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

The literature concerned with studies of the occurrence and function of the cyclic nucleotides in blood vessels is reviewed. Emphasis is placed on the critical evaluation of the evidence which relates to the hypothesis that cyclic nucleotides meditate the effects of drugs and neurotransmitters on vascular contractility. The hypothesis that cyclic AMP mediates vasodilation, especially that induced by beta-adrenergic relaxation, is supported by many experimental approaches, but it is concluded that the evidence remains unconvincing based on the criteria established for such a mediator role. Possible sites of action of cyclic AMP are discussed. The demonstrated action of cyclic AMP on vascular membrane electrophysiology and calcium ion pumps are reviewed as possible causes of relaxation. The role of both nucleotides in vascular disease, especially hypertension is discussed. Finally the needs for further research in this area are suggested.
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PMID:Occurrence and function of cyclic nucleotides in blood vessels. 17 65

Subcellular fractions were obtained from aortas and ventricles of 6-month-old spontaneously hypertensive and normotensive Wistar rats by the use of differential and sucrose density gradient centrifugation. These preparations were studied to determine what alterations in calcium accumulation and enzymatic activities might be associated with hypertension. The total amount of calcium accumulation (in the presence of ATP and 17 muM free calcium) by the plasma membrane-enriched fraction from hypertensive rat aortas significantly less than that from normotensive rats (11.3 +/- 0.4 vs 16.2 +/- 1.6 mumol of calcium/g of protein, n = 8). In contrast the specific activities of the plasma membrane marker enzymes, 5'-nucleotidase and phosphodiesterase I, were 80% and 40% greater, respectively, in the hypertensive than in the normotensive fractions. On the other hand, various fractions from ventricles of the two types of rats were generally similar in enzyme activities and calcium accumulation. The decreased rate of relaxation of aortas from spontaneously hypertensive rats may be caused by the decreased rate of calcium transport demonstrated in this study.
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PMID:Calcium accumulation and enzymatic activities of subcellular fractions from aortas and ventricles of genetically hypertensive rats. 17 22

A 53-year-old male with Cushing's syndrome due to ectopic ACTH production from medullary carcinoma of the thyroid was reported. The clinical course and results of detailed endocrinological studies and immunohistochemical findings about the cancer tissue were described. An abnormally high concentration of calcitonin, ACTH and beta-MSH in both plasma and cancer tissue (thyroid, lymph nodes and liver) were documented by radioimmunoassay. Urinary 17-OHCS was as high as 38.4 mg/day and showed no supression following dexamethasone 8 mg/day administration. ORAL METYRAPONE (3 G/DAY) CAUSED NO RESPONSE IN URINARY 17-OHCS. Parallel increments in plasma calcitonin, ACTH and beta-MSH were observed following calcium and gastrin loading. Total thyroidectomy with modified radical neck dissection caused minimal changes of plasma levels of calcitonin, ACTH and beta-MSH and no improvement in the clinical manifestations of Cushing's syndrome. An aortogram revealed metastatic tumors in the liver. A second operation, total adrenalectomy, resulted in an improvement of the clinical and laboratory findings such as hypokalemia, high blood pressure, muscle atrophy and moon face. Immunofluorescent study showed different distribution patterns in calcitonin- and ACTH-positive cells in the primary focus but similar patterns in the liver metastasis.
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PMID:[A case of medullary thyroid carcinoma with ectopic ACTH syndrome (author's transl)]. 20 14

As compared to fatty tissue cells of animals with normal pressure, those of SHR rats were found to be characterized by a higher lipolytic response and a larger increase in the cAMP content on exposure to the effect of ACTH. As compared to the controls, adrenalectomized SHR rats had an increased basal cAMP content and an increased lipolytic response of the adipocytes following adrenaline administration. In inhibition of phosphodiesterase in the fatty cells of adrenalectomized rats with normal pressure, the cAMP content grew by 20% as compared to that in SHR rats subjected to the operation. It is suggested that the changes in intracellular distribution of calcium, shown in this model of hypertension, may be the direct cause of the altered sensitivity of the "target" cells to the effect of hormones.
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PMID:[Mechanism of the change in adipocyte sensitivity to ACTH and adrenaline in spontaneous genetic hypertesion in rats]. 21 34

High calcium diet induces an hypertension lasting one week in normal rats. In mineralocorticoid treated rats (DOCA + NaCl), the same diet prevents for 10 weeks the increase of arterial blood pressure. Parathyroid activity (estimated by urinary cAMP) is decreased after the high calcium diet. These results confirm the role of the parathyroid glands in mineralocorticoid hypertension in the rat.
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PMID:[Arterial blood pressure and high calcium diet in normal and mineralcorticoid (DOCA and sodium chloride hypertensive rats]. 22 48

A retrospective review of 500 patients with primary hyperparathyroidism seen from 1951 to 1975 was conducted; the effect of routine screening of calcium and phosphate levels (initiated in 1968) on the incidence and spectrum of the disease was analyzed. The majority of the patients (77%) were diagnosed in the eight-year period after routine biochemical screening was instituted. Comparing the group of patients diagnosed before the advent of biochemical screening and those diagnosed since screening was instituted, we found: (1) a small but significant increase in the number of asymptomatic patients diagnosed (from 2% to 12%); (2) no change in the incidence of related medical disorders, i.e., nephrocalcinosis and hypertension; (3) no change in the incidence of primary hyperplasia and adenoma; and (4) no change in the mean serum calcium level, the mean age at diagnosis, or the number or location of the involved parathyroid glands. Although routine calcium screening has identified significantly more cases of primary hyperparathyroidism, screening apparently does not enable diagnosis at an earlier stage.
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PMID:Twenty-five year experience with primary hyperparathyroidism at Columbia Presbyterian Medical Center. 26 10

An attempt is made to elucidate the cellular mechanisms which may account for the well-documented correlation between sodium metabolism and peripheral vascular resistance. As a starting point, the evidence that the Na electrochemical gradient across the vascular smooth muscle cell plasma membrane (sarcolemma) plays an important role in cell calcium regulation is reviewed. Because there is significant resting tension ("tone") in most resistance vessels, the ionized Ca2+ level ([Ca2+]1) in the smooth muscle fibers in these vessels must be maintained above the contraction threshold. Consequently, the Ca transport system in the sarcolemma, presumably an Na-Ca exchange mechanism, must be set so as to hold [Ca2+]1 at this suprathreshold level. Any change in the Na gradient will then be reflected as a change in [Ca2+]1 and, therefore, in steady vessel wall tension and peripheral resistance. The correlation between Na metabolism and hypertension could then be accounted for if a circulating agent, perhaps the "natriuretic hormone," affects the Na gradient (across the sarcolemma) and, therefore, [Ca2+]1 and tension.
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PMID:Sodium ions, calcium ions, blood pressure regulation, and hypertension: a reassessment and a hypothesis. 32 93

The prevalence of clinical and sub-clinical occlusive arterial disease and of risk factors implicated in the pathogenesis of arteriosclerosis was assessed in 21 patients with chronic renal failure, 27 on maintenance haemodialysis and 51 renal allograft recipients. Clinical occlusive arterial disease was present in 27 patients, and sub-clinical arterial disease in 34. Myocardial infarction, cerebral thrombosis and lower limb arterial thrombosis had occurred only in the transplant recipients; these patients had, however, been followed for a longer period of time than the other two groups. In the allograft recipients, the cumulative incidence of any occlusive arterial disease was 416 per 1000, and that of coronary heart disease was 267 per 1000 at six years. Hypertension was present in 76 per cent of patients prior to renal replacement therapy. Following institution of definitive therapy, hypertension was of shorter duration and less common in haemodialysis patients than in renal transplant recipients. Uraemic and haemodialysis patients with occlusive arterial disease had required antihypertensive medication for significantly longer than those free of arterial disease. Transplant recipients with hypertension had a greater mean serum creatinine, were receiving a larger maintenance dosage of corticosteroids and less frequently had undergone prior bilateral nephrectomy than those transplant patients without hypertension. Serum lipid levels were elevated in 62 per cent of patients. In the uraemic and haemodialysis patients hypertriglyceridaemia was the predominant abnormality while in the transplant recipients combined hypertriglyceridaemia/hypercholesterolaemia was more frequent. Despite regular aluminium hydroxide therapy 81 per cent of uraemic and haemodialysis patients had a calcium X phosphate product higher than normal. Arterial and/or soft tissue calcification as demonstrable in 20-38 per cent of patients within each group, but could not be related to the calcium X phosphate product of radiographic evidence of hyperparathyroidism. Glucose intolerance was present in 71 per cent of the uraemic and haemodialysis patients and 33 per cent of the transplant recipients. Hyperuricaemia, cigarette smoking, obesity and a sedentary existence were also prevalent. The majority of patients had several risk factors implicated in the pathogenesis of arteriosclerosis. Occlusive arterial disease is a major problem in patients with end stage renal disease, being no less common after transplantation than with long-term maintenance dialysis. The aetiology is multifactorial.
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PMID:Occlusive arterial disease in uraemic and haemodialysis patients and renal transplant recipients. A study of the incidence of arterial disease and of the prevalence of risk factors implicated in the pathogenesis of arteriosclerosis. 32 93

Verapamil is a novel antiarrhythmic and antianginal agent which, although introduced in 1962, has only recently gained prominence not only as a significant agent in cardiovascular therapeutics but also as a powerful tool to examine the nature of some of the biophysical phenomena at the membrane of cardiac and other excitable tissues. Verapamil is the prototype of those agents which selectively inhibit membrane transport of calcium, an action which accounts for the drug's peripheral and coronary vasodilator properties, its effect on excitation-contraction coupling and hence its negative inotropic propensity, as well as its depressant effects on the sinus node and atrioventricular conduction. Its pharmacological effects are largely independent of the autonomic nervous system. The main therapeutic uses of the drug are in the management of atrial tachyarrhythmias, angina, and possibly hypertension. The overall exp:rimental and clinical data suggest that verapamil will become an important and safe addition to existing drug regimens, especially as an agent of choice for the short-term treatment of most cases of paroxysmal supraventricular tachycardias. The initial experience in other arrhythmias, angina and hypertension, is also sufficiently encouraging to justify further detailed clinical trials to define its potential role in cardiovascular therapeutics.
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PMID:Verapamil: a review of its pharmacological properties and therapeutic use. 34 45

End-stage kidneys in patients who are receiving long-term intermittent treatment with hemodialysis are metabolic structures that participate in many body processes and that themselves develop and change despite severe excretory deficiencies. Nephron loss is severe. Other lesions in such kidneys include the following: smooth muscle nodules that arise in necrotic arteries and arterioles; embryonal hyperplasia of Bowman's capsular epithelium; remodeling of the arteries and veins; tubular atrophy; dilation and cyst formation (acquired cystic disease); arteriolar granular cell hyperplasia and hypertension; deposits of oxalate, calcium, and immune complexes; interstitial fibrosis with collagen and smooth muscle; mucoid change; and cellular infiltration. This list does not include all pathologic conditions found in the end-stage--dialysis kidney. The necessity of and the criteria for an experimental model of human long-term intermittent hemodialysis for end-stage renal disease, presently lacking, are indicated.
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PMID:New therapies and new pathologies: end-stage--dialysis kidneys. 36 73


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