the heart rate was significantly reduced when compared to the normotensive control group (p < 0.05). The day-night difference of the systolic and diastolic blood pressure was significantly lower in the group with pheochromocytoma and hyperthyroidism than in the essential hypertensive controls (p < 0.05); the day-night difference of the heart rate was similar. In the patients with primary hyperaldosteronism the day-night differences of the systolic and diastolic blood pressure and of the heart rate was similar to those in essential hypertensive controls. We conclude that endocrine disorders affecting sympathetic activity like pheochromocytoma or hyperthyroidism influence the circadian blood pressure rhythm, whereas the renin-aldosterone-system has no major impact on the diurnal blood pressure variation. The results therefore support the hypothesis that circadian blood pressure variation is mainly mediated by a modulation of the sympathetic tone.

Adrenal Gland Neoplasms↗
PubMed1983

Unilateral hypersecretion of aldosterone associated with adrenal hyperplasia as a cause of primary aldosteronism.

In 3 patients with longstanding hypertension and spontaneous or diuretic-induced hypokalemia, the diagnosis of primary aldosteronism was established by the dual criteria of non-suppressible plasma aldosterone level and suppressed plasma renin activity. Preoperative studies of the etiology for the hyperaldosteronism using the postural plasma aldosterone test and adrenal venous steroid measurements gave conflicting results. On the basis of the differential adrenal venous steroid content, which suggested an unilateral adrenal source for the aldosterone hypersecretion, presumed to be adrenal adenoma, each patient was operated upon. In each case the excised adrenal revealed adenomatous or macronodular hyperplasia. Reinvestigation of the patients 3 to 12 months after the adrenalectomy showed that the dynamics of the renin-aldosterone axis was now restored to the normal state even though the patients remained hypertensive. These findings indicate that unilateral hypersecretion of aldosterone associated with adrenal hyperplasia can occur in some patients with primary aldosteronism simulating that due to an aldosteronoma. Such observations also raise questions about the pathogenesis of the adrenal hyperplasia and seem to add further complexity to the evaluation of patients with hyperaldosteronism.

Adrenal Cortex↗
PubMed1985

Malignant hypertension due to an aldosterone producing adrenal adenoma.

Malignant hypertension in Conn's syndrome is rare. We report an 18 year old boy who presented with visual and renal impairment due to malignant hypertension which subsequently proved to be secondary to an aldosterone secreting adrenal adenoma. Diagnosis was delayed in this patient as plasma renin concentrations (PRC) were not invariably low and it is emphasized that suppression of PRC is not always a feature of primary hyperaldosteronism. The diagnosis of primary hyperaldosteronism is only excluded adequately by the demonstration of suppression of aldosterone secretion.

Adenoma↗
PubMed1999

[The Conn syndrome. The clinical and surgical aspects of 18 cases of adrenal adenoma].

OBJECTIVES: Presentation of a series of 18 patients who underwent surgery of aldosterone-producing adrenal adenoma (Conn's syndrome) over the last 10 years. Assessment of the most significant clinical and pathological aspects from a surgical point of view. METHODS: Retrospective study evaluating a broad range of features: clinical, analytical, hormonal, imaging, types of anaesthesia, approaches, technique used, intra and post-operative morbidity and mortality, evolution and pathoanatomical diagnosis. RESULTS: The most frequent clinical data of primary hyperaldosteronism were: 94.4% volume-dependent HBP, 50% headaches and dizziness, 27.8% epistasis and/or episodes of angor or acute myocardial infarction, and 22.2% heart failure. The biochemical study and hormonal testing evidenced: hypokalemia in 88.9%, metabolic alkalosis 66.7% and hypernatremia in 61.1%. Mean aldosterone levels were 517.5 pg/mL, and urinary levels 85.9 mcg/day. Resting plasma renin activity (PRA) < 0.2 ng/mL/h in 77.8% cases and positive aldosterone stimulation test in 61.1%: captopril test positive. Imaging diagnosis was based in CAT which was conclusive in 88.9% and ultrasound which was diagnostic in 27.8% cases. The surgical approach was: lumbotomy (over the 11th or 12th rib) in 14 patients and transpleurodiaphragmatic in all remaining patients. The intraoperative complications reported were placement of endothoracic tube due to iatrogenic pneumothorax in two occasions. Duration of the procedure (mean 136.1 min) and post-operative hospitalization (mean 7.76 days), as well as post-surgery follow-up for up to 96 months were also studied. At final time point there was 66.7 asymptomatic patients, 33.3% cases of HBP, and no deaths. CONCLUSIONS: Primary hyperaldosteronism due to adrenal adenoma is an uncommon reason for HBP, but in most cases can be cured with surgery. Biochemical and hormonal testing is determinant to research a diagnosis. Ultrasound and CAT are essential for imaging diagnosis, and occasionally NMR can be of help. Lumbotomy is considered the choice approach for these small tumours as it is a familial technique for urologists with a low complications rate.

Adenoma↗
PubMed1999

[Hypertension and mineralocorticoids. Usefulness of renin and aldosterone measurements].

Recently, some genetic forms of hypertension have been well characterized. These forms can be globally called mineralocorticoid hypertension and are due to different alterations of the renin-angiotensin-aldosterone system (SRAA). Among these, classic primary hyperaldosteronism and its glucocorticoid remediable variety, in which hypertension is secondary to aldosterone production, must be considered. There are also conditions in which mineralocorticoid activity does not depend on aldosterone production. These conditions generate a hyporeninemic hyperaldosteronism, observed in Liddle syndrome, apparent mineralocorticoid hypertension, 11- and 17-hydroxylase deficiency, among others. The detection of these forms of hypertension is only feasible if the renin-angiotensin-aldosterone system is assessed, measuring renin and aldosterone levels. This article reviews these forms of hypertension, their clinical workup and their relevance in the usual hypertensive patients.

Aldosterone↗
PubMedDate not supplied

[Hyperplastic changes and aldosterone content in the adrenal cortex in essential hypertension and primary aldosteronism].

Autopsy and operative material (adrenalectomy for hyperaldosteronism) was studied to elucidate morphology, incidence of nodules, aldosterone content in the adrenal of patients with essential hypertension (EH). It was established than nodular masses in the adrenals in the form of micro and macronodules are present in 80% of EH patients. Aldosterone content in the adrenals in both nodules and in the adjacent cortex is significantly higher than in the adrenals of patients without EH. This fact as well as increased cell nuclei size in the fascicular and glomerular zones indicate high secretory activity of the adrenals in EH. Clinicomorphological comparisons in patients after adrenalectomy because of hyperaldosteronism syndrome allow to conclude that grave forms of EH may be followed by aldosteronism syndromes with nodular hyperplasia of the adrenal cortex being the basis of the syndrome. Indications to adrenalectomy require clear criteria of differential diagnosis with primary aldosteronism.

Adrenal Cortex↗
PubMed2000

[Transtubular potassium gradient in the diagnosis of potassium metabolism disorders].

The transtubular potassium gradient (TTKG) is a simple physiologically based clinical test to study the renal excretion of potassium. This article reviews the most important physiological changes influencing TTKG, the hypokalaemia and hyperkalaemia, the effect of mineralocorticoids, alkalosis, action of diuretics among other drugs etc. The authors studied the abnormalities of TTKG occurring in clinical conditions (renal patients with nephrotic edema, "dry" patients with renal diseases, liver cirrhosis associated with ascites, and primary hyperaldosteronism) and compare them to the results obtained in healthy people. They consider the test to be useful in the recognition of conditions with hypoaldosteronism (including the various types of pseudohypoaldosteronisms and aldosterone resistance) and hyperaldosteronism as well as renal diseases, in accordance with the data published in the literature. On the basis of their own results, they found the method of determination of TTKG informative and helpful also when investigating the site of actions and the effect mechanisms of the diuretics.

Diagnosis, Differential↗
PubMed2000

Diabetes mellitus in primary aldosteronism.

BACKGROUND: Information concerning diabetes mellitus associated with primary aldosteronism is scarce. OBJECTIVES: To determine the prevalence of diabetes mellitus in its two main pathogenetic forms of primary aldosteronism and to evaluate its association with several clinical variables. PATIENTS: Fifty in-patients (31 female and 19 male, aged 16-66), diagnosed during the years 1980-1998 as aldosterone producing adenoma (n = 26) or as idiopathic hyperaldosteronism (n = 24). METHODS: Morning fasting plasma glucose was measured by glucoso oxidase method in all patients. In the presence of higher values, confirmatory measurements were performed on the next day. The results were evaluated retrospectively by the diagnostic criteria of American Diabetes Association, 1997. Statistical significance of the association between diabetes mellitus and clinical variables was evaluated by chi-square test. RESULTS: Diabetes mellitus was ascertained in 6 patients out of 50 (12%; interval of 95% confidence 5-24%). Diabetes was accompanied significantly more often with idiopathic hyperaldosteronism (10-47%) than with aldosterone producing adenoma (0-13%). Patients with the family history of diabetes suffered more often (9-76%) from this disease than those without the history (1-19%). Obesity, longer (> 5 years) duration of hypertension and hypokalaemia did not affect the occurrence of diabetes. CONCLUSIONS: The occurrence of diabetes in primary aldosteronism was connected significantly with its idiopathic subtype and positive family history of diabetes. (Tab. 2, Ref. 11.)

Adolescent↗
PubMed2000

The aldosterone/renin ratio as a screening test for primary aldosteronism.

OBJECTIVE: To investigate the utility of random outpatient plasma aldosterone and renin measurements in screening for primary aldosteronism (PA) in hypertensive patients. DESIGN: Clinical records of hypertensive patients who had aldosterone and renin determinations over a 3-year period were analysed retrospectively. The patients were arbitrarily classified into five groups defined according to the aldosterone level and the aldosterone/renin (A/R) ratio: PA (plasma aldosterone > 500, A/R ratio > or = 1,000; essential hypertension (EHT) (aldosterone < 1,000, A/R < 1000); secondary hyperaldosteronism (SHA) (aldosterone > or = 1,000, A/R < 400); low-renin hypertension (LRHT) (aldosterone < 500, A/R > or = 1,000); miscellaneous hyperaldosteronism (MHA) (aldosterone > or = 1,000, A/R 400-1000). SETTING: A hypertension clinic in a large teaching hospital. PATIENTS AND RESULTS: The sample of 216 hypertensives were classified as follows: EHT 51%, LRHT 8%, PA 32%, SHA 7%, and MHA 3%. Mean plasma potassium values were significantly lower (P < 0.0001) in the PA group compared with essential hypertensives, but plasma K+ was of little utility in identifying individual patients with PA, as 71% were normokalaemic. Adrenal computed tomography scans were performed on 38 of 69 patients with PA, and revealed definite unilateral or bilateral adrenal masses in 7 and probable unilateral masses in a further 4. Five patients underwent unilateral adrenalectomy, confirming adrenal adenomas in 4 and nodular hyperplasia in 1. The minimum prevalence of PA due to adrenal adenoma or hyperplasia was 3.3% of all hypertensives and 10.1% of patients with biochemical PA defined by A/R ratio. Patients with biochemical PA had more target organ damage, and in general responded more favourably to regimens with spironolactone than to conventional therapy. CONCLUSIONS: A random outpatient aldosterone and renin measurement identifies a group of hypertensives with biochemical PA in which there is a significant prevalence of adrenal adenomas, increased prevalence of target organ damage and a good response to spironolactone. These results have major implications for the investigation and management of patients with severe or resistant hypertension.

Adult↗
PubMed2000

[Excess of mineralocorticoids in essential hypertension: clinical-diagnostic approach].

BACKGROUND: Primary hyperaldosteronism is more frequent among subjects with essential hypertension than previously thought. The prevalence, according to local and international evidence could fluctuate between 9 and 10%. AIM: To investigate if subjects with essential hypertension have different aldosterone and renin plasma levels than normotensive subjects. PATIENTS AND METHODS: One hundred twenty five subjects with essential hypertension, not receiving medications for at least two weeks prior to the study and 168 age and sex matched normotensive controls were studied. Blood was drawn between 9 and 10 AM during a sodium free diet to determine plasma aldosterone, plasma renin activity and potassium. RESULTS: Plasma aldosterone was higher in hypertensive subjects than controls (11.6 +/- 7.6 and 9.9 +/- 5.1 ng/dl respectively; p = 0.04). Plasma renin activity was lower in hypertensives than controls (1.42 +/- 1.28 and 1.88 +/- 1.39 ng/ml/b respectively; p < 0.001). Thus, plasma aldosterone/plasma renin activity ratio was higher in hypertensives (13.8 +/- 13.5 and 8.3 +/- 7.8; p < 0.001). A pathological ratio was defined as over 25, corresponding to the mean plus two standard deviations of the control group. Primary hyperaldosteronism was found in 5/125 hypertensives (4%) and 1/168 normotensive subject (0.6%). None had hypokalemia. CONCLUSIONS: Subjects with essential hypertension have higher plasma aldosterone and lower plasma renin activity than normal controls. A plasma aldosterone/plasma renin activity over 25 was defined as abnormal.

Adult↗
PubMed2001

[Effect of insulin in hypertension with high and low levels of renin].

BACKGROUND: Setback in insulin resistance has been described in patients with essential hypertension. The aim of our study was to verify at the receptor and postreceptor levels the presence of insulin resistance in patients with high or low renin activity. METHODS AND RESULTS: Six patients with the renal artery stenosis (20 to 65 years, average age was 51 +/- 12 years, BMI: 27 +/- 2.0 kg.m2) and six patients with primary hyperaldosteronism (28 to 61 years, average age was 50 +/- 13 years, BMI: 26.9 +/- 3.2 kg.m2) were investigated. Their diagnose was confirmed by laboratory examination, computer tomography, and duplex sonography. Blood pressure was monitored for 24 hours with Spacelab tonometer (SBP: 161 +/- 29 mmHg, DBP: 98 +/- 12 mmHg versus SBP: 168 +/- 21 mmHg, DBP: 103 +/- 9 mmHg; plasma renin activity was 8.1 +/- 5.6 versus 0.3 +/- 0.4 ng.ml-1.h-1, p < 0.001; recumbent plasma aldosterone level was 98 +/- 31 versus 358 +/- 103 pg.ml-1, p < 0.001, normal value till 150 pg/ml, serum potassium was 3.9 +/- 0.4 and 3.5 +/- 0.6 mmol/l). All patients had normal course of the oral glucose tolerance test. Six volunteers of corresponding age and BMI formed the control group. Patients had normal values of the basal morning glycemia (4.9 +/- 0.5 and 5.0 +/- 0.6 versus 4.9 +/- 0.6 mmol/l), basal insulinemia level was 28.8 +/- 12.4 and 21.0 +/- 10.2 versus 15.9 +/- 8.8 mU.l-1 in healthy controls. Insulin effect was tested using isoglycemic hyperinsulinemic clamp method on Biostator with insulin infusion of 1 mU.kg.min-1. Plasma potassium concentration was kept at constant physiological levels using linear infusion pump (in patients with primary hyperaldosteronism after the prior supplementation). In patients with high-renin or low-renin hypertension, the glucose consumption during clamping was lower than that of healthy controls (M, glucose disposal rate: 23.7 +/- 4.8 and 19.5 +/- 3.4 versus 33.0 +/- 5.7 mumol.kg.-1.min-1, p < 0.001), increase of the metabolic glucose clearance (MCRG: 5.1 +/- 1.5 and 3.9 +/- 0.7 versus 7.9 +/- 1.4 ml.kg-1.min-1, p < 0.001) and tissue insulin sensitivity index (M/I: 24.3 +/- 10.1 and 26.4 +/- 8.3 versus 38.4 +/- 10.1 mumol.kg-1.min-1 to mU.l-1 x 100, p < 0.001). CONCLUSIONS: Patients with high-renin and low-renin hypertension have the insulin effectiveness significantly impaired. Such insulin resistance probably does not depend on the renin activity, plasma aldosterone concentration or on serum potassium level. The ethiopathogenesis of the described changes will be the aim of our next study.

Adult↗
PubMedDate not supplied

[Excretion of aldosterone in the urine, renin activity in the plasma and some indices of the metabolism of potassium and sodium in patients with the iodiopathic edema syndrome].

It appeared that urinary aldosterone excretion was increased in 23 of 35 patients with a syndrome of idiopathic edema. The plasma renin activity failed to differ from the norm; consequently it can be supposed that the renin-angiotensin system played no significant role in the mechanism of hyperaldosteronism development in this form of pathology. A negative sodium balance was revealed in some of the patients with an edema syndrome and hyperaldosteronism.

Adult↗