摘要:

The reviews by Drs. Touyz and Schiffrin, Dzau, Karczewskiet al., and Mulrow were edited by Dr. Ganten and Dr. Luft and those by Drs. Nakaoet al., Simonson and Dunn, Fischer and Badr, and O'Sheaet al., by Dr. Kurokawa.

ISSN:1062-4821    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

During the past year, there has been significant progress in the knowledge of mechanisms involved in the intracellular transduction of extracellular signals. These advances have allowed a more detailed understanding of how receptors involved in contraction and relaxation of smooth muscle cells couple to intracellular effector systems and of the growth response that characterizes the behavior of blood vessels in hypertension. A large measure of this progress relates to identifying receptor subtypes of regulatory proteins that modulate activation of intracellular or membrane enzymes participating in contraction, relaxation, and growth as well as new pathways of signal transduction. Major new findings in mechanisms of cell signaling and growth in vascular smooth muscle are discussed in part I, and their involvement in hypertension are discussed in part II.

ISSN:1062-4821    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Essential hypertension is characterized by various cell membrane abnormalities associated with receptor characteristics, enzymatic activity, and transmembrane ion exchange. These processes are interrelated with cellular signal transduction. Defects in the tightly controlled intracellular signaling pathways and their implications in the pathogenesis of hypertension are reviewed.

ISSN:1062-4821    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Structural changes of the heart and blood vessels participate in the long-term regulation of the cardiovascular system. In hypertension and myocardial dysfunction, the adaptive process of cardiac and vascular remodeling may contribute to the pathophysiology and complications of these diseases. Recent investigations have enhanced our understanding of the cellular and molecular biology of vascular smooth muscle and cardiac myocyte growth. Mechanical and neurohormonal factors can independently stimulate hypertrophy-hyperplasia in vascular and cardiac myocytes. Increased pressure-stretch of cardiac myocyte and vascular smooth muscle cells can activate protooncogene expressions that may mediate the growth response. Vasoactive substances also regulate cardiovascular growth. In general, endogenous vasoconstrictors (eg, angiotensin, endothelin) act as growth promoters, and endogenous vasodilators (eg, nitric oxide, prostacyclin, atrial natriuretic peptide) act as growth inhibitors of vascular smooth muscle and, possibly, cardiac myocytes. Recent data have demonstrated that the vasoconstrictive agents, such as angiotensin, activate protooncogenes and autocrine growth factors that mediate vascular growth. Furthermore, the development of vascular hypertrophy versus hyperplasia is dependent on the relative activation of endogenous proliferative growth factor (eg, platelet-derived growth factor, basic fibroblast growth factor) versus antipro-liferative factor (eg, transforming growth factor-β) by the growth stimulus. Taken together, these data demonstrate that complex interactions of local mediators, which participate in the pathophysiology of cardiovascular diseases, control cardiovascular growth.

ISSN:1062-4821    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

This review discusses phosphorylation of target proteins in the plasma membrane, the sarcoplasmic reticulum, and the myofilaments of cardiac and vascular smooth muscle cells known to be important in regulating contraction and relaxation. Substantial data have been obtained on the regulation of calcium uptake mechanisms of the sarcoplasmic reticulum in cardiac as well as vascular smooth muscle, suggesting a central role of phospholamban for relaxation in the cardiovascular system. As shown for cardiac muscle, the calcium release from the sarcoplasmic reticulum is also under β-adrenergic control via phosphorylation of the ryanodine receptor. The developmental switching from the skeletal to the cardiac isoform of the cardiac thin-filament protein troponin I marks the onset of β-adrenergic regulation of myofilaments through phosphorylation. Further examples for the genetic control of systems regulated by protein phosphorylation are presented. The review emphasizes the power of molecular-biologic approaches in combination with traditional methods to achieve significant progress in this field of cardiovascular research.

ISSN:1062-4821    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

The standard concept of the renin-angiotensin system is that renin is secreted by the juxtaglomerular cells of the kidney into the circulation, where it cleaves angiotensin to release angiotensin I. The angiotensin I is converted to angiotensin II by a converting enzyme located on the plasma membrane of the endothelial cell. The released angiotensin II binds to receptors on target cells to initiate a series of intracellular actions that result in a specific cell function. The kidney was conceived to secrete renin with the circulatory angiotensin II returning to the kidney to alter renal function. It is now clear that all the components of the renin-angiotensin system can be synthesized within the kidney. In fact, angiotensin II is formed in very high concentrations in the renal interstitial space. Local angiotensin II production can have profound influences on renal function,ie, alter glomerular hemodynamics, reduce sodium excretion, and constrict small arterioles. In certain disease states, the local action of angiotensin II may have harmful effects on the kidney, and blockade of the renin-angiotensin system can be beneficial to the kidney.

ISSN:1062-4821    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

The natriuretic peptide system is a complicated system comprising at least three endogenous peptides, atrial natriuretic peptide, brain natriuretic peptide, and C-type natriuretic peptide and three receptors, the atrial natriuretic peptide-A receptor (guanylyl cyclase A), the atrial natriuretic peptide-B receptor (guanylyl cyclase B), and the clearance receptor. The accumulated evidence indicates that this system is implicated in the control of blood pressure, body fluid homeostasis, and vascular remodeling as both cardiac hormone and local regulator.

ISSN:1062-4821    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

In the past year, major advances have been made in understanding the role of endothelin peptides in renal homeostasis. Numerous cells in the kidney secrete endothelin, which binds to two receptor subtypes on neighboring cells in an autocrine or paracrine mode. Endothelin is a potent vasoconstrictor of the renal vasculature that reduces renal blood flow and glomerular filtration rate. Endothelin also affects renal sodium and water handling. Finally, we may have to extend our concept of the renal actions of endothelin to include its growth factor actions.

ISSN:1062-4821    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Basic and clinical investigations into the roles of arachidonate-derived compounds in regulating renal function under normal and pathophysiological conditions continued to expand over the past year. Exciting new insights regarding the pathobiology of thromboxane A2revealed new roles for this potent cyclooxygenase-derived vasoconstrictor in the glomerular dysfunction that accompanies inflammatory disorders and insulin-dependent diabetes. Major advances have extended our understanding of the proinflammatory actions of leukotriene B4and other 5-lipoxygenase compounds in mediating glomerular injury during experimental glomerulonephritis. Intriguingly, emerging evidence suggests the presence of an anti-inflammatory arm in the lipoxygenase pathway,ie, 15-lipoxygenase, products of which may act as endogenous leukotriene antagonists. New information has also become available about the renal biology of cytochrome P-450 metabolites of arachidonic acid as well as about nonenzymatically generated biologically potent eicosanoids, the F2-isoprostanes.

ISSN:1062-4821    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Growth hormone and a number of polypeptide growth factors exert actions on renal development, growth, and metabolism and on repair processes following renal injury. There is increasing evidence that under selected circumstances, these agents play roles in the pathogenesis of kidney disease and that under others, they may be useful in its treatment. Growth hormone, platelet-derived growth factor, or transforming growth factor-β may be causative of glomerulosclerosis. The reduction in epidermal growth factor expression within the kidney in the setting of acute ischemic injury could delay regeneration, and replacement may be therapeutic. Insulinlike growth factor I may play a role in the regenerative response to acute renal injury. Pharmacologic properties of growth hormone or insulinlike growth factor I to enhance glomerular filtration rate and renal plasma flow and to increase skeletal growth may be harnessable for treating chronic renal failure and its complications. It is likely that strategies designed to employ growth hormone or growth factors as pharmacologic agents or to block their activities will assume increasingly important roles in therapy for renal disease.

ISSN:1062-4821    

出版商:OVID    

年代:1993

数据来源: OVID