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

Over 10,000 male civil servants and municipal employees in Israel, aged 40 years and above, underwent an extensive clinical, biochemical, anthropometric, sociodemographic and psychosocial evaluation in 1963, 1965 and 1968. Follow-up for mortality was continued through 1986. Over 23 years, a number of previously established risk factors for coronary heart disease (CHD) incidence were found to predict mortality. The long-term follow-up assisted in illustrating temporal patterns. A single causal assessment of blood pressure retained high prediction for long-term mortality. Blood lipids, while significantly associated with both coronary and all-cause mortality, exhibited a small contribution to the latter, when compared to hypertension, cigarette smoking habits and diabetes. Weak associations of long-term coronary mortality with the dietary intake patterns of fatty acids, as reported at baseline, were probably fully mediated by the effect of the diet on serum cholesterol. Religious orthodoxy appeared to provide a degree of immunity, part of which was independent of life-style correlates. A number of now well-established associations in cardiovascular epidemiology were first demonstrated, or amplified, in the study. Patterns of ethnic diversity in the risk factor and prevalence rates of CHD persisted, as viewed from the angle of mortality rates, over nearly a quarter of a decade, highlighting the enigma of a migrant country as a cardiovascular melting pot.
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PMID:Factors predictive of long-term coronary heart disease mortality among 10,059 male Israeli civil servants and municipal employees. A 23-year mortality follow-up in the Israeli Ischemic Heart Disease Study. 832 74

The recent literature concerning Raynaud's syndrome is reviewed. Raynaud's syndrome is as common as hypertension and diabetes. In spite of its generally benign character, it causes a lot of discomfort to individuals and sickness absenteeism to society, especially in the colder regions of the world. The etiology remains an enigma 130 years after its first description, perhaps even more so than ever before, the many new theories proposed in the literature. Clearly, in a condition where seventy different etiologic theories are advocated, the culprit lesion is obviously missing, or there is not a culprit lesion but an accumulation of conditions having nothing in common but a few symptoms. Moreover a Raynaud attack may result, not from a single event, but from a cascade of events, just as, for example, hemostasis does. Controversy about diagnosis exists all over. For example, how does one make a diagnosis? Patient history has been considered unreliable. A standardized cold test, though highly reproducible in the authors' hands, is far from common property. Raynaud's syndrome is a condition for which thirty-eight therapies have been advocated in the last three years, but the curative answer is still to come.
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PMID:Raynaud's syndrome, an enigma after 130 years. 844 29

We have recently characterized a novel angiotensin II/vasopressin (Ang II/AVP) dual receptor coupled to adenylate cyclase and responding with equal sensitivity to Ang II and AVP. To gain insight into putative renal physiological roles of the dual Ang II/AVP receptor, we determined its pharmacological binding properties and renal immunocytochemical distribution. The effective displacement of [3H]AVP by [1-deamino-Val14,D-Arg8]-vasopressin (DVDAVP), a specific antidiuretic AVP analogue, supports a V2-type AVP receptor characteristic of the Ang II/AVP receptor. Displacement of 125I-Ang II by losartan but not by PD 123319 defines the Ang II/AVP receptor as a novel AT1 receptor isoform coupled to adenylate cyclase, in contrast to prototype Ca(2+)-mobilizing AT1 receptors. Neither Ang II nor AVP displace each other, corroborating the predicted discrete binding domains for Ang II and AVP but presenting an enigma for the dissection of putative Ang II- and AVP-specific hierarchical roles of the dual Ang II/AVP receptor. The renal cytolocalization of the Ang II/AVP receptor to the outer medullary thick ascending limb tubules and inner medullary collecting ducts is consistent with the well-established AVP stimulation of sodium and water reabsorption in these tubules. These data suggest that the Ang II/AVP receptor might provide the molecular basis for the observed similar stimulatory effects of Ang II and AVP on renal tubular sodium and fluid reabsorption at physiological hormone concentrations.
Hypertension 1997 Apr
PMID:Renal immunocytochemical distribution and pharmacological properties of the dual angiotensin II/AVP receptor. 909 83

Angiotensin II (Ang II) plays an important role in regulating cardiovascular hemodynamics and structure. Multiple lines of evidence have suggested the existence of Ang II receptor subtypes, and at least 2 distinct receptor subtypes have been defined on the basis of their differential pharmacological and biochemical properties and designated as type 1 (AT1) and type 2 (AT2) receptors. To date, most of the known effects of Ang II in adult tissues are attributable to the AT1 receptor. Recent cloning of the AT2 receptor contributes to reveal its physiological functions, but many functions of the AT2 receptor are still an enigma. AT1 and AT2 receptors belong to the 7-transmembrane, G protein-coupled receptor family. However, accumulating evidence demonstrates that the function and signaling mechanisms of these receptor subtypes are quite different, and these receptors may exert opposite effects in terms of cell growth and blood pressure regulation. We will review the role of the AT2 receptor in the cardiovascular system and the molecular and cellular mechanisms of AT2 receptor action.
Hypertension 1999 Feb
PMID:Recent progress in angiotensin II type 2 receptor research in the cardiovascular system. 1002 16

The southeastern region of the United States has been recognized for 6 decades as an area of excess cerebrovascular mortality rates. While the reasons for the disease variation remain an enigma, South Carolina has consistently been the forerunner of the "Stroke Belt." To determine the effects of nativity (birthplace) on stroke mortality rates in South Carolina, proportional mortality ratios (PMRs) were calculated for stroke deaths in South Carolina during 1980-1996 according to birthplace and stratified by gender, race, age, and educational status. The analyses revealed a graded risk of stroke by birthplace, with the highest PMRs (95% CI) among individuals born in South Carolina (104.8 [103.4 to 106.3]), intermediate PMRs in those born in the Southeast other than South Carolina (92.5 [90.2 to 94.9]), and lowest PMRs for those born outside the Southeast (77.4 [74.9 to 80.1]). The lower stroke PMRs for individuals born outside the Southeast were more striking in blacks (51.8 [45.2 to 59.3]) than in whites (84.9 [82.0 to 88.0]) and for men (73.3 [69.5 to 77.3]) than women (83.5 [79.9 to 87.3]). The findings, particularly in blacks, were not explainable by gender, differences in age, and/or markers of educational and socioeconomic status. These findings suggest that nativity is a significant risk marker for the geographic variation in stroke mortality. Moreover, the regional disparities for nativity and subsequent stroke mortality appear to be greater in blacks than in whites and for men than for women. An understanding of factors linking birthplace to risk for cerebrovascular mortality could facilitate efforts directed at stroke prevention.
Hypertension 1999 Jul
PMID:Impact of nativity and race on "Stroke Belt" mortality. 1040 24

There is a wealth of experimental and clinical information showing that hypertension, hyperglycaemia, hyperthermia and intracranial hypertension are each independent indicators of a poor prognosis after stroke, but there is an astonishing lack of evidence from randomised controlled trials to tell us how to manage these problems, bearing in mind their frequency in stroke patients. The therapeutic options will, in most cases, not involve patented drugs, and financial support for running the necessary randomised controlled trials will have to come from government or charity sponsors rather than from the pharmaceutical industry. It is vital that academic researchers now devise studies of appropriate design and size to answer these important questions. In the absence of randomised data, severe hyperglycaemia and pyrexia should be treated, whilst acute hypertension is probably best left untreated unless very severe or complicated by other medical conditions. The management of cerebral oedema remains an enigma.
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PMID:Optimising homeostasis. 1109 91

Preeclampsia-eclampsia is still one of the leading causes of maternal and fetal morbidity and mortality. Despite active research for many years, the etiology of this disorder exclusive to human pregnancy is an enigma. Recent evidence suggests there may be several underlying causes or predispositions leading to the signs of hypertension, proteinuria, and edema, findings that allow us to make the diagnosis of the "syndrome" of preeclampsia. Despite improved prenatal care, severe preeclampsia and eclampsia still occur. Although understanding of the pathophysiology of these disorders has improved, treatment has not changed significantly in over 50 years. Although postponement of delivery in selected women with severe preeclampsia improves fetal outcome to a degree, this is not done without risk to the mother. In the United States, magnesium sulfate and hydralazine are the most commonly used medications for seizure prophylaxis and hypertension in the intrapartum period. The search for the underlying cause of this disorder and for a clinical marker to predict those women who will develop preeclampsia-eclampsia is ongoing, with its prevention the ultimate goal. This review begins with the clinical and pathophysiologic aspects of preeclampsia-eclampsia (Part 1). In Part 2, the experimental observations, the search for predictive factors, and the genetics of this disorder will be reviewed.
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PMID:Preeclampsia. Part 1: clinical and pathophysiologic considerations. 1221 68

Preeclampsia-eclampsia is still one of the leading causes of maternal and fetal morbidity and mortality. Despite active research for many years, the etiology of this disorder exclusive to human pregnancy is an enigma. Recent evidence suggests there may be several underlying causes or predispositions leading to the signs of hypertension, proteinuria, and edema, findings that allow us to make the diagnosis of the "syndrome" of preeclampsia. Despite improved prenatal care, severe preeclampsia and eclampsia still occur. Although understanding of the pathophysiology of these disorders has improved, treatment has not changed significantly in over 50 years. Although postponement of delivery in selected women with severe preeclampsia improves fetal outcome to a degree, this is not done without risk to the mother. In the United States, magnesium sulfate and hydralazine are the most commonly used medications for seizure prophylaxis and hypertension in the intrapartum period. The search for the underlying cause of this disorder and for a clinical marker to predict those women who will develop preeclampsia-eclampsia is ongoing, with its prevention the ultimate goal. This review began with the clinical and pathophysiologic aspects of preeclampsia-eclampsia (Part 1). Now, in Part 2, the experimental observations, the search for predictive factors, and the genetics of this disorder are reviewed.
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PMID:Preeclampsia. Part 2: experimental and genetic considerations. 1221 69

The pathogenesis of pain in chronic pancreatitis remains an enigma. The cause of pain is almost certainly multifactorial and may vary at different stages of the disease process. These factors may include the release of excessive oxygen-derived free radicals, tissue hypoxia and acidosis, inflammatory infiltration with influx of pain transmittent substances into damaged nerve ends, and the development of pancreatic ductal and tissue fluid hypertension due to morphological changes of the pancreas. Investigations into the causes of pain have been limited by changes in the dynamics with the progression of the disease process, limitations in studying functional and morphological changes of the pancreas in the clinical setting, and the psychosomatic profile of patients. Many of these patients are addicted to alcohol, and suffer from personality disorders. The difficulty in quantifying pain, which is at best subjective, further compounds the issue, especially when assessing the efficacy of treatment.
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PMID:Pathogenesis of pain in chronic pancreatitis: ongoing enigma. 1457 90

High blood pressure is common in the western world and is a major risk factor for the development of stroke. Lowering blood pressure reduces the risk of first and recurrent stroke. High blood pressure is also common in acute stroke and is independently associated with a poor prognosis, in part due to promoting early recurrence and the development of fatal cerebral oedema in patients with ischaemic stroke and, possibly, re-bleeding in those with haemorrhagic stroke. However, the management of blood pressure remains an enigma--its lowering could improve outcome by reducing recurrence or worsen outcome by reducing regional perfusion in the face of dysfunctional cerebral autoregulation. Conversely, raising blood pressure might improve outcome by raising regional perfusion or worsen it by inducing cerebral oedema and early recurrence. Administration of some vaso-active drugs (beta-receptor antagonists and calcium channel blockers) can worsen outcome and reduce cerebral blood flow. In contrast, other drug classes--angiotensin- converting enzyme inhibitors, angiotensin receptor antagonists and nitrates--appear to lower blood pressure without reducing measures of cerebral perfusion. In the absence of definitive trial data, which is urgently needed, blood pressure should not be routinely lowered unless it is extreme (systolic blood pressure >220 mm Hg) or associated with arterial dissection or cardiac ischaemia or failure, in which case cautious lowering (<15%), perhaps with an angiotensin-converting enzyme inhibitor, angiotensin receptor antagonist or nitrate, is appropriate.
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PMID:High blood pressure as risk factor and prognostic predictor in acute ischaemic stroke: when and how to treat it? 1469 80


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