摘要:

Recent investigations cast some doubts on the status of insulin resistance as a trigger in hyperinsulinemia-associated hypertension or obesity-related hypertension, or both. Major epidemiological studies have shown that central adiposity is a powerful risk factor for stroke or coronary artery disease when accompanied by hypertension or hypertriglyceridemia. New heredity studies have failed to identify a common gene that may explain obesity-related hypertension.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

The role of extracellular fluid status and sodium balance in various forms of hypertension often has been difficult to define precisely because of the limitations of direct measurements of these factors. Isotopic measurements of various fluid volume compartments in the body have suffered from being insensitive and imprecise. Estimates of sodium content have also been difficult because of the ready diffusion of this ion among many body compartments. Studies of sodium balance utilizing metabolic ward techniques have been too time-consuming and arduous for large-scale investigations. Thus, inferences on the role of sodium and volume in blood pressure have been derived largely from indirect observations based on the response of blood pressure to manipulation of sodium or volume status, or both, and by changes in dietary sodium, or administration of intravenous sodium loads or diuretics. Such studies, while indirect and often crude in precision, have yielded important new insights into the etiology and pathogenesis of hypertension. The roles of agents that influence renal handling of sodium and water, and vascular biology are also being investigated for their influence on sodium homeostasis.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

In spite of our comprehensive understanding of renovascular hypertension, diagnostic tests based on the pathophysiology of the disease have been disappointing in their sensitivity and specificity. They are particularly unreliable in the setting of bilateral disease and renal dysfunction. The recent results of vascular surgery and renal angioplasty combined with the use of metallic stents have shown dramatic benefits in revascularization even in the setting of renal artery occlusion, ostial renal artery stenosis, and renal dysfunction. Timely diagnosis and intervention are imperative, and, therefore, we recommend the early use of arteriography using digital subtraction angiographic techniques for the definitive diagnosis.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

At least three distinct cellular mechanisms are currently thought to be responsible for the initiation of atherosclerotic lesions in humans: (1) accumulation of lipids and plasma-derived lipoproteins in the arterial intima; (2) smooth muscle cell migration from the media into the intima, and smooth muscle cell proliferation or accumulation, or both, within the intima; and (3) accumulation of platelet and/or fibrin deposits in the intima. Independent of the triggering factor, it appears that the first step in atherogenesis involves activation of repair mechanisms in the blood vessel in an attempt to restore vascular homeostasis, which involves a delicate balance of growth promoting and growth inhibitory activities of the vascular wall cells. The healing process involves a series of specific and temporally coordinated events, such as platelet aggregation, monocyte adhesion and migration across endothelial cells, and migration and proliferation of vascular smooth muscle cells, which are normally orchestrated by a variety of growth factors, cytokines, adhesion molecules, and extracellular matrix proteins in a controlled, although not yet fully understood, manner. Alteration in any of these steps during the healing process can lead to changes in the patterns of protein synthesis, processing, and secretion in these cells. These in turn result in connective tissue deposition, lipid accumulation, cell death, mineralization, and finally the development of advanced, occluding atherosclerotic plaques.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Diabetes is characterized by hyperglycemia, a relative lack of insulin, and an inclination to vascular disease and neuropathy. The link between diabetes and vascular disease is not understood, but autonomic dysfunction could partly account for alterations in reactivity of diabetic blood vessels to neurotransmitters and circulating hormones. Changes in local control of vascular tone, such as imbalance in production of relaxing and contracting factors by the endothelium, may be related to the initiation and maintenance of abnormal vascular reactivity characteristically seen in diabetic vascular complications. The emphasis is to discuss functional changes of blood vessel adrenergic neuroeffector mechanisms and endothelial cell dysfunction, together with the complex interrelationship of cyclooxygenase catalysis, protein kinase C activity, sodium-potassium ATPase activity, and flux through the polyol pathway. This review focuses on the common mechanisms by which hyperglycemia causes changes in vascular function.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

The activation of the mitogen-activated protein kinase cascade is one of the major signalling pathways by which growth factors transmit their mitogenic messages from the cell membrane to the nucleus. Two major breakthroughs reported in the past months are the cross-communication between the mitogen-activated protein kinase cascade and the cAMP-protein kinase A signal pathway, and the role of α- and βγ-complexes of heterotrimeric G proteins in activating the mitogen-activated protein kinase pathway. These signalling strategies have now also been demonstrated in renal mesangial cells. Another important step has been the identification of a candidate gene for polycystic kidney disease. Knowledge of the molecular mechanisms of action of growth factors in the kidney will promote greatly our understanding of the aetiology of renal disease.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID