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

Selenium is a vestigial element indispensable for man and animal, having adverse effects when in bigger quantities. Among the diseases resulting from selenium deficiency in animals the most important are nutritional muscular dystrophy, exudative disthesis (most common in poultry), and nutritional hepatic dystrophy. In the man chronic intoxication occurs most of all, which is observed in selenium bearing regions. Taking into consideration geographic distribution on some of the diseases beneficial influence of selenium is observed in cardiac and vascular diseases, and hypertension. The correlation between selenium deficiency and mortality caused by neoplasm is also notable. It is unquestionable that selenium inhibits the activity of enzymes, especially those containing sulfohydryl groups. The stabilization of lysosomal membranes leads to the presumption that selenium prevents peroxidation processes in tissues and cell membranes. The influence of selenium on reproduction is also worth noticing. Its supply turns out to be effective in cases of infertility of sheep, and partly in rats, pigs, and poultry. The embryo dies in pigs fed on fodder poor in selenium and vitamin E. The degeneration of the ovaries and placenta accretion occur in cows in cases of selenium deficiency. The excess of selenium can affect negatively the reproductive system. The element is thought to be a teratogenic agent. Since it permeates through the placenta and lactic gland easily, the symptoms of selenosis appear in new-born animals; many of them have developmental anomalies occurring at the same time. In birds the decrease in laying eggs and their incubation occur in case of selenium deficiency.
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PMID:The influence of selenium on the reproduction of rats. 136 82

1. Calpains (calcium-activated cysteine proteinases) have evolved by gene fusion events involving calmodulin-like genes, cysteine proteinase genes and other sequences of unknown origin. 2. The enzymes are composed of two non-identical subunits, each of which contains functional calcium-binding sequences. 3. Calpains are inhibited by the endogenous protein inhibitor, calpastatin and some calmodulin antagonists are also inhibitors of calpain. A number of synthetic proteinase inhibitors also inhibit calpains. 4. Calpains can be activated by phospholipids, an endogenous protein activator and some amino acid derivatives. 5. Various protein substrates for calpains have been recognized in vitro, but the identity of in situ substrates remains unclear. 6. Proposals have been made for calpain function, including involvement in signal transduction, platelet activation, cell fusion, mitosis and cytoskeleton and contractile protein turnover. 7. Calpain and calpastatin expression is altered in a number of abnormal states including muscular dystrophy, muscle denervation and tenotomy, hypertension and platelet abnormalities.
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PMID:Calpains (intracellular calcium-activated cysteine proteinases): structure-activity relationships and involvement in normal and abnormal cellular metabolism. 227 16

Clinical uses of calcium channel blockers are expanding. In addition to the established uses in patients with arrhythmias, angina pectoris or hypertension, newer and to some extent investigational uses indicate widespread application. For instance, their use has been reported in hypertrophic cardiomyopathy and cold cardioplegia, as well as in pulmonary hypertension, antiplatelet therapy, asthma, achalasia and oesophageal spasm, increased intraocular pressure and in cerebral vasospasm. Their use in obstetrical practice has been proposed. Thus, the presentation of a patient who is treated with calcium channel blockers and who requires anaesthesia will become more common. Calcium channel blockers may, under certain circumstances, potentiate haemodynamic and MAC depressive effects of inhalation agents. There is also evidence that the effects of neuromuscular blocking agents may be potentiated. The anaesthetist should be aware that the potential for interactions exists with digoxin, propranolol, quinidine, theophylline or dantrolene. Of interest and some significance are the anaesthetic implications of pathophysiological alterations that can be induced by calcium channel blockers, by affecting lower oesophageal tone, intracranial hypertension, bronchomotor tone (asthma), muscular dystrophy, neuromuscular function, hypoxic pulmonary vasoconstriction, malignant hyperthermia, inhibition of platelet aggregation and hyperkalemia. Despite these significant potential anaesthetic implications and because, at this time, in some instances withdrawal has clearly demonstrated increase in the signs of myocardial ischaemia, it would not seem necessary to recommend preoperative discontinuation of calcium channel blocker medication in patients presenting for anaesthesia. It is, however, appropriate that there is a high index of awareness of potential problems, unless there is some modification in inhalation anaesthetic concentrations and neuromuscular blocker dosage. Monitoring of cardiovascular and neuromuscular functions is essential. Calcium channel blockers would appear to be currently the drugs of choice for angina pectoris, arrhythmias or hypertension in patients with associated chronic obstructive pulmonary disease.
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PMID:Anaesthetic implications of calcium channel blockers. 286 80

Although Ca in small quantities plays a fundamental role in cell activation, excessive intracellular Ca accumulation results in severe cellular damage and is a major factor in the pathophysiology of multiple diseases. Paradoxically, high Ca intake may be beneficial in unrelated disorders such as arterial hypertension, nephrolithiasis and in the prevention of colon cancer. Parathyroid hormone (PTH) could be the link capable to explain this paradox. PTH stimulates cellular calcium influx. Under normal conditions, this effect takes place only in target tissues for the hormone, but in the presence of altered cell-membrane permeability for calcium, normal plasma PTH may be detrimental, enhancing cellular calcium influx. Thus, the suppression of PTH secretion by a high Ca intake would result in a reduced PTH-induced cellular Ca accumulation in genetically predisposed tissues with a loose cellular Ca control. Thus, parathyroid ablation in dystrophic hamster reduces the elevated muscle Ca observed in muscular dystrophy and causes histological improvement without altering the serum Ca concentration. The amount of dietary Ca required is not firmly established, but anthropological observations suggest a daily intake of approximately 1600 mg, much higher than the present average Ca intake in Western societies. Thus, a higher Ca intake would be beneficial in the treatment, and more importantly, in the prevention of multiple diseases.
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PMID:[New perspectives in calcium metabolism]. 820 35

WW domains are recently described protein-protein interaction modules; they bind to proline-rich sequences that usually also contain a tyrosine. These domains have been detected in several unrelated proteins, often alongside other domains. Recent studies suggest that WW domains in specific proteins may play a role in diseases such as hypertension or muscular dystrophy.
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PMID:WW domains. 873 47

Patients with neuromuscular disease may suffer from nocturnal respiratory failure despite normal daytime respiratory function. The physiological reduction in muscle tone during sleep may be life-threatening in a patient with impaired muscle strength. Nocturnal respiratory failure may occur in patients with the postpolio syndrome, amyotrophic lateral sclerosis, myasthenia gravis, myotonic dystrophy, and muscular dystrophy. Diagnosis of obstructive, central and mixed apneas, hypopneas, and hypoventilation is best made using polysomnography. Therapeutic options include noninvasive ventilation such as continuous positive airway pressure, bilevel positive airway pressure, intermittent positive pressure ventilation and, rarely, tracheostomy, oxygen, or protriptyline. Evaluation by a sleep specialist should be initiated in any neuromuscular patient with nocturnal symptoms such as air hunger, intermittent snoring or breathing, orthopnea, cyanosis, restlessness, and insomnia. Daytime symptoms may include morning drowsiness, headaches and excessive daytime sleepiness. Polycythemia, hypertension, and signs of heart failure may also be seen. Effective treatment is available, and may improve the quality of life, and possibly increase survival.
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PMID:Nocturnal respiratory failure as an indication of noninvasive ventilation in the patient with neuromuscular disease. 967 Mar 10

WW domains are protein modules that bind proline-rich ligands. WW domain-ligand complexes are of importance as they have been implicated in several human diseases such as muscular dystrophy, cancer, hypertension, Alzheimer's, and Huntington's diseases. We report the results of a protein array aimed at mapping all the human WW domain protein-protein interactions. Our biochemical approach integrates parallel synthesis of peptides, protein expression, and high-throughput screening methodology combined with tools of bioinformatics. The results suggest that the majority of the bioinformatically predicted WW peptide ligands and most WW domains are functional, and that only about 10% of the measured domain-ligand interactions are positive. The analysis of the WW domain protein arrays also underscores the importance of the amino acid residues surrounding the WW ligand core motifs for specific binding to WW domains. In addition, the methodology presented here allows for the rapid elucidation of WW domain-ligand interactions with multiple applications including prediction of exact WW ligand binding sites, which can be applied to the mapping of other protein signaling domain families. Such information can be applied to the generation of protein interaction networks and identification of potential drug targets. To our knowledge, this report describes the first protein-protein interaction map of a domain in the human proteome.
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PMID:A map of WW domain family interactions. 1499 88

Autosomal dominant polycystic kidney disease (ADPKD) is the most frequent life- threatening, hereditary disease. ADPKD is more common than sickle cell anemia, cystic fibrosis, muscular dystrophy, hemophilia, Down's syndrome, and Huntington's disease combined. ADPKD is a multisystemic disorder characterized by the progressive development of renal cysts and marked renal enlargement. Structural and functional renal deterioration occurs in ADPKD patients and is the fourth leading cause of end-stage renal disease (ESRD) in adults. Aside from the renal manifestations, extrarenal structural abnormalities, such as liver cysts, cardiovascular abnormalities, and intracranial aneurysms may lead to morbidity and mortality. Recent studies have identified prognostic factors for progressive renal impairment including gender, race, age, proteinuria, hematuria, hypertension and increased left ventricular mass index (LVMI). Early diagnosis and better understanding of the pathophysiology of the disease provides the opportunity to aggressivly treat hypertension with renin-angiotensin-aldosterone system inhibitors and thereby potentially reduce LVMI, prevent cardiovascular morbidity and mortality and slow progression of the renal disease.
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PMID:Developments in the management of autosomal dominant polycystic kidney disease. 1872 45

The calcium ion (Ca(2+)) is the simplest and most versatile intracellular messenger known. The discovery of Ca(2+) sparks and a related family of elementary Ca(2+) signaling events has revealed fundamental principles of the Ca(2+) signaling system. A newly appreciated "digital" subsystem consisting of brief, high Ca(2+) concentration over short distances (nanometers to microns) comingles with an "analog" global Ca(2+) signaling subsystem. Over the past 15 years, much has been learned about the theoretical and practical aspects of spark formation and detection. The quest for the spark mechanisms [the activation, coordination, and termination of Ca(2+) release units (CRUs)] has met unexpected challenges, however, and raised vexing questions about CRU operation in situ. Ample evidence shows that Ca(2+) sparks catalyze many high-threshold Ca(2+) processes involved in cardiac and skeletal muscle excitation-contraction coupling, vascular tone regulation, membrane excitability, and neuronal secretion. Investigation of Ca(2+) sparks in diseases has also begun to provide novel insights into hypertension, cardiac arrhythmias, heart failure, and muscular dystrophy. An emerging view is that spatially and temporally patterned activation of the digital subsystem confers on intracellular Ca(2+) signaling an exquisite architecture in space, time, and intensity, which underpins signaling efficiency, stability, specificity, and diversity. These recent advances in "sparkology" thus promise to unify the simplicity and complexity of Ca(2+) signaling in biology.
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PMID:Calcium sparks. 1892 88

Cellular responses to mechanical forces are crucial in embryonic development and adult physiology, and are involved in numerous diseases, including atherosclerosis, hypertension, osteoporosis, muscular dystrophy, myopathies and cancer. These responses are mediated by load-bearing subcellular structures, such as the plasma membrane, cell-adhesion complexes and the cytoskeleton. Recent work has demonstrated that these structures are dynamic, undergoing assembly, disassembly and movement, even when ostensibly stable. An emerging insight is that transduction of forces into biochemical signals occurs within the context of these processes. This framework helps to explain how forces of varying strengths or dynamic characteristics regulate distinct signalling pathways.
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PMID:Dynamic molecular processes mediate cellular mechanotransduction. 2177 77


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