Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Unilateral renal artery stenosis can lead to a non-functional kidney which secretes large amounts of renin. Four cases are presented in which the high renin state resulted in hypertension, proteinuria from the intact contralateral kidney, and secondary aldosteronism. The proteinuria was in the nephrotic range, which is unusual in renovascular hypertension, but gradually disappeared after correction of the high renin state by removal of the renin-secreting kidney or administration of an ACE inhibitor. Accordingly, when there is marked proteinuria in the presence of new-onset or rapidly progressive hypertension, hypokalaemic alkalosis, and a high peripheral PRA, renal artery stenosis should be considered since the proteinuria may be reversible after nephrectomy, repair of the ischaemic kidney or medical therapy.
 ...
PMID:Reversible nephrotic syndrome due to high renin state in renovascular hypertension. 773 87

Familial glucocorticoid resistance results from the partial inability of glucocorticoids to exert their effects on their target tissues throughout the organism. The condition is associated with compensatory elevations of circulating ACTH and cortisol, with the former causing excess abnormal secretion of steroids with mineralocorticoid and androgen activity. The manifestations of glucocorticoid resistance vary from asymptomatic to chronic fatigue, to varying degrees of hypertension and/or hypokalaemic alkalosis and hyperandrogenism. The latter can be manifest in women as acne, hirsutism, menstrual irregularity, oligoanovulation and infertility, in men as infertility, and in children as precocious puberty. Different molecular defects of the highly conserved glucocorticoid receptor gene, altering its concentration and functional characteristics, appear to cause the syndrome of familial glucocorticoid resistance. Depending on the molecular defect, this syndrome is transmitted by an autosomal dominant or recessive trait. There are recent suggestions that non-generalized forms of glucocorticoid resistance may exist, resulting in autoimmune-inflammatory phenomena or psychiatric manifestations.
 ...
PMID:Hormone-nuclear receptor interactions in health and disease. Glucocorticoid resistance. 798 Aug 39

In physiological conditions, the regulation of acid-base balance in brain maintains a noteworthy stability of cerebral pH. During systemic metabolic acid-base imbalances cerebral pH is well controlled as the blood/brain barrier is slowly and poorly permeable to electrolytes (HCO3- and H+). Cerebral pH is regulated by a modulation of the respiratory drive, triggered by the early alterations of interstitial fluid pH, close to medullary chemoreceptors. As blood/brain barrier is highly permeable to Co2, CSF pH is corrected in a few hours, even in case of severe metabolic acidosis and alkalosis. Conversely, during ventilatory acidosis and alkalosis the cerebral pH varies in the same direction and in the same range than blood pH. Therefore, the brain is better protected against metabolic than ventilatory acid-base imbalances. Ventilatory acidosis and alkalosis are able to impair cerebral blood flow and brain activity through interstitial pH alterations. During respiratory acidosis, [HCO3-] increases in extracellular fluids to control cerebral pH by two main ways: a carbonic anhydrase activation at the blood/brain and blood/CSF barriers level and an increase in chloride shift in glial cells (HCO3- exchanged for Cl-). During respiratory alkalosis, [HCO3-] decreases in extracellular fluids by the opposite changes in HCO3- transport and by an increase in lactic acid synthesis by cerebral cells. The treatment of metabolic acidosis with bicarbonates may induce a cerebral acidosis and worsen a cerebral oedema during ketoacidosis. Moderate hypocapnia carried out to treat intracranial hypertension is mainly effective when cerebral blood flow is high and vascular CO2 reactivity maintained. Hypocapnia may restore an altered cerebral blood flow autoregulation. Instrumental hypocapnia requires a control of cerebral perfusion pressure and cerebral arteriovenous difference for oxygen, to select patients for whom this kind of treatment may be of benefit, to choose the optimal level of hypocapnia and to avoid any deleterious effect. If hypocapnia is maintained over several days, an adaptation of CSF pH may limit the therapeutic effect on the cerebral blood flow and the intracranial pressure.
 ...
PMID:[Acid-base equilibrium and the brain]. 809 67

A 62-year-old male with small cell lung cancer (SCLC) associated with Cushing's syndrome and diabetes insipidus (DI) is reported. The patient was referred to our hospital for treatment of SCLC. A diagnosis of paraneoplastic Cushing's syndrome was made on the basis of an elevated serum ACTH (623.5 pg/ml) level, elevated excretion of urinary 17-OHCS (18.01 mg/day), obesity, hypertension, hyperglycemia, persistent hypokalemia, alkalosis, and no history of diabetes mellitus. He was also diagnosed as having DI based on polyuria and polydipsia, low specific gravity of the urine (1.007-1.010), low serum ADH (1.4 pg/ml) level, normal plasma osmolarity (29 mOsm/kg H2O), and the results of water deprivation test. DI and a left visual field defect was suggestive of metastasis to the pituitary region, but no lesion was detected by either CT scan or MRI scan. The patient failed to show a good response to intensive chemotherapy, and died of the tumor five months after commencing chemotherapy. Post-mortem examination revealed metastases to the hypothalamic-neurohypophyseal region, lungs, liver, adrenal glands, bone, bone marrow, and hilar and mediastinal lymph nodes.
 ...
PMID:[A case of small cell lung cancer associated with diabetes insipidus and Cushing's syndrome]. 839 May 89

The case is described of a 40-year-old female with severe hypertension and hypokalaemic metabolic alkalosis, due to prolonged liquorice ingestion. The pseudo-aldosterone-like effects of liquorice have always been attributed to glycyrrhizic acid, but its biochemical substrate has remained elusive. It is now known that glycyrrhetenic acid, the hydrolytic metabolite of glycerrhizic acid, is the active component of liquorice which causes inhibition of the peripheral metabolism of cortisol. Cortisol binds with the same affinity as aldosterone to the mineralocorticoid receptor resulting in a hypermineralocorticoid condition. Ingestion of liquorice may therefore result in retention of sodium and water, hypertension, hypokalaemia, alkalosis and suppression of the renin-aldosterone system. The literature on liquorice-induced hypertension is briefly reviewed with emphasis on the biochemical features of this mineralocorticoid excess syndrome.
 ...
PMID:Liquorice-induced hypertension--a new understanding of an old disease: case report and brief review. 854 95

A Japanese boy with apparent mineralocorticoid excess (AME) is described. He was born with intrauterine growth retardation (IUGR) and elevated serum level of creatine phosphokinase (CPK). He was studied at 2 years of age because of polyurea and polydipsia of one year's duration and was found to have hypokalaemic alkalosis and sustained hypertension. His plasma renin activity and aldosterone levels were always low and his ratio of urinary tetrahydrocortisol plus allo-tetrahydrocortisol to that of tetrahydrocortisone was very high. Therefore, AME due to 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) deficiency was diagnosed. He was successfully treated with a combination of spironolactone and nifedipine for at least 16 months. His blood pressure, plasma pH and serum potassium levels were normalized by this treatment, but serum CPK level remained high. We researched the birth records of previously reported AME cases and found that IUGR is a characteristic feature of AME. The mechanism by which IUGR occurs in AME is discussed and we speculate that 11 beta-HSD might be deficient in the placenta and/or fetal tissues, as well as in the kidney, in AME. An explanation for the elevated CPK could not be found.
 ...
PMID:Apparent mineralocorticoid excess due to 11 beta-hydroxysteroid dehydrogenase deficiency: a possible cause of intrauterine growth retardation. 872 36

In a 38-year-old woman who was hospitalized because of hypertension and hypokalaemic alkalosis, the intake of liquorice (200 g per day) was proven to be the cause. A liquorice provocation test produced all the expected clinical and biochemical abnormalities. Some kinds of liquorice contain glycyrrhetic acid which inhibits the enzyme 11-beta-hydroxysteroid dehydrogenase (e.g. in the kidney) leading to decreased transformation of cortisol into cortisone. The mineralocorticoid action of cortisol causes a drop in serum potassium and an increase in serum sodium concentration, together with a metabolic alkalosis, which in the patient described led to retention of water resulting in weight increase and hypertension.
 ...
PMID:[Hypertension caused by licorice consumption]. 902 43

The basic clinical pathophysiology of primary aldosteronism (PAL) was described by Conn in terms of autonomous production of aldosterone, secondary suppression of renin and development of hypertension with hypokalaemic alkalosis. Conn recognised a normokalaemic form of the syndrome and suggested that it might masquerade as essential hypertension and be not uncommon. This was hotly disputed at the time, and normokalaemic PAL considered rare until recently, and, as a consequence, overlooked. The advent of a simple screening test, the aldosterone-renin ratio, led to recognition that normokalaemic forms are not uncommon. In fact, PAL may be the commonest specifically treatable and potentially curable form of hypertension so far identified. In all patients with PAL confirmed by lack of suppressibility ("autonomy") of aldosterone production, Familial Hyperaldosteronism Type I (FH-I, glucocorticoid-remediable hyperaldosteronism, reviewed elsewhere in this issue) should first be excluded by dexamethasone suppression or genetic testing. Capable of causing fatal stroke in young people affected by this dominantly inherited disorder, it can be reversed by doses of glucocorticoids such as dexamethasone which partially suppress endogenous ACTH without producing "steroid" side-effects. The remaining varieties of PAL may eventually also be shown to have a genetic basis, but are currently treated either by excision of a solitary aldosterone-secreting tumour or by antagonism of aldosterone's action in the renal tubule. It is possible that both adrenal cortices are genetically predisposed to overproduction of aldosterone in all varieties of PAL, whether because of anomalous regulation of aldosterone secretion or because of a tendency towards hyperplasia and neoplasia. Aldosterone-producing adenomas (APA's) can be divided into two main subtypes based on morphology and biochemical behaviour. The first subtype to be morphologically and biochemically characterised is composed predominantly of fasciculata-like cells and is unresponsive to angiotensin II (ALL-U-APA). The more recently characterised subtype is composed predominantly of glomerulosa-like cells, is responsive to angiotensin II (AII-R-APA) and could previously have been misdiagnosed as bilateral hyperplasia. The renin gene is often overexpressed in the second variety of adenoma, and in surrounding non-tumorous cortex, and the two subgroups show different allelic frequencies for RFLP's of the constitutive renin gene and the constitutive ANP gene locus. Unilateral, solitary, benign adrenal cortical adenomas producing aldosterone (APA's) represent a potentially surgically curable form of hypertension. Adrenal venous sampling (AVS) should always be performed because APA's are biochemically recognisable by adrenal venous steroid measurement before they are identifiable by computerised tomography or scintigraphy, and adrenal masses seen on CT may not be responsible for PAL. The secretory activity of adrenal masses must therefore be established by AVS before surgical removal. Discovery of an adrenal mass on CT requires formulation of a plan, whether or not it is found to be secreting hormones in excess. Independently of the treatment of the patient's hypertension, an apparently nonfunctioning adrenal mass ("incidentaloma") should be removed if 2.5 cm or more in diameter, because of the risk of cancer. Smaller masses require long-term follow-up. Primary aldosteronism not lateralising on AVS should be treated with low dose spironolactone, or with amiloride. For any such patients intolerant of medical treatment, laparoscopic removal of the adrenal showing higher production of aldosterone on AVS is an option worthy of consideration.The resultant reduction in mass of tissue autonomously secreting aldosterone should improve hypertension, as aldosterone productions falls below a critical level, and may even be curative in the short, medium or long term, depending on the rate of growth and activity of au
 ...
PMID:Primary aldosteronism. 922 Dec 68

Calcium is necessary for the prevention and treatment of diseases such as osteoporosis, hypertension, and, possibly, colon cancer. Supplementation is useful when dietary calcium intake is low, as is the current situation in North America. There are many factors to consider before recommending any one form of supplement. A consideration for calcium carbonate tablets is whether the tablet disintegrates and whether or not a lack of food or acid in the stomach will hinder utilization. Other forms of calcium, particularly the chelated calcium salts, are better absorbed in fasting achlorhydric subjects but have less calcium per gram of supplement. Interaction of calcium with other mineral nutrients and the presence of contaminating metals has focused attention on safety. Based on present evidence, chelated calcium and refined calcium carbonate tablets (including those labeled as antacids) may be safely and effectively ingested by most people at doses generally recommended for treatment or prevention of osteoporosis. One should not exceed 2,000 mg of calcium, except at the advice of their health care provider, as inadvertent mineral deficiencies may arise. Persons at risk for developing milk-alkali syndrome, such as thiazide users and persons with renal failure, should be identified and monitored for alkalosis and hypercalcemia when using calcium supplements.
 ...
PMID:Calcium supplementation. 927 39

It has been recognised that high haemoglobin oxygen capacity is essential for the development of high blood pressure in spontaneously hypertensive rats. In the present study we have found increased concentration of 2,3 diphosphoglycerate (2,3-DPG) in red blood cells of spontaneously hypertensive rats (SHR) of Okamoto-Aoki strain. As 2,3-DPG is the major factor decreasing haemoglobin affinity to oxygen, our finding suggests that at given value of pO2 oxygen delivery to the tissue of SHR would be increased. Therefore increased concentration of 2,3-DPG in red blood cells of SHR would be of the pathophysiological meaning by promoting autoregulatory increase in total vascular resistance in this strain of rats. The mechanism responsible for enhanced synthesis of 2,3-DPG in SHR remains unclear. Intracellular alkalosis due to either hypocapnia and/or an enhanced activity of Na+/H+ antiporter occurring in SHR are the most plausible explanations for the above finding.
 ...
PMID:The increased concentration of 2,3-diphosphoglycerate in red blood cells of spontaneously hypertensive rats. 944 32


<< Previous 1 2 3 4 5 6 7 8 Next >>