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

Pronounced hypoaldosteronism was found in three young women with hypertension and symptoms of mineralocorticoid overproduction--i.e., hyporeninaemia, hypokalaemia, and a fall in blood-pressure after diuretic therapy. Plasma 11-deoxycorticosterone and 18-hydroxy-11-dooxycorticosterone concentrations were normal Treatment with dexamethasone induced a return to normal of blood-pressure and plasma-potassium and an increase in plasma-renin activity and urinary aldosterone excretion. The data suggest that hypertension in these patients is maintained by overproduction of an unknown adrenocorticotropindependent mineralocortocoid.
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PMID:Dexamethasone-responsive hypertension in young women with suppressed renin and aldosterone. 7 49

A 57-year-old woman with hypertension and moderate renal insufficiency had chronic unexplained hyperkalaemia. Metabolic balance studies confirmed a diagnosis of hyporeninaemic hypoaldosteronism. Two observations suggested that impaired renal prostaglandin production contributed to the pathogenesis of the patient's disorder. Baseline renal-prostaglandin synthesis (as determined by urinary excretion of P.G.E and P.G.F) was was substantially depressed when compared with that in nine normal females. Infusion of low doses of P.G.A1 produced a significant increase in serum-aldosterone and urinary potassium excretion; it also led to a dramatic fall in blood-pressure and serum-potassium. It appears from these studies that a defect in renal prostaglandin synthesis has an important role in the pathogenesis of hyporeninaemic hypoaldosteronism.
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PMID:Possible role for impaired renal prostaglandin production in pathogenesis of hyporeninaemic hypoaldosteronism. 8 82

1. Pronounced hypoaldosteronism was found in five young women with low-renin hypertension and characteristic features of the mineralocorticoid hypertensive syndrome. 2. There was no overproduction of the mineralocorticoids 11-deoxycorticosterone and 18-OH-11-deoxycorticosterone. 3. Dexamethasone restored blood pressure to normal, decreased body weight, increased plasma potassium, and increased plasma renin activity and aldosterone excretion in all patients. 4. The data suggest overproduction of an unknown adrenocorticotrophic hormone-dependent mineralocorticoid maintaining hypertension in these patients.
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PMID:Evidence for an unidentified, adrenocorticotrophic hormone-dependent mineralocorticoid maintaining hypertension in young women with hypoaldosteronism. 28 66

The renin-angiotensin-aldosterone system appears to function normally in uncomplicated diabetes mellitus. Alterations in this system, however, have been observed in several of the microvascular and electrolyte complications associated with this disease. Plasma renin activity (PRA) and aldosterone are decreased in diabetic with nephropathy and hypertension, in those with neuropathy including orthostatic hypotension, and in those with hypoaldosteronism. PRA is low in rats with uncontrolled, nonketotic diabetes, and pressor responsiveness to angiotension II is increased in patients with diabetic retinopathy. Potential mechanisms responsible for the decreased PRA include plasma volume expansion, hyalin destruction of the juxtaglomerular cells, defective synthesis of renin, and inadequate catecholamine stimulation of renin, and inadequant cathecholamine stimulation of renin release. In diabetic ketoacidosis, PRA and aldosterone are stimulated secondary to the associated dehydration with hypovolemia. This report reviews the current status of the function of the renin-angiotensin-aldosterone system in diabetes mellitus and proposes a possible role for the altered function of this system in the pathophysiology of several diabetic complications.
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PMID:Renin-angiotensin-aldosterone system in diabetes mellitus. 82 63

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

Thirteen patients were followed for 4-46 months after removal of an aldosterone producing adenoma. Normotension was achieved in all cases but two in whom moderate diastolic hypertension was easily managed on diuretic therapy. All were cured of hypokalemia and symptoms related to low plasm potassium. Persistaent selective hypoaldosteronism was seen in one patient. A gratifying regression of symptoms and signs related to arterial hypertension was seen. Medical treatment with aldosterone antagonists may "cure" the patient to the same extent as surgery. The present results encourage the use of surgical treatment in these young patients since a life-long drug therapy--with its attendant problems--is the only alternative.
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PMID:Conn's syndrome. A follow-up of thirteen surgically treated cases. 107 48

The radioimmunological dosages of renin and of aldosterone are used nowadays in clinical practice for research purposes only. The measurement of activity of plasma renin may be considered a significant indication of the concentration of the enzime in plasma and, indirectly, of its secretion. Several factors take a part in the regulation of renin secretion (mean arterial pressure, introduction of sodium and potassium, the sympathetic nervous system, ADH and concentration of angiotensin II in plasma). In pathological conditions such factors may cause alteration of the renin-angiotensin II system, thus determining hyperreninisms and hyporeninisms, whether associated with arterial hypertension or not. Several factors take a part on aldosterone secretion too (ACTH, sodiaemia, potassiaemia, renin-angiotensin II system). In pathological conditions the alteration of the regulation system may lead to hyperaldosteronism or to hypoaldosteronism of primary or secondary type. A survey of recent research on the physiopathology of the renin-aldosterone system is also given.
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PMID:[Renin and aldosterone]. 123 75

Hyperkalemia is commonly encountered in patients who receive a renal transplant and the immunosuppressive drug, cyclosporine. There is also a high incidence of hypertension (which is thought to be due to expansion of the extracellular fluid volume) and hyperchloremic metabolic acidosis in this group of patients. This constellation of findings led to the suspicion of the possibility that their basis might be type II hypoaldosteronism. To test this hypothesis, 12 patients with hyperkalemia (plasma K+, 5.1 +/- 0.2 mmol/L at the time of study) while receiving cyclosporine were studied. Patients who had diabetes mellitus, those receiving drugs known to cause hyperkalemia (e.g., beta blockers, angiotensin-converting enzyme inhibitors, K(+)-sparing diuretics), or those with a serum creatinine greater than 200 mumol/L were excluded. The renal response to hyperkalemia was inappropriate because the transtubular K+ concentration gradient (TTKG) was only 4.3 +/- 0.4 compared with a TTKG of 13 +/- 1, 2 h after 50 mmol of KCl was given to normal subjects. The TTKG, after administration of 200 micrograms of fludrocortisone, was still very low (5.6 +/- 0.6) in the patients compared with that of controls (12 +/- 1). After administration of 250 to 500 mg of acetazolamide to increase the delivery of bicarbonate to the distal nephron, the TTKG rose significantly to 11 +/- 1 in patients on cyclosporine, compared with 17 +/- 1 in the controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Studies to determine the basis for hyperkalemia in recipients of a renal transplant who are treated with cyclosporine. 162 52

In a clinical case of arterial hypertension with hypopotassiaemia and hyporeninaemic hypoaldosteronism due to the use of a dermatological cream containing 9-alpha-fluoroprednisolone, late identification of the iatrogenic cause forced attention on the differential diagnosis of the less frequent hyporeninaemic hypoaldosteronism.
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PMID:[Arterial hypertension and hyporeninemic hypoaldosteronism. Description of a clinical case]. 200 35

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


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