Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One of the most exciting aspirations of current medical science is the regeneration of damaged body parts. The capacity of adult tissues to regenerate in response to injury stimuli represents an important homeostatic process that until recently was thought to be limited in mammals to tissues with high turnover such as blood and skin. However, it is now generally accepted that each tissue type, even those considered post-mitotic, such as nerve or muscle, contains a reserve of undifferentiated progenitor cells, loosely termed stem cells, participating in tissue regeneration and repair. Skeletal muscle regeneration is a coordinate process in which several factors are sequentially activated to maintain and preserve muscle structure and function upon injury stimuli. In this review, we will discuss the role of stem cells in muscle regeneration and repair and the critical role of specific factors, such as IGF-1, vasopressin and TNF-alpha, in the modulation of the myogenic program and in the regulation of muscle regeneration and homeostasis.
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PMID:Stem cell-mediated muscle regeneration and repair in aging and neuromuscular diseases. 1770 92

Neurogenic stress causes sudden acceleration of heart rate and elevation of arterial blood pressure. that may markedly increase the work load of the heart. Several recent clinical studies document significant role of stress in evoking sudden cardiovascular complications. It has been also shown that the cardiovascular responses to stress are significantly exaggerated during the post-infarct cardiac failure. This review emphasises important neuromodulatory role of some neuropeptides in regulation of the cardiovascular system during stress. A number of experimental data provide evidence that intensity of the cardiovascular responses to stress is regulated by neuropeptides. Vasopressin, angiotensin II and interleukin-1beta (IL-1beta) appear to be responsible for exaggeration of the cardiovascular responses to stress whereas oxytocin seems to act in the opposite way. Recent studies performed in our Department provide evidence for differential involvement of angiotensin II AT(1), vasopressin V(1a), IL-1 and oxytocin receptors in regulation of the cardiovascular responses to the alarming stress. Current evidence suggests that the enhanced stimulation of central AT(1) and V(1) receptors as well as the attenuated stimulation of oxytocin receptors account for exaggeration of the cardiovascular responses to the sudden alarming stress during the post-infarct state. Growing number of data indicate that angiotensin II significantly interacts with vasopressin, interleukin-1 and TNF-alpha systems in the central cardiovascular control under resting conditions. Some of the neuropeptides interact also during stress.
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PMID:Role of neuropeptides in central control of cardiovascular responses to stress. 1925 65

Acute renal failure (ARF) is frequently associated with polyuria and urine concentration defects and it is a severe complication of sepsis because it increases the mortality rate. Inhibition of NF-kappaB activation has been suggested to provide a useful strategy for the treatment of septic shock. However, the impact on sepsis-induced ARF is still unclear. Therefore, we examined the effect of pyrrolidine dithiocarbamate (PDTC) and of small interfering RNA (siRNA) silencing NF-kappaB p50/p105 on sepsis-induced downregulation of vasopressin V(2) receptors and aquaporin (AQP)-2 channels using a cecal ligation and puncture (CLP) mouse model. CLP caused a time-dependent downregulation of renal vasopressin V(2) receptor and of AQP2 expression without alterations in plasma vasopressin levels. Renal activation of NF-kappaB in response to CLP was attenuated by PDTC pretreatment, which also attenuated the downregulation of V(2) receptor and AQP2 expression. Furthermore, a strong nuclear staining for the NF-kappaB p50 subunit throughout the whole kidney in response to CLP was observed. siRNA against NF-kappaB p50 attenuated the CLP-induced nuclear translocation of the p50 subunit and the CLP-induced downregulation of V(2) receptor and AQP2 expression. Additionally, PDTC and siRNA pretreatment inhibited the CLP-induced increase in renal TNF-alpha and IL-1beta concentration and NOS-2 mRNA abundance. Moreover, PDTC and siRNA pretreatment ameliorated CLP-induced hypotension and ARF. Our findings suggest that NF-kappaB activation is of importance for the downregulation of AQP2 channel and vasopressin V(2) receptor expression during sepsis. In addition, our data indicate that NF-kappaB inhibition ameliorates sepsis-induced ARF.
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PMID:Inhibition of NF-kappaB ameliorates sepsis-induced downregulation of aquaporin-2/V2 receptor expression and acute renal failure in vivo. 1982 75

In spite of significant progress in pharmacotherapy the incidence of newly diagnosed cases of cardiovascular diseases and cardiovascular morbidity is alarmingly high. Treatment of hypertension or heart failure still remains a serious challenge. Continuous attempts are made to identify the mechanisms that decide about susceptibility to pathogenic factors, and to determine effectiveness of a specific therapeutic approach. Coincidence of cardiovascular diseases with metabolic disorders and obesity has initiated intensive research for their common background. In the recent years increasing attention has been drawn to disproportionately greater number of depressive disorders and susceptibility to stress in patients with coronary artery disease. An opposite relationship, i.e. a greater number of sudden cardiovascular complications in patients with depression, has been also postulated. Progress in functional neuroanatomy and neurochemistry provided new information about the neural network responsible for regulation of cardiovascular functions, metabolism and emotionality in health and under pathological conditions. In this review we will focus on the role of neuromodulators and neurotransmitters engaged in regulation of the cardiovascular system, neuroendocrine and metabolic functions in health and in pathogenesis of cardiovascular diseases and obesity. Among them are classical neurotransmitters (epinephrine and norepinephrine, serotonin, GABA), classical (CRH, vasopressin, neuropeptide Y) and newly discovered (orexins, apelin, leptin IL-1beta, TNF-alpha, ghrelin) neuropeptides, gasotransmitters, eicozanoids, endocannabinoids, and some other compounds involved in regulation of neuroendocrine, sympatho-adrenal and parasympathetic nervous systems. Special attention is drawn to those factors which play a role in immunology and inflammatory processes. Interaction between various neurotransmitter/neuromodulatory systems which may be involved in integration of metabolic and cardiovascular functions is analyzed. The survey gives evidence for significant disturbances in release or action of the same mediators in hypertension heart failure, obesity, diabetes mellitus, metabolic syndrome, starvation, chronic stress, depression and other psychiatric disorders. With regard to the pathogenic background of the cardiovascular diseases especially valuable are the studies showing inappropriate function of angiotensin peptides, vasopressin, CRH, apelin, cytokines and orexins in chronic stress, cardiovascular and metabolic diseases. The studies surveyed in this review suggest that multiple brain mechanisms interact together sharing the same neural circuits responsible for adjustment of function of the cardiovascular system and metabolism to current needs.
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PMID:Brain and cardiovascular diseases: common neurogenic background of cardiovascular, metabolic and inflammatory diseases. 2108 94

At present, a constant progress in pathophysiology understanding and treatment of the chronic heart failure (CHF) is arising. The current CHF pharmacotherapy is complex, involving factors affecting the renin-angiotensin-aldosterone system (RAAS), beta-blockers, diuretics and vasodilatators. There are also significant efforts to introduce in CHF pharmacology novel therapeutic strategies, based on the other neurohormonal mechanisms activated in CHF. They include vasopressin receptor antagonists (VRA; vaptans), endothelin receptor antagonists (ERA; sentans), agents relating to the natriuretic peptides system (neutral endopeptidase inhibitors; NEPI and vasopeptidase inhibitors; VPI) and anticytokines agents (anti TNF-alpha immunoglobulin or TNF-alpha scavenger receptor; Etanercept). In this article we briefly describe the modem approach to CHF systemic treatment.
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PMID:Neuroendocrine activation as a target of modern chronic heart failure pharmacotherapy. 2164 84


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