11. |
Regulation of vesicular transport by GTP-binding proteins |
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Current Opinion in Nephrology and Hypertension,
Volume 4,
Issue 5,
1995,
Page 421-425
Jennifer Stow,
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摘要:
Intracellular protein trafficking occurs in a series of transport vesicles. Vesicle trafficking is regulated both by heterotrimeric and monomeric CTP-binding proteins (G proteins). Recent studies have explored effector systems used by heterotrimeric G proteins and by monomeric ADP-ribosylation factor G proteins for regulation of vesicle budding. New members of the Rab monomeric G protein family have been identified in polarized cells and new evidence confirms the function of Rab proteins in vesicle targeting. From these data we can begin to reconstruct the signal transduction pathways that regulate intracellular transport.
ISSN:1062-4821
出版商:OVID
年代:1995
数据来源: OVID
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12. |
Are angiotensin-converting enzyme inhibitors the renal protective antihypertensive drugs of choice? |
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Current Opinion in Nephrology and Hypertension,
Volume 4,
Issue 5,
1995,
Page 427-431
John Bauer,
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ISSN:1062-4821
出版商:OVID
年代:1995
数据来源: OVID
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13. |
Corticosteroid hypertension |
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Current Opinion in Nephrology and Hypertension,
Volume 4,
Issue 5,
1995,
Page 432-437
John Funder,
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摘要:
Over the past year, the focus in corticosteroid hypertension has been on the cloning of the enzyme 11 fi-hydroxysteroid dehydrogenase, and the demonstration of a variety of mutations or deletions in the sequence coding for this enzyme in the syndrome of apparent mineralocorticoid excess. This syndrome is the third single-gene cause of human hypertension to be characterized, with glucocorticoid remediable aldosteronism (1992) and Liddle's syndrome (1994). The three conditions are characterized by inappropriate control of aldosterone secretion (glucocorticoid remediable aldosteronism), sodium retention (Liddle's syndrome) or aldosterone action (apparent mineralocorticoid excess), and underline a potential role of an aldosterone: salt imbalance in mineralocorticoid hypertension. No comparable mechanisms of hypertension following glucocorticoid receptor occupancy have been documented to date.
ISSN:1062-4821
出版商:OVID
年代:1995
数据来源: OVID
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14. |
Hypertension in postmenopausal women: pathophysiology and management |
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Current Opinion in Nephrology and Hypertension,
Volume 4,
Issue 5,
1995,
Page 438-442
Suzanne Oparil,
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摘要:
Hypertension, particularly systolic hypertension, afflicts over 50% of postmenopausal women and is an important risk factor for cardiovascular disease in this group. Hormone replacement therapy with estrogen or an estrogen/progestin combination does not alter blood pressure but has beneficial effects on other cardiovascular risk factors, so should be considered in all postmenopausal women unless contraindicated.
ISSN:1062-4821
出版商:OVID
年代:1995
数据来源: OVID
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15. |
Hypertension after cardiac transplantation: pathophysiology and management |
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Current Opinion in Nephrology and Hypertension,
Volume 4,
Issue 5,
1995,
Page 443-451
Mikael Sander,
Ronald Victor,
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摘要:
This article reviews the current state of knowledge concerning cyclosporine A-induced hypertension after heart transplantation, its pathophysiology and management. The hypothesis is presented that a common molecular mechanism mediates both the immunosuppressive and the hypertensive actions of cyclosporine. The calcium-calmodulin dependent phosphatase, calcineurin, is the common cellular target mediating the salient immunosuppressive effects of both cyclosporine A and FK5O6. Calcineurin is even more plentiful in nonlymphoid tissues such as the nervous system, muscle, and kidney. Because these are the main target sites for cyclosporine A-induced toxicity, it has been hypothesized recently that inhibition of calcineurin mediates cyclosporine A-induced toxicity. This hypothesis is supported by increasing experimental evidence, at both the whole animal and cellular levels, indicating that the toxicity profile of cyclosporine A is duplicated by FK506 but not by rapamycin, a structural analog of FK506 which is a potent immunosuppressive agent but has no effect on calcineurin. Recent multicenter trials demonstrate that in the clinical setting the hypertensive and other side effects of cyclosporine A are duplicated by FK506. The clinical toxicity of rapamycin is as yet unknown.
ISSN:1062-4821
出版商:OVID
年代:1995
数据来源: OVID
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16. |
Orthostatic hypotension: epidemiology, pathophysiology and management |
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Current Opinion in Nephrology and Hypertension,
Volume 4,
Issue 5,
1995,
Page 452-454
Giris Jacob,
David Robertson,
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摘要:
Orthostatic hypotension is characterized by low upright blood pressure levels and symptoms of cerebral hypoperfusion. Whereas orthostatic hypotension is heterogeneous, correct pathophysiologic diagnosis is important because of therapeutic and prognostic considerations. Although therapy is not usually curative, it can be extraordinarily beneficial if it is individually tailored. Management of the Shy-Drager syndrome (multiple-system atrophy) remains a formidable challenge.
ISSN:1062-4821
出版商:OVID
年代:1995
数据来源: OVID
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17. |
Benign prostatic hyperplasia: pathophysiology and pharmacological treatment |
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Current Opinion in Nephrology and Hypertension,
Volume 4,
Issue 5,
1995,
Page 455-459
Finn Madsen,
Reginald Bruskewitz,
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摘要:
Recent studies have confirmed that a-blocker therapy and antihormonal therapy are effective and safe treatment modalities in patients with symptomatic benign prostatic hyperplasia. New data suggest that the clinical response to medical therapy lasts for at least 3 years without any increase in side effects during this period.
ISSN:1062-4821
出版商:OVID
年代:1995
数据来源: OVID
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18. |
Hypertension in autosomal dominant polycystic kidney disease |
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Current Opinion in Nephrology and Hypertension,
Volume 4,
Issue 5,
1995,
Page 460-464
Patrick Parfrey,
Brendan Barrett,
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摘要:
Hypertension occurs frequently in autosomal dominant polycystic kidney disease. Increased activity of the renin-angiotensin system contributes to the development and maintenance of hypertension before the development of renal failure. Angiotensin-converting enzyme inhibitors are indicated for treatment of hypertension before the development of renal failure, but in severe renal failure these agents may cause further deterioration in renal function. Treatment of hypertension may not retard the progression of renal failure but is necessary for the prevention of cardiovascular disease.
ISSN:1062-4821
出版商:OVID
年代:1995
数据来源: OVID
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