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| 1. |
Aldosterone Antagonism and Arterial Stiffness: Response |
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Hypertension: Journal of The American Heart Association,
Volume 43,
Issue 2,
2004,
Page 3-4
William,
White Daniel,
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ISSN:0194-911X
出版商:OVID
年代:2004
数据来源: OVID
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| 2. |
Vitamin C in Heart Failure: Hype or Hope?: Response: Vitamin C in Heart Failure: Hope? |
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Hypertension: Journal of The American Heart Association,
Volume 43,
Issue 2,
2004,
Page 5-6
Gianfranco,
Piccirillo Marialuce,
Nocco Antonio,
Moisè Marco,
Lionetti Camilla,
Naso Silvia,
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ISSN:0194-911X
出版商:OVID
年代:2004
数据来源: OVID
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| 3. |
Antioxidant Activities and Oxidative Stress Byproducts in Human Hypertension: Response |
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Hypertension: Journal of The American Heart Association,
Volume 43,
Issue 2,
2004,
Page 7-8
Jesep,
Redon Maria,
Tormos Felipe,
Chaves Olga,
Espinosa Antonio,
Iradi Guillermo,
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ISSN:0194-911X
出版商:OVID
年代:2004
数据来源: OVID
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| 4. |
Correction |
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Hypertension: Journal of The American Heart Association,
Volume 43,
Issue 2,
2004,
Page 9-9
&NA;,
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PDF (90KB)
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ISSN:0194-911X
出版商:OVID
年代:2004
数据来源: OVID
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| 5. |
Blood Pressure Management in Patients With Acute Ischemic Stroke |
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Hypertension: Journal of The American Heart Association,
Volume 43,
Issue 2,
2004,
Page 137-141
Larry Goldstein,
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PDF (46KB)
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ISSN:0194-911X
出版商:OVID
年代:2004
数据来源: OVID
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| 6. |
Salt Intake, Endothelial Cell Signaling, and Progression of Kidney Disease |
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Hypertension: Journal of The American Heart Association,
Volume 43,
Issue 2,
2004,
Page 142-146
Paul Sanders,
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摘要:
Abstract—It has been known for decades that increased dietary intake of salt (NaCl) shortens the life span of rats in a dose-dependent fashion. This review focuses specifically on the recently described biological effect and consequences of increased salt ingestion on the endothelium through a mechanism that is independent of blood pressure. Changes in salt intake are recognized by endothelial cells in the vascular tree and glomeruli through a physical process that promotes a series of signaling events involved in transcriptional regulation of genes that include transforming growth factor-&bgr;1 (TGF-&bgr;1) and the endothelial isoform of nitric oxide synthase (NOS3). A balance is struck between TGF-&bgr;1 and NOS3 as salt intake varies and creates a negative feedback loop, because TGF-&bgr;1 increased expression of NOS3 and NO inhibited production of TGF-&bgr;1 in healthy rats. Changes in this feedback system have been observed in salt-sensitive hypertension and appear to impact end-organ damage, particularly the kidney. The data support an important benefit to reduction of salt intake in the setting of chronic kidney disease.
ISSN:0194-911X
出版商:OVID
年代:2004
数据来源: OVID
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| 7. |
The Sympathetic Nervous System and HypertensionRecent Developments |
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Hypertension: Journal of The American Heart Association,
Volume 43,
Issue 2,
2004,
Page 147-150
Gerald DiBona,
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ISSN:0194-911X
出版商:OVID
年代:2004
数据来源: OVID
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| 8. |
Increased Aortic Stiffness: An Unfavorable Cardiorenal Connection |
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Hypertension: Journal of The American Heart Association,
Volume 43,
Issue 2,
2004,
Page 151-153
Gary Mitchell,
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PDF (18KB)
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ISSN:0194-911X
出版商:OVID
年代:2004
数据来源: OVID
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| 9. |
Neurogenic Hypertension: Is the Enigma of Its Origin Near the Solution? |
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Hypertension: Journal of The American Heart Association,
Volume 43,
Issue 2,
2004,
Page 154-155
Guido Grassi,
Giuseppe Mancia,
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ISSN:0194-911X
出版商:OVID
年代:2004
数据来源: OVID
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| 10. |
Rho/Rho-Kinase Pathway in the Brainstem Contributes to Hypertension Caused by Chronic Nitric Oxide Synthase Inhibition |
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Hypertension: Journal of The American Heart Association,
Volume 43,
Issue 2,
2004,
Page 156-162
Koji Ito,
Yoshitaka Hirooka,
Takuya Kishi,
Yoshikuni Kimura,
Kozo Kaibuchi,
Hiroaki Shimokawa,
Akira Takeshita,
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摘要:
Abstract—Central nervous system mechanisms are involved in hypertension caused by chronic inhibition of nitric oxide (NO) synthesis. Chronic inhibition of NO synthesis might also activate the Rho/Rho-kinase pathway in the vasculature. We recently demonstrated that activation of the Rho/Rho-kinase pathway in the nucleus tractus solitarii (NTS) contributes to hypertensive mechanisms in spontaneously hypertensive rats. The aim of the present study was to determine whether activation of this pathway also contributes to neurogenic hypertensive mechanisms caused by chronic NO synthesis inhibition. The NO synthase inhibitorN&ohgr;-nitro-l-arginine methyl ester (l-NAME) was administered to Wistar-Kyoto rats in their drinking water (1 mg/mL) for 2 weeks. Bilateral microinjection of Y-27632, a specific Rho-kinase inhibitor, into the NTS elicited decreases in arterial pressure, heart rate, and renal sympathetic nerve activity in control rats and l-NAME–treated rats. The magnitude of the decrease, however, was significantly greater in l-NAME–treated than in control rats. In another group of rats, the specific Rho-kinase inhibitor, Y-27632, was administered intracisternally for 2 weeks with a mini-osmotic pump from the beginning of treatment with l-NAME. Y-27632 co-treatment significantly attenuated the increase in arterial pressure. Furthermore, the expression level of membranous RhoA and phosphorylation of the target proteins of Rho-kinase, the ERM (ezrin, radixin, moesin) family members, was significantly greater in l-NAME–treated rats than in control rats. These results indicate that activation of the Rho/Rho-kinase pathway in the NTS contributes to neurogenic hypertension caused by chronic NO synthase inhibition.
ISSN:0194-911X
出版商:OVID
年代:2004
数据来源: OVID
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