Seminars in vascular medicine最新文献

{"title":"Cortisol, 11beta-hydroxysteroid dehydrogenases, and hypertension.","authors":"Stan H M van Uum,&nbsp;Jacques W M Lenders,&nbsp;Ad R M M Hermus","doi":"10.1055/s-2004-835369","DOIUrl":"https://doi.org/10.1055/s-2004-835369","url":null,"abstract":"<p><p>Hypersecretion of cortisol is associated with hypertension. In addition, an abnormal cortisol metabolism may play a role in the pathogenesis of hypertension. The 11beta-hydroxysteroid dehydrogenase (11beta-HSD) isozymes catalyze interconversion of cortisol and cortisone and play an important role in the regulation of the effects of cortisol. Activity of 11beta-HSD type 2, converting active cortisol in inactive cortisone, is crucial in preventing access of cortisol to the renal mineralocorticoid receptors (MRs). Decreased activity of this isozyme in the kidney, either congenitally in Apparent Mineralocorticoid Excess syndrome or acquired following licorice consumption, allows cortisol access to the MRs, resulting in hypokalemic hypertension. In normotensive subjects, an association has been demonstrated between blood pressure increase on a high-salt diet and a mild decrease of renal 11beta-HSD2 activity. In ectopic adrenocorticotropic hormone (ACTH), plasma cortisol levels are very high, resulting in mineralocorticoid hypertension caused by saturation of the available renal 11beta-HSD2 capacity. Activity of the 11beta-HSDs has also been demonstrated in many extrarenal sites. Several studies have demonstrated extrarenal effects of cortisol on blood pressure, as well as a possible role for altered extrarenal 11beta-HSD activities in the pathogenesis of hypertension. More studies are needed to clarify the role of 11beta-HSDs in the pathogenesis of hypertension.</p>","PeriodicalId":87139,"journal":{"name":"Seminars in vascular medicine","volume":"4 2","pages":"121-8"},"PeriodicalIF":0.0,"publicationDate":"2004-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-2004-835369","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40913916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adrenomedullin: its role in the cardiovascular system.","authors":"Bernard M Y Cheung,&nbsp;Carol Y Y Li,&nbsp;Louisa Y F Wong","doi":"10.1055/s-2004-835370","DOIUrl":"https://doi.org/10.1055/s-2004-835370","url":null,"abstract":"<p><p>Adrenomedullin is a 52-amino acid peptide that was first isolated from human pheochromocytoma. Subsequently, it was found to be distributed widely in the body, including throughout the cardiovascular system. It belongs to a family of peptides that include calcitonin gene-related peptide and amylin. Adrenomedullin causes vasorelaxation and influences vascular proliferation and interacts closely with nitric oxide, and it may have a role in the pathophysiology of hypertension, ischemic heart disease, and cardiac and renal failure. Nonpeptide agonists or antagonists of adrenomedullin may have potential therapeutic application. The role of adrenomedullin in septicemic shock also merits further investigation.</p>","PeriodicalId":87139,"journal":{"name":"Seminars in vascular medicine","volume":"4 2","pages":"129-34"},"PeriodicalIF":0.0,"publicationDate":"2004-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-2004-835370","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40913917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of the somatotropic system in cognition and other cerebral functions.","authors":"Wouter M Creyghton,&nbsp;P Sytze van Dam,&nbsp;Hans P F Koppeschaar","doi":"10.1055/s-2004-835375","DOIUrl":"https://doi.org/10.1055/s-2004-835375","url":null,"abstract":"<p><p>Growth hormone (GH) and insulin-like growth factor 1 (IGF-1) receptors can be found in several areas of the brain. GH receptors are mainly found in the choroid plexus, thalamus, hypothalamus, pituitary, putamen, and hippocampus, whereas IGF-1 receptors are mainly concentrated in the hippocampus and parahippocampal areas. In early life, GH and IGF-1 have an important role in the development and differentiation of the central nervous system. In the more developed central nervous system, GH and IGF-1 are thought to have a variety of functions such as a neuroprotective function, an appetite increasing function, various cognitive functions, and perhaps a blood flow-regulating function. In GH-deficient children and adults, improvement of cognitive functions was observed after the administration of GH. Furthermore, specific cognitive functions in healthy older subjects may improve after increasing GH or IGF-1 levels.</p>","PeriodicalId":87139,"journal":{"name":"Seminars in vascular medicine","volume":"4 2","pages":"167-72"},"PeriodicalIF":0.0,"publicationDate":"2004-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-2004-835375","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40913901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Drink to prevent: review on the cardioprotective mechanisms of alcohol and red wine polyphenols.","authors":"Dylan W de Lange,&nbsp;Albert van de Wiel","doi":"10.1055/s-2004-835376","DOIUrl":"https://doi.org/10.1055/s-2004-835376","url":null,"abstract":"<p><p>Moderate alcohol consumption has convincingly been associated with decreased cardiovascular mortality in epidemiological studies and metaanalyses. This decreased mortality has been attributed to changes in lipid profiles, decreased coagulation, increased fibrinolysis, inhibition of platelets, increased nitric oxide, and antioxidant capacities of alcoholic beverages. Most of these laboratory and animal studies, as well as small intervention trials in human volunteers, have revealed many interesting mechanisms that contribute to the cardioprotective effects of alcohol, red wine, or red wine polyphenolic compounds. An update on putative mechanisms is presented in this review.</p>","PeriodicalId":87139,"journal":{"name":"Seminars in vascular medicine","volume":"4 2","pages":"173-86"},"PeriodicalIF":0.0,"publicationDate":"2004-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-2004-835376","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40913902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Familial combined hyperlipidemia: controversial aspects of its diagnosis and pathogenesis.","authors":"Carlos A Aguilar Salinas,&nbsp;Margarita Zamora,&nbsp;Rita A Gómez-Díaz,&nbsp;Roopa Mehta,&nbsp;Francisco J Gómez Pérez,&nbsp;Juan A Rull","doi":"10.1055/s-2004-835379","DOIUrl":"https://doi.org/10.1055/s-2004-835379","url":null,"abstract":"<p><p>Familial combined hyperlipidemia is the most frequent cause of primary dyslipidemia in Mexico. Its manifestations include hypercholesterolemia, hypertriglyceridemia, or a combination of both. Despite its high frequency, a proper diagnosis is rarely made. Assessment of the lipid profiles of at least three first-degree relatives is necessary. The diagnosis of familial combined hyperlipidemia in a family not only leads to the identification of other affected family members but, more important, allows cardiovascular risk stratification of those affected. Prospective studies have confirmed the atherogenicity of the disease. A critical review of the current literature in this field is presented in this article. Although three screenings of the genome have been completed, the genes responsible for this disorder have not been identified. Limitations with respect to the characterization of affected subjects and the heterogeneity of the disease are among possible explanations. However, familial combined hyperlipidemia, because of its high prevalence, must be given greater priority. It represents a great challenge for physicians involved in the treatment of dyslipidemic patients.</p>","PeriodicalId":87139,"journal":{"name":"Seminars in vascular medicine","volume":"4 2","pages":"203-9"},"PeriodicalIF":0.0,"publicationDate":"2004-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-2004-835379","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40913905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The emerging role of lipoproteins in atherogenesis: beyond LDL cholesterol.","authors":"Stephen Nicholls,&nbsp;Pia Lundman","doi":"10.1055/s-2004-835377","DOIUrl":"https://doi.org/10.1055/s-2004-835377","url":null,"abstract":"<p><p>Low-density lipoprotein cholesterol has a well-established role in atherogenesis and the development of coronary heart disease. However, despite effective lowering of low-density lipoprotein cholesterol, many patients continue to have cardiovascular events. It has subsequently emerged that several additional dyslipidemic states promote atherogenesis. In particular, the atherogenic lipoprotein phenotype comprising an elevation of triglycerides and triglyceride-rich lipoproteins; decreased concentrations of high-density lipoprotein cholesterol; and increased small, dense low-density lipoprotein cholesterol, in addition to impaired postprandial lipemia, have been demonstrated to have profound effects on the arterial wall. As such, these factors have become important targets in the development of effective strategies to prevent atherosclerotic cardiovascular disease.</p>","PeriodicalId":87139,"journal":{"name":"Seminars in vascular medicine","volume":"4 2","pages":"187-95"},"PeriodicalIF":0.0,"publicationDate":"2004-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-2004-835377","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40913903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The lost promise of hormone replacement therapy and heart disease.","authors":"Angela H E M Maas","doi":"10.1055/s-2004-835371","DOIUrl":"https://doi.org/10.1055/s-2004-835371","url":null,"abstract":"<p><p>Since the first secondary prevention trials were published in 1998, the prospect of hormone replacement therapy to prevent atherosclerotic heart disease in postmenopausal women has changed dramatically. Early harmful effects of hormone replacement therapy and lack of beneficial effects on coronary heart disease event rates in high-risk women have challenged the beneficial results gleaned from observational studies in the past. In this article, the effects of estrogens on lipids, hemostatic parameters, inflammation, and the vascular wall are described. The discrepancies that have arisen between the previous observational studies and recent randomized clinical trials are discussed: The current available data indicate that estrogens are beneficial to healthy endothelium but are harmful once atherosclerotic disease has developed.</p>","PeriodicalId":87139,"journal":{"name":"Seminars in vascular medicine","volume":"4 2","pages":"135-44"},"PeriodicalIF":0.0,"publicationDate":"2004-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-2004-835371","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40913918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiovascular Endocrinology","authors":"M. T. B. Twickler1","doi":"10.1055/s-2004-835366","DOIUrl":"https://doi.org/10.1055/s-2004-835366","url":null,"abstract":"Cardiovascular disease (CVD) is a major cause of morbidity and mortality all over the world. Despite growing knowledge about the origins of CVD, only a modest decrease in cardiovascular mortality, as a percentage of total mortality, has been found in recent decades. Several factors have been proposed to explain this trend in the epidemiology of CVD, such as adaptation of a Western lifestyle and the abundant availability of dietary calories. Cardiovascular prevention programs that should decrease the occurrence of cardiovascular disease have less than expected results: Initial decrease in smoking behavior is again growing among young individuals, with weight gain and, subsequently, an alarming growth in obesity. Moreover, patients who have classic risk factors, such as hypertension and dyslipidemia, are still insufficiently treated, leading the intervention programs to consequently have a smaller effect. Most CVD programs focus on atherosclerotic disease and its direct consequences on restenosis, and on reevents of ischemic coronary artery disease. However, a shift in cardiovascular morbidity and mortality is observed in a trend away from acute ischemic coronary artery disease toward a more chronic cardiovascular disease, such as heart failure. Recently, better treatment options for complications related to acute ischemic coronary disease were introduced, such as fibrinolytic therapy, use of coronary stents events, and emergency percutaneous transluminal coronary arteriography. In contrast to primary and secondary prevention programs that act through reducing effects of classical atherogenic risk factors, additional processes are involved in chronic heart disease concerning, for example, remodeling of damaged cardiac muscle. More insight is obtained from recent studies about biological processes that are part of the origin of remodeling and adaptation in cardiac performance, such as paracrine and autocrine growth factors and components of hormonal systems. Indeed, these factors within cardiac tissue are closely integrated in several adaptive processes that have an effect on heart and hemodynamic properties. This progress in research creates an increase in cross talk between distinct clinical departments, such as endocrinology, internal medicine, and cardiology, with a subsequent development of research and clinical programs that cross classic clinical borders. These academic initiatives could be organized within a medical infrastructure named cardiovascular endocrinology. Recent progress in molecular biology offers us novel tools to create new therapeutic strategies and to redefine in more detail the origin of CV diseases. Elucidation of involved genes and related proteins that participate in cardiac physiology enable us to learn more about future interventions to treat heart failure and atherosclerotic disease more efficiently. Indeed, more sensitive techniques showed, for example, the role of apoptosis and postnatal differentiation of functional","PeriodicalId":87139,"journal":{"name":"Seminars in vascular medicine","volume":"4 1","pages":"105 - 106"},"PeriodicalIF":0.0,"publicationDate":"2004-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-2004-835366","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"58009027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-density lipoprotein as a key component in the prevention of premature atherosclerotic disease in the insulin resistance syndrome.","authors":"Boris Hansel,&nbsp;Anatol Kontush,&nbsp;Marcel Th B Twickler","doi":"10.1055/s-2004-835381","DOIUrl":"https://doi.org/10.1055/s-2004-835381","url":null,"abstract":"in vitro in vivo","PeriodicalId":87139,"journal":{"name":"Seminars in vascular medicine","volume":"4 2","pages":"215-23"},"PeriodicalIF":0.0,"publicationDate":"2004-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-2004-835381","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40992087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acromegaly and heart failure: revisions of the growth hormone/insulin-like growth factor axis and its relation to the cardiovascular system.","authors":"Th B Twickler,&nbsp;M J M Cramer,&nbsp;S P Senden,&nbsp;P A Doevendans,&nbsp;W R de Vries,&nbsp;D W Erkelens,&nbsp;H P F Koppeschaar","doi":"10.1055/s-2004-835368","DOIUrl":"https://doi.org/10.1055/s-2004-835368","url":null,"abstract":"<p><p>Cardiomyopathy is a major cause of death in overt acromegaly. Recent progress in research has increasingly revealed the molecular mechanisms concerning growth hormone and insulin-like growth factor in the development of heart failure. In this article, we propose mechanisms according to which heart failure occurs, and we aim to extrapolate this knowledge to more general processes involved in heart failure.</p>","PeriodicalId":87139,"journal":{"name":"Seminars in vascular medicine","volume":"4 2","pages":"115-20"},"PeriodicalIF":0.0,"publicationDate":"2004-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-2004-835368","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40913409","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}