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

One female patient--with slight pure mitral stenosis, mild hypertension and ischemic cardiomyopathy and disabling pulmonary emphysema--developed at 54 years of age permanent atrial fibrillation, had a gratuitous mitral commissurotomy four months later, sustained chronic fibrillation for 13 years, then spontaneously resumed sinus node command at age 67 without any discernible reason. Sinus rhythm was being maintained at follow-up nine months later. Her cardiac status of fair compensation under modest digitoxin and diuretic therapy has neither improved nor worsened with the return of atrial systole. The duration, in this observation, of permanent auricular fibrillation before spontaneous return of sinus rhythm, is one of the longest ever published, exceeded, to the best of my knowledge, only by one case of Lewis and by another one of Reeve and associates. Such an exceptional event points out a fascinating enigma: how can major longstanding atrial dysrhythmias (fibrillation, flutter), whose causes and pathogenesis seem at least partly elucidated, spontaneously disappeer in atria so badly diseased? I think we must humbly confess that no satisfactory explanation is at present available for this disconcerting phenomenon.
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PMID:Spontaneous resumption of sinus rhythm in an elderly patient after 13 years of permanent atrial fibrillation. 47 82

Coronary heart disease (CHD) remains an uncommon disorder in the South African Black population. It has been suggested that herein lies an enigma, since it is believed that these people are considerably exposed to the conventional risk factors for CHD. To test this belief I have assessed the exposure of Black people, in time and degree, to the following CHD risk factors: affluence, age, hypertension, hyperlipidaemia, dietary excess, smoking, physical inactivity, diabetes, obesity, hyperuricaemia and hyperinsulinism. Among males only hypertension, and among females only hypertension and obesity, emerged as prominent factors. However, neither of these is significantly atherogenic in the social, nutritional and metabolic milieu in which Blacks generally live, and obesity is a doubtful atherogenic factor, even in westernized populations. It is therefore concluded that the rarity of CHD in Blacks is not enigmatic, but is appropriate to their environmental circumstances.
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PMID:The rarity of coronary heart disease in South African blacks. 69 6

A young woman presented with a novel multisystem disease: painful periostitis, osteosclerosis, hypertension, and renal dysfunction. The similarity of some of this clinical picture to fluoride intoxication led to the discovery of massively elevated fluoride levels in serum, urine, and bone. Although initially an enigma, the source of fluoride was later found to be the illicit use of an anesthetic agent, methoxyflurane. This agents is one of a class of organofluorides that, by virtue of biotransformation, is a known cause of inorganic fluoride exposure. Though the drug is potentially nephrotoxic as generally used, exposure to it is transient and has not previously led to discernible bone disease.
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PMID:Subacute fluorosis: a consequence of abuse of an organofluoride anesthetic. 71 28

The hemodynamic hallmark of hypertension complicating the treatment of renal anemia with recombinant human erythropoietin (rHu-EPO) is increased total peripheral vascular resistance, but the mechanisms underlying the arteriolar vasoconstriction are still an enigma. We studied body fluid volumes, plasma renin activity, plasma norepinephrine, and calcium metabolism in platelets in 40 previously normotensive hemodialysis patients before and after 12 weeks of rHu-EPO treatment. Partial correction of anemia caused a rise in arterial pressure (94 +/- 6 mmHg vs 124 +/- 7 mmHg, p less than 0.05) and in platelet cytosolic calcium concentration (113 +/- 5 nM vs 171 +/- 18 nM, p less than 0.05) in eight patients. Hypertensive patients had significantly higher plasma noradrenaline concentrations, but they did not differ significantly in body fluid volumes and plasma renin activities. There was a close correlation between free calcium concentration in platelets and mean arterial pressure in patients developing rHu-EPO-induced-hypertension (r = 0.95). Short-term antihypertensive treatment resulted in a reduction of free calcium concentrations in platelets and a concomitant fall in blood pressure. The main results of the present studies suggest that rHu-EPO-induced hypertension might be associated with altered cellular calcium homeostasis and hyperactivity of the sympathetic nervous system. If rHu-EPO therapy induces alterations of pressor factors or the hormone itself raises the cytosolic calcium not only in platelets but also in vascular smooth muscle cells, altered cellular calcium influx may contribute to the arteriolar vasoconstriction.
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PMID:Correlation of blood pressure in end-stage renal disease with platelet cytosolic free calcium concentration during treatment of renal anemia with recombinant human erythropoietin. 163 25

The pathogenesis of primary Raynaud's phenomenon remains an enigma. Most evidence favors a local abnormality in the digital arteries as opposed to an increased activity of the sympathetic nervous system. The local fault may involve the alpha 2-adrenergic receptors, which are most important in reflex sympathetic vasoconstriction. Cooling blood vessels increase the sensitivity of alpha 2-adrenergic receptors, increased levels of alpha 2-adrenergic receptors are present in primary Raynaud's disease, and patients show an increased sensitivity to alpha 2-adrenergic receptor agonists on finger blood flow. Serotonin has also been implicated, but the evidence is not compelling. In secondary Raynaud's phenomenon, vasospastic attacks can often be explained by a low arterial distending pressure, a thickened vessel wall, or absence of beta-adrenergic receptor activity. Diagnosis of primary Raynaud's disease relies on a typical history and normal physical examination, laboratory studies, and nailfold capillaroscopy. Finger systolic blood pressures during local cooling with ischemia may be helpful to document vasospastic attacks but does not distinguish primary from secondary Raynaud's phenomenon. The treatment of Raynaud's phenomenon is usually conservative. Pavlovian conditioning or biofeedback may be beneficial. When drug therapy is necessary, the calcium channel entry blocker nifedipine or sympatholytic agents have been shown to decrease the frequency and duration of vasospastic attacks in about two thirds of patients, although subjective improvement does not usually correlate with objective testing. Direct-acting vasodilators have not been shown to be of definite benefit. New therapies include prostaglandins, captopril, and the serotonergic antagonist ketanserin. Surgical sympathectomy has not been beneficial.
Hypertension 1991 May
PMID:Raynaud's phenomenon. An update. 202 4

A study was carried out to evaluate the relationship between blood pressure, plasma renin activity, serum aldosterone and patterns of urinary sodium and potassium excretion rates in urban Zulus, rural Zulus and Indians in order to explain the high prevalence of hypertension in the urban adult Zulu (25%) compared to the rural adult Zulu (10%). Urinary sodium and potassium were not significantly different between urban and rural Zulus. There was no association between sodium excretion and blood pressure. Urinary potassium correlated negatively with blood pressure in rural Zulus and Indians but not in urban Zulus. The urinary sodium:potassium ratio was significantly lower in rural Zulus than in urban Zulus. The sodium:potassium ratio of Indians was not significantly different from that of Zulus. Plasma renin activity levels were significantly lower in urban than in rural Zulus. This difference is an enigma but may be due to an environmental factor. Serum aldosterone correlated positively with plasma renin activity and negatively with the urinary sodium:potassium ratio.
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PMID:A study of urinary sodium and potassium excretion rates among urban and rural Zulus and Indians. 390 Jan 99

Occlusion of the internal carotid or middle cerebral artery was seen in 44 young adults of both sexes from a rural population in Ceylon over a period of four years. None had hypertension, diabetes, prediabetes, or hypercholesterolaemia. There were 19 men with internal carotid occlusions, most being due to atherosclerotic thrombosis. The high incidence of atherosclerosis in these patients on a marginal diet remains an enigma, and we suggest that carbohydrate-induced hyperlipidaemia might be an important aetiological factor. There were 13 men with middle cerebral occlusions, the aetiology of which remains obscure. Occult embolism or atherothrombosis are suggested as possible causative factors. Of the 12 women five had middle cerebral artery occlusions in the last trimester of pregnancy and two had internal carotid artery occlusions in the puerperium. The pattern of ischaemic strokes in women aged 15-45 was similar to that observed in Western countries, though our patients differed ethnologically and in dietary habits.
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PMID:Strokes in young adults. 507 49

Despite decades of intense research, the etiology of essential hypertension remains one of the major enigmas of clinical medicine. On the basis of recent advances in the vascular biology of hypertension two important paradigms have emerged that offer promise in solving this enigma: 1) the concept of vascular remodeling, and 2) the concept of vascular autocrine-paracrine factors as determinants of vascular resistance. These concepts are interrelated because vascular autocrine-paracrine factors appear to mediate the process of vascular remodeling. This review focuses on these two emerging paradigms and their potential importance in elucidating the pathogenic mechanisms of hypertension.
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PMID:Autocrine-paracrine factors and vascular remodeling in hypertension. 792 89

This article reviews literature on the highly differentiated nature of the luteal cell types and their regulation in the mid-cycle corpus luteum of ruminants. The blood vessels of the corpus luteum are composed primarily of endothelial cells with few intraluteal arterioles or arteries. Blood flow to the corpus luteum does not seem to be regulated by tropic hormones, metabolic activity, or autonomic nerves, but it is dependent on maintenance of high blood pressure. The density of luteal capillaries and lack of luteal arterioles allows an elevated, relatively unregulated luteal blood flow. Steroidogenesis in the ruminant corpus luteum manifests both dependence on and independence from the actions of LH. Initial luteinization, growth, and development of the corpus luteum is dependent on LH action, but progesterone production by the mid-cycle corpus luteum of ruminants is relatively independent of acute LH stimulation. This apparent enigma may be due to distinct functional properties of the steroidogenic cell types in the corpus luteum. Progesterone production by the large luteal cells is relatively independent of LH action, but the small luteal cells respond to LH stimulation. Much of the progesterone produced by the mid-cycle corpus luteum is produced by the large luteal cells and may not be acutely dependent on LH stimulation. Progesterone production by both cell types is dependent on lipoproteins delivered by the abundant luteal blood supply. Thus, distinct cellular features of the mid-cycle corpus luteum produce considerable steroidogenic capacity.
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PMID:Cell types and hormonal mechanisms associated with mid-cycle corpus luteum function. 792 67

Although the pathogenesis of the diabetes mellitus syndrome remains poorly understood, both insulin-dependent diabetes mellitus and non-insulin-dependent diabetes mellitus predispose the individual to a similar spectrum of complications, including hypertension, macrovascular and microvascular disease, cataracts cardiomyopathy, neuropathy, and premature aging, suggesting that these complications develop along a pathway common to both diabetic conditions. Yet not all diabetic persons are affected by all of these complications or to the same degree. What causes this marked variability in the clinical manifestations of the diabetes syndrome remains an enigma. Accumulating data from animal models of diabetes and from studying patients with diabetes reveal that intracellular calcium levels are increased in most tissues. The activities of the membrane, adenosine triphosphatase (ATPase) associated cation pumps, which determine intracellular calcium level (i.e., calcium-ATPase and [sodium + potassium]-ATPase), are also altered. The nature of the alteration is often tissue specific and may depend on the level of blood glucose or insulin, or both. In this review we discuss the potential contribution of these changes in intracellular calcium regulation, whether acquired or genetically determined, to the pathogenesis of the diabetes syndrome, to the abnormalities in insulin secretion and action (mainly in non-insulin-dependent diabetes), and to the complications of both diabetes syndromes. Altered intracellular calcium metabolism may represent a common, underlying abnormality linking the metabolic, cardiovascular, ocular, and neural manifestations of the diabetic disease process.
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PMID:Diabetes mellitus: a disease of abnormal cellular calcium metabolism? 762 30


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