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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The results of this study demonstrate that only in healthy normotensive subjects during extended orthostatism that the renin-angiotensin-aldosterone system remains integral and is characterized by a significant increase in serum angiotensin-converting enzyme (SACE), plasma renin activity (PRA) and plasma aldosterone (PA). SACE modification do not seems to directly follow that of PRA (as shown by the absence of a direct correlation between SACE and PRA). In essential hypertension, the behavior of SACE seems to change, without demonstrating a significant increase in the mean levels of this enzyme. Finally in hypertension of known origin, such as primary hyperaldosteronism, the low levels of SACE in the recumbent position (not stimulated by orthostatism) seem to depend (by mechanism of negative biofeedback) on the increased serum levels of PA, which is moreover verified in the same group for PRA.
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PMID:[The behavior of serum angiotensin-converting enzyme in normotensive subjects, in subjects with essential hypertension and in subjects with primary hyperaldosteronism on the orthostatic test]. 133 43

Only a few studies deal with electrocardiographic (ECG) signs of left ventricular hypertrophy (LVH) in patients with primary hyperaldosteronism, although it may be presumed that many factors such as arterial hypertension, hypokalemia, increased blood volume, and decreased activity of the renin-angiotensin system can modify LVH pattern in this entity. For that reason, we evaluated ECG signs of LVH in 55 patients with primary hyperaldosteronism hospitalized in our department from 1971 to 1990. These data were compared with age, serum potassium level, plasma renin activity (PRA) and-in 14 patients-with left ventricular mass, measured echocardiographically. We found inverse correlation between serum potassium concentration and the Sokolow-Lyon index: SV1 + RV5/6 (r = -0.47, p < 0.001). Among 24 patients with only abnormal QRS voltage, without ST-T changes suggestive of LVH, 19 (79.2%) had hypokalemia. In multivariate analysis, potassium concentration was the single independent predictor of an abnormal QRS voltage: -0.743, p = 0.01 vs. 0.153 (age), -0.337 (PRA) and 0.454 (LV mass). Our observations suggest that hypokalemia is an important factor influencing an amplitude of QRS complexes and may be responsible for false-positive LVH diagnosis.
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PMID:Influence of serum potassium on the electrocardiographic pattern of left ventricular hypertrophy in primary hyperaldosteronism. 139 82

The mechanisms of hypertension during primary hyperaldosteronism and Cushing's syndrome are not completely understood. An enhanced vascular sensitivity to noradrenaline has been described in both situations. Neuropeptide Y (NPY) induces direct vasoconstriction and potentiates the action of noradrenaline. Sodium retention and dexamethasone have been shown to increase circulating NPY levels in animals and the expression of NPY in neuroendocrine cells. In order to determine if NPY could be involved in the enhanced vascular sensitivity to noradrenaline associated with adrenocortical hyperactivity, we measured plasma NPY in patients with Cushing's syndrome (n = 26) and primary hyperaldosteronism (n = 15) and compared it with that of hypertensive patients with pheochromocytomas (n = 13) or essential hypertension (n = 51) and with normotensive controls (n = 47). The concentration of NPY-Like immunoreactivity (NPY-Li) (mean +/- S.E.) in controls was 39.6 +/- 3.0 pg/ml. Elevated concentrations were found in 77% of the samples collected from pheochromocytoma patients (1180.4 +/- 394.0 pg/ml). NPY-Li levels in patients with essential hypertension (35.0 +/- 2.6 pg/ml), primary hyperaldosteronism (31.3 +/- 3.9 pg/ml) and Cushing's syndrome (33.1 +/- 4.8 pg/ml) were not different from that of controls. NPY-Li levels in hypertensive and normotensive patients with Cushing's syndrome were similar (38.5 +/- 7.5 vs 24.2 +/- 3.7 pg/ml). No correlation was found between the NPY-Li level and the mean blood pressure at the time of sampling. Our results suggest that NPY is unlikely to be involved in the pathogenesis of hypertension associated with primary hyperaldosteronism and Cushing's syndrome.
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PMID:Plasma concentration of neuropeptide Y in patients with adrenal hypertension. 147 6

Patients (pts) with essential hypertension normally exhibit a typical diurnal variation with a nocturnal blood-pressure (BP) decreased. A lack of this periodicity is often reported in pts with secondary hypertension. 24-h BP measurement was therefore performed in 308 pts with essential hypertension, and in 172 pts with secondary hypertension, in order to evaluate the diagnostic value of nocturnal BP decrease. Diagnoses of the secondary hypertensives were: renoparenchymatous hypertension (n = 29), diabetic nephropathy (n = 24), morbus Conn (n = 6), renal artery stenosis (n = 32), pheochromocytoma (n = 5), hemodialysis pts (n = 30), and kidney transplantation (n = 44). Pts with essential hypertension showed a mean systolic and diastolic BP decrease during the nighttime period of 22 +/- 7 mmHg and 17 +/- 5 mmHg, respectively. In contrast, the corresponding values in secondary hypertension were 5.7 +/- 9.2 mmHg (systolic decrease) and 5.2 +/- 5.9 (diastolic decrease). Pts with pheochromocytoma who had a nighttime increase in BP demonstrated the greatest difference from the essential hypertensives, followed by pts with either diabetic nephropathy or after kidney transplantation. A lack of nocturnal BP decline (less than 10% of the daytime values) was detected in 69.8% of pts with secondary hypertension, but only in 5.2% of pts with essential hypertension. In summary, these results suggest that the absence of a nighttime decline in BP during 24-h ambulatory monitoring is an indication of secondary hypertension and should lead to further investigations. Furthermore, a nightly hypertension is associated with a higher risk of complications.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diagnostic significance of absent nocturnal blood pressure decrease in 24-hour long-term blood pressure measurement]. 151 20

1. An unusual clinical case is described in which renal artery stenosis (RAS) was found to coexist with adrenocortical hyperplasia, resulting in hypertension. 2. Partial relief of the hypertension was achieved by correction of RAS, and then further relief by extirpation of one adrenal gland affected by unilateral hyperplasia, in interventions 8 months apart. 3. Biochemical features typical of primary hyperaldosteronism were observed both before and after RAS repair but were not present after unilateral adrenalectomy. 4. The association of these two lesions could have occurred by chance, through genetic linkage, or by progression from RAS to tertiary aldosteronism.
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PMID:Concurrence of primary aldosteronism and renal artery stenosis. 152 61

This is a report of a rare and unusual case of adrenal pathology. A patient presented with clinical and biological signs of primary aldosteronism and computed body tomography scan led to our suspecting the presence of a left adrenocortical carcinoma. The in vitro studies performed on the resected tumour showed very low synthesis of mineralocorticoids and glucocorticoids. The patient could not be reexamined until 15 months later, when he still suffered hypertension; another tomography scan revealed a mass on the right adrenal gland. The studies performed on this second tumour confirmed the diagnosis of Conn's adenoma: active in vitro biosynthesis of 18-hydroxy-corticosterone and aldosterone from exogenous tritiated precursors.
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PMID:Concurrent adrenocortical carcinoma and Conn's adenoma in a man with primary hyperaldosteronism. In vivo and in vitro studies. 152 66

We present a case in which a patient, having already sustained an episode of malignant hypertension, was subsequently found to have an underlying Conn's adenoma. Ablation of the adenoma improved control of her hypertension. When a second adenoma developed in her remaining adrenal gland, control of her hypertension deteriorated.
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PMID:Conn's syndrome can cause malignant hypertension. 158 35

The paper summarizes data from the recent literature on pathogenetic variants of primary hyperaldosteronism, screening, diagnosis and therapy of this secondary form of arterial hypertension. On examples from their own practice the authors draw attention to the that the diagnosis and treatment of this disease is not always as straightforward as might appear from the literature. The solution is simple, effective screening in every hypertensive patient by examination of the kalaemia before treatment of arterial hypertension is started. In case of hypokalaemia the subsequent procedure should be the concern of specialized departments.
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PMID:[Primary hyperaldosteronism, problems in diagnosis and therapy in clinical practice]. 159 22

In the 1950s, after years of suspicion and work by many investigators regarding a potent mineralocorticoid hormone from the adrenal cortex, aldosterone was at last isolated and chemically identified [40, 41]. Soon after, Jerome Conn was the first to report [11] the clinical correlate of excessive secretion of aldosterone from a benign adrenocortical tumor manifested by hypertension and hypokalemia with the increased urinary excretion of aldosterone. This tumor is often called as aldosteronoma, and the disorder produced by it has been called primary aldosteronism by Conn. In the vast majority of patients harboring such tumors, the hypertension is cured by the resection of the tumor [12, 51], although some suggest that the hypertension may recur in a proportion of apparently cured patients [3, 36]. Thus, primary aldosteronism represents one of a few potentially curable forms of hypertension. Since aldosterone is elaborated normally by the zona glomerulosa cells of the adrenal, it has been assumed that all aldosteronomas originate from the cells of the glomerulosa zone. A clonal origin of aldosteronomas has also been suggested [28]. Some earlier and recent developments, however, indicate that functionally there may be more than one type of aldosteronomas and that their cellular origins might be different.
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PMID:Cellular origin of aldosteronomas. 160 Mar 48

The paper is concerned with the results of determination of a value of Na+/H(+)-metabolism in 66 patients with arterial hypertension of different genesis, including 21 patients with stage 11 essential hypertension, 8 patients with renal hypertension, 25 patients with Itsenko-Cushing syndrome or disease, 7 patients with pheochromocytoma, and 5 patients with primary hyperaldosteronism. The control group consisted of 11 healthy persons without predisposition to essential hypertension. It was shown that a value of Na+/H(+)-metabolism in patients with essential hypertension exceeded a 3.8-fold the control values. In patients with hyperglucocorticism, pheochromocytoma, arterial hypertension of renal genesis, the rate of Na+/H(+)-metabolism was significantly decreased as compared to that of a group of patients with essential hypertension. It could be used in differential diagnosis of the hypertensive syndrome. The problem of the diagnostic value of this indicator in primary hyperaldosteronism needs further investigation.
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PMID:[Determination of the value of Na+/H+-metabolism in erythrocytes of patients with arterial hypertension of endocrine origin]. 165 73


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