ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Nitric oxide synthases are a family of complex cytochrome P45o-like hemeproteins that catalyze the five-electron oxidation of L-arginine to form nitric oxide. Nitric oxide synthase apoenzyme is dependent on molecular oxygen, nicotinamide adenine dinucleotide phosphate hydrogen, flavins and tetrahydrobiopterin, and it functions as a dimer. Three human nitric oxide synthase isoforms have been identified to date. The endothelial constitutive, neuronal, and inducible nitric oxide synthase isoforms are found on human chromosomes 7, 12 and 17, respectively. Characterization of the structural organization of the human nitric oxide synthase genes reveals that, although they are structurally related, the mechanisms by which they are regulated are distinct. Expression of the mRNA for endothelial constitutive nitric oxide synthase is regulated at the level of transcription and mRNA stability. The mRNA transcripts derived from the neuronal nitric oxide synthase gene are characterized by a remarkable degree of structural diversity. Levels of inducible nitric oxide synthase mRNA are controlled by interacting combinations of cytokines and biological mediators at the level of gene transcription and mRNA stability.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Nitric oxide seems to play a crucial role in sodium homeostasis and hence blood pressure regulation by controlling the tone of glomerular arterioles and mesanglum, medullary circulation, pressure natriuresis, tubuloglomerular feedback, renin release, and tubular function. Thus, deficiency of the L-arginine-nitric oxide pathway may be involved in the pathogenesis of such diseases as salt-sensitive hypertension, whereas activation of the nitric oxide system may either protect against or contribute to progression of various renal diseases.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Aldosterone is a type of steroid hormone that acts primarily in renal collecting ducts to stimulate reabsorption of Na+as well as secretion of K+and H+. It binds with intracellular receptors in the nucleus that stimulate the expression of several genes. Transcription and subsequent translation result in the production of new proteins that modulate the activity of ionic transport systems located in the apical and basolateral membranes of the target epithelial cells. This review focuses on the cellular mechanisms of aldosterone action on Na+, K+, and H+transport in mammalian renal collecting ducts. Although the cellular actions of aldosterone conform to the general mode of steroid hormone action, numerous questions relating to each step in the process remain unanswered.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Mineralocorticoid receptors in the distal nephron have no intrinsic specificity for mineralocorticoids over glucocorticoids (cortisol in humans; corticosterone in rodents), but are protected from glucocorticoids by the enzyme 11β-hydroxysteroid dehydrogenase, which inactivates these steroids to cortisone and 11-dehydrocorticosterone, respectively. Recent work has demonstrated that the enzyme is expressed as multiple tissue-specific isoforms, some of which catalyse the reverse conversion of cortisone to cortisol. These isoforms may allow 11β-hydroxysteroid dehydrogenase to modulate access of ligands to glucocorticoid and mineralocorticoid receptors, as well as to amplify and attenuate tissue responses. 11β-hydroxysteroid dehydrogenase-mediated protection of mineralocorticoid receptors fails in congenital 11 β-hydroxysteroid dehydrogenase deficiency and after inhibition of the enzyme by liquorice. In these circumstances, cortisol-dependent mineralocorticoid excess and hypertension ensue. Recent studies suggest that similar deficiencies of 11β-dehydrogenase activity may contribute to pathophysiology in common clinical syndromes, illustrating the potential significance of this novel mechanism for development of hypertension.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Recent developments in angiotensin II receptor research are discussed in the context of our knowledge in preceding years. Cloning of non-mammalian angiotensin II receptors without high affinity for non-peptide antagonists has permitted a new approach to the delineation of ligand-binding domains. Cloning of the second major isoform of angiotensin II receptor, AT2, and identification as a seven transmembrane domain receptor with only 32% sequence homology with the first isoform, AT1, provide the first concrete step toward our understanding of the roles of AT2. The discovery of phospholipase C-mediated pathway for AT1in vascular smooth muscle cell signaling introduces an entirely unexpected angle to future research. New aspects of AT1gene regulation and receptor desensitization and internalization are evolving. Molecular mechanisms and physiological implications of the differential expression of AT1Aand AT1Bare being clarified. The recent discovery of human AT1Bmay make studies on animal models interesting and more meaningful. The first paper on the genetic role of the AT1gene in human hypertension has just been published. A promising future is expected in the further development of angiotensin-receptor research in relation to cardiac, renal, and vascular function by employing techniques of molecular biology.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Urinary calcium excretion is regulated homeostatically. Regulation is achieved, in part, by the action of parathyroid hormone on Ca2+absorption in the distal nephron. Parathyroid hormone increases Ca2+absorption in the cortical portion of the thick ascending limb of Henle's loop in all species studied, in the murine distal convoluted tubule, and in the rabbit connecting tubule. All of these sites contain parathyroid hormone-stimulated adenylate cyclase. Both cellular and paracellular pathways of Ca2+absorption are regulated by parathyroid hormone in the cortical portion of the thick ascending limb of Henle's loop. In both distal convoluted and connecting tubule cells, parathyroid hormone regulates transcellular Ca2+absorption by controlling the insertion and open probability of luminal plasmalemmal Ca2+ion channels. These channels are stimulated and inhibited by L-type calcium channel agonists and antagonists, repectively, but differ from similar channels in excitable cells in that membrane depolarization does not activate them. Parathyroid hormone also increases the driving force for diffusional Ca2+ion entry from the luminal fluid into the cytosol by increasing the intracellular negative electrical potential (at least in murine distal convoluted tubule cells) by increasing the chloride ion conductance of the basolateral cell membrane. The effects of parathyroid hormone on the other components of cellular Ca2+transport, via both protein kinases A and C and their interactions, remain to be examined.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID