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1. |
Response: Rapid Nongenomic Effects of Aldosterone on Human Forearm Vasculature |
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Hypertension: Journal of The American Heart Association,
Volume 43,
Issue 5,
2004,
Page 30-30
Bernhard Schmidt,
Roland Schmieder,
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ISSN:0194-911X
出版商:OVID
年代:2004
数据来源: OVID
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2. |
The JNC-7 Guidelines and the Optimal Target for Systolic Blood Pressure: Response |
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Hypertension: Journal of The American Heart Association,
Volume 43,
Issue 5,
2004,
Page 31-31
Aram Chobanian,
Edward Roccella,
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ISSN:0194-911X
出版商:OVID
年代:2004
数据来源: OVID
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3. |
Assessing the Sensitivity of Spontaneous Baroreflex Control of the Heart: Deeper Insight Into Complex Physiology |
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Hypertension: Journal of The American Heart Association,
Volume 43,
Issue 5,
2004,
Page 32-34
Gianfranco Parati,
Marco Di Rienzo,
Paolo Castiglioni,
Malika Bouhaddi,
Catherine Cerutti,
Andrei Cividjian,
Jean-Luc Elghozi,
Jacques-Olivier Fortrat,
Arlette Girard,
Ben Janssen,
Claude Julien,
John Karemaker,
Ferdinando Iellamo,
Dominique Laude,
Elena Lukoshkova,
Massimo Pagani,
Pontus Persson,
Luc Quintin,
Jacques Regnard,
J. Ruediger,
Philip Saul,
Marco Vettorello,
Karel Wesseling,
Giuseppe Mancia,
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PDF (20KB)
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ISSN:0194-911X
出版商:OVID
年代:2004
数据来源: OVID
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4. |
Response: Assessing the Sensitivity of Spontaneous Baroreflex Control of the Heart: Deeper Insight Into Complex Physiology |
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Hypertension: Journal of The American Heart Association,
Volume 43,
Issue 5,
2004,
Page 34-34
J. Taylor,
Ruth Lipman,
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PDF (20KB)
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ISSN:0194-911X
出版商:OVID
年代:2004
数据来源: OVID
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5. |
Correction |
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Hypertension: Journal of The American Heart Association,
Volume 43,
Issue 5,
2004,
Page 35-35
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PDF (17KB)
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ISSN:0194-911X
出版商:OVID
年代:2004
数据来源: OVID
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6. |
Diagnosis and Localization of Pheochromocytoma |
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Hypertension: Journal of The American Heart Association,
Volume 43,
Issue 5,
2004,
Page 907-910
David Goldstein,
Graeme Eisenhofer,
John Flynn,
Gary Wand,
Karel Pacak,
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摘要:
Abstract—This Hypertension Grand Rounds shows how applying new clinical laboratory techniques helped to diagnose pheochromocytoma in a difficult case. In the setting of long-standing, sustained hypertension, the patient had a hypertensive paroxysm during anesthesia induction for surgery, leading to suspicion of a pheochromocytoma. Conventional testing, including CT scanning and fractionated urinary metanephrine test, was not diagnostic. The patient had another hypertensive paroxysm during subsequent anesthesia induction, requiring intensive care. Consistently elevated plasma levels of free normetanephrine provided the first and only biochemical evidence for a pheochromocytoma in this case. 6-[18F]Fluorodopamine positron emission tomography and123I-metaiodobenzylguanidine scintigraphy subsequently agreed on the existence of a small left adrenal mass, which when removed surgically proved to be a pheochromocytoma. Postoperatively, plasma levels of normetanephrine normalized, and there were no further hypertensive paroxysms, although the patient remained hypertensive. This case illustrates the superiority of plasma levels of free (unconjugated) metanephrines, compared with other biochemical tests, to detect pheochromocytoma. It also confirms that functional imaging by 6-[18F]fluorodopamine or123I-metaiodobenzylguanidine scanning can localize pheochromocytoma in difficult cases in which other imaging tests are not diagnostic.
ISSN:0194-911X
出版商:OVID
年代:2004
数据来源: OVID
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7. |
Obesity and Hypertension-Induced Restrictive CardiomyopathyA Harbinger of Things to Come |
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Hypertension: Journal of The American Heart Association,
Volume 43,
Issue 5,
2004,
Page 911-917
Bernhard Pilz,
Jan-Hinrich Bräsen,
Wolfgang Schneider,
Friedrich Luft,
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PDF (2167KB)
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ISSN:0194-911X
出版商:OVID
年代:2004
数据来源: OVID
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8. |
Novel Mechanisms Responsible for Postmenopausal Hypertension |
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Hypertension: Journal of The American Heart Association,
Volume 43,
Issue 5,
2004,
Page 918-923
Jane Reckelhoff,
Lourdes Fortepiani,
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PDF (316KB)
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摘要:
Abstract—Blood pressure increases in many women after menopause. Hypertension is one of the major risk factors for cardiovascular disease. However, the mechanisms responsible for the postmenopausal increase in blood pressure are yet to be elucidated. Various humoral systems have been proposed to play a role in postmenopausal hypertension, such as changes in estrogen/androgen ratios, increases in endothelin and oxidative stress, and activation of the renin-angiotensin system (RAS). In addition, obesity, type II diabetes, and activation of the sympathetic nervous system are common in postmenopausal women and may also play important roles. However, progress in elucidating the mechanisms responsible for postmenopausal hypertension has been hampered by the lack of a suitable animal model. The aging female spontaneously hypertensive rat (SHR) exhibits many of the characteristics found in postmenopausal women. In this review, some of the possible mechanisms that could play a role in postmenopausal hypertension are discussed, as well as the characteristics of the aged female SHR as a model to study.
ISSN:0194-911X
出版商:OVID
年代:2004
数据来源: OVID
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9. |
Modulation of the Inflammatory Response in Cardiovascular Disease |
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Hypertension: Journal of The American Heart Association,
Volume 43,
Issue 5,
2004,
Page 924-931
D. Granger,
Thorsten Vowinkel,
Thomas Petnehazy,
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摘要:
Abstract—There is a growing body of evidence that inflammation might play an important role in the initiation and progression of cardiovascular diseases (CVDs). The designation of CVD as a chronic inflammatory process is further supported by evidence that the risk factors for CVD cause endothelial cells throughout the vascular tree to assume an inflammatory phenotype. These activated endothelial cells characteristically exhibit oxidative stress and increased adhesiveness for circulating leukocytes. Although initial efforts to define the mechanisms underlying the inflammatory phenotype in diseased endothelial cells have focused on the linkage between oxidative stress and adhesion molecule activation/expression, recent work has implicated a variety of additional factors that can modulate the magnitude and/or nature of the inflammatory responses in CVD. Platelets, angiotensin II, and the CD40/CD40 ligand signaling system are gaining recognition as contributors to the pathogenesis of CVD. These factors appear to converge with known pathways that link oxidative stress with adhesion molecule expression and help to explain the apparent integration of coagulation with inflammation in CVD. These factors also hold the promise of offering multiple sites for therapeutic intervention in CVD.
ISSN:0194-911X
出版商:OVID
年代:2004
数据来源: OVID
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10. |
Dietary Sodium and Blood Pressure |
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Hypertension: Journal of The American Heart Association,
Volume 43,
Issue 5,
2004,
Page 932-935
Daniel Jones,
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PDF (27KB)
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ISSN:0194-911X
出版商:OVID
年代:2004
数据来源: OVID
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