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

Not all the varied clinical disorders in which aldosterone and the mineralocorticoid hormones are involved have been reviewed. Only those disorders in which the mineralocorticoid hormones and their regulatory factors are the principal cause of the biochemical and clinical abnormalities have been examined. These are many and varied. Appreciation of the extent and magnitude of their involvement in the regulation of blood pressure, body fluids, and electrolyte composition continues to grow. The major direct clinical impact of the mineralocorticoid hormones appears to be in two areas: hypertension and potassium homeostasis. Their part in the mosaic of hypertension is established in primary hyperaldosteronism, but they also appear to affect and modify the hypertensive process in primary or essential hypertension. The probe continues. Hypoaldosteronism is more than the rare occurrence associated with Addison's disease. It may be the clue to the presence of nonaldosterone mineralocorticoid excess syndromes, and is obviously of critical importance in an increasing number of patients with chronic renal failure of varied aetiologies.
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PMID:A perspective on aldosterone abnormalities. 97 45

The overall control of body sodium relies on mechanisms that have close links to blood pressure control and hypertension. The Strauss concept of a basal level of body sodium, below which any available sodium is retained and above which any extra sodium is excreted (at a rate exponentially related to the amount present in the body), has been confirmed in rat studies. Total body sodium, on an average sodium intake, thus consists of basal plus extra: the proportions of these can vary and this makes interpretation of total body sodium difficult. Basal body sodium is, in theory, the level at which delivery of sodium to the distal nephron equals distal reabsorption of sodium. The latter is largely determined by aldosterone and, indeed, basal body sodium is high in primary aldosteronism and low in Addison's disease. The half-life of extra sodium is short in primary aldosteronism and long in Addison's disease: it is also short in some hypertensive subjects but in general lengthens with age. The exact mechanisms involved are still uncertain. Most of this work is based on step reductions in sodium intake. Step increases in sodium intake appear to lead to more complicated adjustment processes, with a delay in commencing excretion followed by some under-damping of the system before a new higher level of body sodium and a new equilibrium of intake and excretion is reached.
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PMID:The control of body sodium in relation to hypertension: exploring the Strauss concept. 170 18

Plasma renin activity (PRA) and plasma volume (PV) were determined in 22 adult patients treated for Addison's disease (AD) and reporting at the clinic for follow-up. Mean PRA was thrice the upper limit of normal (9.1 +/- 7.1 ng/ml/h (SD)) and mean PV was decreased (87% +/- 11 (SD)), consistent with residual hypovolemia in most patients, despite conventional treatment with both fluorocortisol (FF) and cortisone acetate. There was an inverse relationship between PRA and PV. Both PRA and PV were significantly correlated with FF dosage. On the other hand, no correlation was found between PV and either systolic or diastolic blood pressure (BP), while PRA was significantly correlated with systolic but not diastolic BP. Four patients were persistently hypertensive (diastolic BP greater than 100 mmHg) with elevated PRA in 3, associated with a definitely low PV in two cases. Two of these patients were progressively taken off FF, so as to control BP. Thus, in view of the not infrequent occurrence of arterial hypertension in AD patient on conventional treatment, we would warn against attempts at normalizing PV and PRA by means of FF, irrespective of BP in asymptomatic cases. In fact, when hypertension develops, reduction or sometimes withdrawal of FF may be recommended as a first therapeutic step.
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PMID:Mineralocorticoids in the management of primary adrenocortical insufficiency. 206 74

We report an unusual association of hyperkalemia, mild hyperchloremic acidosis, and hypertension in a young woman. Pseudohyperkalemia, Addison's disease, renal insufficiency, classical hyporeninemic hypoaldosteronism, isolated hypoaldosteronism, and iatrogenic causes were excluded. The patient's findings were compatible with a rare syndrome designated as type II pseudohypoaldosteronism, Gordon's syndrome.
Hypertension 1986 Feb
PMID:Unusual association of hyperkalemia and hypertension. 241 52

The present study was performed to investigate whether or not there were enkephalins in plasma and urine in normal subjects and in patients with various diseases. Two kinds of antisera were developed to detect M-enk and L-enk. One has specific affinity with the C-terminus of methionine-enkephalin sulfoxide (M-O-enk), the oxidized form of M-enk, and the other with the N-terminus of L-enk. M-enk-like substance (MELS) was present in blood and urine in normal subjects, but not L-enk-like substance (LELS). Plasma MELS and its urinary output averaged 38 +/- 14 pg/ml (N = 19) and 605 +/- 235 ng/day (N = 15, M. +/- S.D.), respectively. There was a significant increase in plasma MELS and its urinary output in patients with pheochromocytoma. Plasma MELS did not show any significant increase or decrease in Cushing's disease. Addison's disease, panhypopituitarism or chronic glomerulonephritis. The urinary output of MELS was significantly increased in patients with essential hypertension, renovascular hypertension and primary aldosteronism, but was decreased in central diabetes insipidus.
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PMID:The presence of methionine-enkephalin in plasma and urine in normal human subjects and various patients. 408 13

The adrenal cortex is an important factor in the control of electrolyte and water balance and in blood pressure homeostasis. Not surprisingly, therefore, hyper- and hyposecretion of one or more of its products has extensive repercussions. Hypersecretion of aldosterone, as seen in primary hyperaldosteronism and related diseases, and of other mineralocorticoids such as corticosterone and/or 11-deoxycorticosterone, as seen in 17 alpha-hydroxylase deficiency or 11 beta-hydroxylase deficiency syndromes, respectively, are associated with hypertension, sodium retention, potassium wastage and a metabolic alkalosis. On the other hand, impaired secretion, as in Addison's disease or in congenital deficiencies of other steroid-synthesizing enzymes, leads to hypotension, sodium loss with hypovolaemia, and hyperkalaemia. In each case, these disturbances of electrolyte metabolism may cause neurological and muscle dysfunction. The relationship between glucocorticoid hypertension and electrolyte metabolism is less clear and the importance of the adrenal cortex in the aetiology of essential hypertension is still being assessed.
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PMID:Disorders of the adrenal cortex: their effects on electrolyte metabolism. 609 53

Glucocorticoids have a permissive effect on vascular tone and blood pressure; they enhance vascular responsiveness to vasopressors such as catecholamines without necessarily having an effect when administered alone. This effect does not require central or systemic mediation. Prostacyclin (prostaglandin I2; PGI2), a potent vasodilator, is produced by the vascular endothelium, vascular smooth muscle cells, adipocytes, and other cells. PGI2 production by vascular endothelium and other cells is decreased by glucocorticoids. The hypothesis is proposed that the effect of glucocorticoids on vascular tone is mediated by inhibition of PGI2 production by vascular endothelium (possibly other cells also). The inhibition of PGI2 production by glucocorticoids may contribute to the hypertension of Cushing's syndrome. Loss of this inhibitory effect in glucocorticoid deficiency states (eg, Addison's disease) may cause enhanced PGI2 production, which may contribute to the haemodynamic and gastrointestinal manifestations of these disorders.
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PMID:Inhibition of prostacyclin production mediates permissive effect of glucocorticoids on vascular tone. Perturbations of this mechanism contribute to pathogenesis of Cushing's syndrome and Addison's disease. 613 23

1. The haemodynamic and volume response to ACTH administration was investigated in six patients with mild, untreated essential hypertension and two patients with Addison's disease on maintenance steroids. Blood pressure, heart rate and weight were recorded daily. Plasma volume (125I-HSA) and cardiac output (thermo-dilution) were measured during the control period and on the 5th day of ACTH treatment. 2. In the hypertensive subjects, mean arterial pressure rose from 94.3 +/- 2.2 to 105.7 +/- 2.8 mmHg on the 5th day of ACTH administration (P less than 0.02). Plasma volume rose from 29.8 +/- 2.2 to 34 +/- 2.2 ml/kg. Cardiac index increased from 2.85 +/- 0.21 to 3.32 +/- 0.14 l/min per m2 (P less than 0.05). Cardiac output rose from 5.81 +/- 0.69 to 6.72 +/- 0.59 l/min. Calculated total peripheral resistance, heart rate and body weight were unchanged. No such changes were seen in patients with Addison's disease. 3. The haemodynamic characteristics of ACTH in patients with mild untreated essential hypertension are similar to those in the experimental model of ACTH induced hypertension in sheep.
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PMID:Haemodynamic response to ACTH administration in essential hypertension. 627 65

The renin-angiotensin system is one of a number of interlinked mechanisms regulating vascular resistance and blood volume. Under certain conditions it may become a predominant factor in maintaining vascular tone. Knowledge about these conditions (sodium depletion, mineralocorticoid deficiency, renovascular hypertension and iatrogenic hyperreninaemic states) is important for the safe and effective use of drugs which inhibit the renin-angiotensin system. Measurements of plasma renin activity are useful in the diagnostic assessment of hypertensive patients with hypokalaemia or evidence of renal artery stenosis. They may also have a place in the management of refractory or dialysis-resistant hypertension. Their use in the selection of antihypertensive therapy for the individual patient is controversial. Sequential measurements of plasma renin are helpful in analysing states of electrolyte depletion, and in titrating therapy for Addison's disease.
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PMID:The renin angiotensin system--its physiology and role in disease states. 631 2

Selective hypoaldosteronism is defined as diminished production of aldosterone, and sometimes also of 18-hydroxycorticosterone, with otherwise intact adrenal function. A decrease in the secretion of potassium and H+-ions and in the reabsorption of sodium in the distal nephron may result and lead to hyperkalemia, hyperchloremic acidosis, and impaired renal sodium conservation. The form of hypoaldosteronism which occurs in the adult is characterized by the following additional features: the aldosterone deficiency is due in the majority of cases to a decrease in enzymatically active plasma renin ("hyporeninemic hypoaldosteronism"), while various endogenous mechanisms as well as certain drugs (prostaglandin inhibitors, beta-blockers) may contribute. Other disturbances of the renin-angiotensin system (e.g. during treatment with converting-enzyme inhibitors) may rarely be responsible. Abnormalities in adrenal cortical synthesis may sometimes coexist, but proof that adrenal enzymatic defects play a primary pathogenic role in selective hyperaldosteronism in the adult is lacking. Such patients are frequently older (greater than 50 years), and often have diabetes mellitus and/or nephropathy (diabetic, interstitial, or hydronephrosis). Hyperkalemia and acidosis tend particularly to develop in association with mild to moderate impairment of renal function. The differential diagnosis should include other causes of impaired renal potassium secretion (Addison's disease, renal resistance to mineralocorticoids, potassium-sparing diuretics). Moreover, possible extrarenal factors contributing to hyperkalemia (oral potassium intake and redistribution of intracellular/extracellular space, particularly with associated insulin deficiency) should also be considered. For treatment, dietary potassium restriction is recommended as a general step. Replacement with the mineralocorticoid fludrocortisone acetate usually reverses the hyperkalemia and acidosis, but may sometimes induce sodium retention and hypertension. Loop diuretics, potassium-exchanging preparations and/or bicarbonate may also be useful as alternatives or additives.
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PMID:[Hyporeninemic hypoaldosteronism and the differential diagnosis of hyperkalemia]. 675 13


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