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)

Various lines of evidence implicate impaired renal function as an important prognostic indicator in patients with congestive heart failure (CHF). Conventional diuretics may aggravate renal dysfunction and can result in neurohumoral activation. Evolving new therapeutic strategies that enhance renal function include administration of B-type natriuretic peptide, adenosine and vasopressin antagonists, and ultrafiltration methods. Prospective studies are needed to evaluate whether these new renal-enhancing strategies will improve patient outcome in CHF.
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PMID:Cardiorenal syndrome in decompensated heart failure: prognostic and therapeutic implications. 1603 34

Hyponatremia and increased urine output after calvarial remodeling have been noted in pediatric patients with craniosynostosis. If not treated properly, patients develop hypoosmotic conditions that can lead to cerebral edema, increased intracranial pressure, and collapsed circulation. Postoperative hyponatremia after central nervous system surgery is considered as the syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Recently, however, cerebral salt wasting syndrome (CSWS) instead of SIADH has been reported frequently. CSWS is associated with a decreased serum sodium level, increased urinary sodium level, increased urine output, decreased ECF volume, increased atrial natriuretic peptide (ANP) level, and increased brain natriuretic peptide (BNP) level. We experienced nine patients with craniosynostosis who underwent calvarial remodeling. By postoperative day 1, the ANP and BNP levels increased by 3-6 folds compared with the preoperative levels. They returned to the normal levels by postoperative day 5. The ADH level was within the normal range even after operation. The urinary sodium level increased in all patients by postoperative day 1 and 3. But the serum sodium level, and serum and urine osmolarity were normal due to appropriate replacement of sodium and fluid. After calvarial remodeling, the potential development of CSWS should be considered and distinguished from SIADH. The patients with CSWS require normal saline resuscitation and should prophylactically receive normal saline.
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PMID:Cerebral salt wasting syndrome after calvarial remodeling in craniosynostosis. 1622 64

We report the development of recurrent hyponatremia after intrathecal methotrexate that was not associated with elevated levels of antidiuretic hormone. We speculate that a central nervous system natriuretic peptide may be involved in the pathogenesis of the naturesis following intrathecal methotrexate.
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PMID:Recurrent hyponatremia after intrathecal methotrexate not related to antidiuretic hormone: is a natriuretic peptide activated? 1641 63

Cardiopulmonary bypass surgery has been linked with a number of postoperative complications. One of the frequently reported physiological alterations is the relative diuresis seen in the immediate post-op period. Rarely reported though is the development of full-blown diabetes insipidus in such patients. The etiology is unknown and has only been hypothesized in the past. We present the clinical course of a 54 year old male who developed transient diabetes insipidus post bypass surgery with subsequent recovery following exogenous vasopressin administration. The physiological alteration leading to the development of diabetes insipidus in a small fraction of bypass patients remains unknown. We propose that the variation in natriuretic peptide levels in the post-bypass period could account for the transient event.
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PMID:A case of transient diabetes insipidus following cardiopulmonary bypass. 1643 83

A case of hyponatraemia associated with subarachnoid haemorrhage is presented. The provisional diagnosis of an inappropriate antidiuresis was made and treatment with fluid restriction was instituted. However the patient continued to deteriorate as the diuresis continued and the hyponatraemia worsened, resulting in hypovolaema. The salt wasting syndrome was subsequently diagnosed and saline and fludrocortisone (0.2 mg/day) was initiated, reducing the renal salt loss, increasing the plasma sodium and improving the neurological status of the patient. Cerebral salt wasting syndrome is an important and under-recognised cause of hyponatraemia in neurosurgical patients, particularly in patients with subarachnoid hemorrhage. It is essential to differentiate it from the syndrome of inappropriate antidiuretic hormone secretion to avoid complications of hypovolaemia and reduced cerebral perfusion as illustrated by this case. Brain natriuretic peptide may be responsible for this syndrome although this requires further investigation.
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PMID:Cerebral salt wasting syndrome: a case report. 1660 1

Diuretics are an integral part of the management of symptomatic heart failure. Although they have been used for several decades, there is still some ambiguity and confusion regarding the outcome and the optimal way of using these common agents. There are no large-scale randomized controlled trials that have evaluated the effect of diuretics on mortality and long-term morbidity in diastolic and systolic dysfunction. Nonetheless, in short-term studies furosemide has demonstrated to reduce symptomatic congestive heart failure and hospitalization, and to improve exercise capacity in the setting of systolic dysfunction. In this review, the classes, sites of action and renal effect of diuretics are reviewed and the various indications, optimal doses and recommendations on effective use and disuse are discussed. Namely, this review addresses the effects of emerging diuretic agents such as eplerenone--a selective mineral corticoid receptor antagonist, nesiritide--a brain natriuretic peptide-recombinant, and conivaptan--a vasopressin antagonist, in attempt to provide an update on current knowledge, even though adequate clinic data are not available for all agents.
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PMID:[Use of diuretics in congestive heart failure: renal effects]. 1663 94

Fish endocrinologists are commonly motivated to pursue their research driven by their own interests in these aquatic animals. However, the data obtained in fish studies not only satisfy their own interests but often contribute more generally to the studies of other vertebrates, including mammals. The life of fishes is characterized by the aquatic habitat, which demands many physiological adjustments distinct from the terrestrial life. Among them, body fluid regulation is of particular importance as the body fluids are exposed to media of varying salinities only across the thin respiratory epithelia of the gills. Endocrine systems play pivotal roles in the homeostatic control of body fluid balance. Judging from the habitat-dependent control mechanisms, some osmoregulatory hormones of fish should have undergone functional and molecular evolution during the ecological transition to the terrestrial life. In fact, water-regulating hormones such as vasopressin are essential for survival on the land, whereas ion-regulating hormones such as natriuretic peptides, guanylins and adrenomedullins are diversified and exhibit more critical functions in aquatic species. In this short review, we introduce some examples illustrating how comparative fish studies contribute to general endocrinology by taking advantage of such differences between fishes and tetrapods. In a functional context, fish studies often afford a deeper understanding of the essential actions of a hormone across vertebrate taxa. Using the natriuretic peptide family as an example, we suggest that more functional studies on fishes will bring similar rewards of understanding. At the molecular level, recent establishment of genome databases in fishes and mammals brings clues to the evolutionary history of hormone molecules via a comparative genomic approach. Because of the functional and molecular diversification of ion-regulating hormones in fishes, this approach sometimes leads to the discovery of new hormones in tetrapods as exemplified by adrenomedullin 2.
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PMID:Contribution of comparative fish studies to general endocrinology: structure and function of some osmoregulatory hormones. 1690 50

Ovarian hyperstimulation syndrome is a complication of the ovulation stimulation, most commonly by gonadotrophins. It frequently occurs in patients included in in vitro fertilization program. The exact mechanism of development of this syndrome has not been elucidated yet. The basic pathogenic mechanism of development of this syndrome is vasodilation of the ovarian blood vessels. Dilated ovarian blood vessels become permeable. Permeability of dilated ovarian blood vessels is more increased by released ovarian mediators. Due to increased permeability of the blood vessels, there is leakage of the intravascular fluid into the extravascular areas resulting in hypovolemia, edema and ascites. Hypovolemia leads to renal perfusion decrease. Increased salt and water reabsorption occurs in the renal tubules so oliguria develops. Decreased arterial blood volume results in stimulation of the renin-angiotensin-aldosterone system, the sympathetic nervous system as well as the antidiuretic hormone. The activation of the sympathetic nervous system via beta adrenergic receptors stimulates renin release and aldosterone secretion. Renin stimulates release of angiotensin I which transforms into angiotensin II. Angiotensin II increases the pressure and stimulates aldosterone secretion. In patients with this syndrome, there is an elevated plasma endothelin and natriuretic peptide level. Endothelin is an important vasoconstrictor. It increases secretion of renin, aldosterone, catecholamines, antidiuretic hormone, and atrial natriuretic peptide, and enhances the vasoconstrictive effect of norepinephrine and angiotensin II. The platelet number increase together with the elevated factor of blood coagulation and hyperviscosity in a severe form of this syndrome may result in development of intravascular thrombosis. The treatment consists of maintenance of circulatory function, i.e. the increase of effective arterial blood volume by applying the plasma volume expanders.
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PMID:[The significance of the ovarian arteriolar vasodilatation in pathogenesis of the ovarian hyperstimulation syndrome]. 1700 17

The heart adapts to increased pressure overload by hypertrophic growth of terminally differentiated cardiomyocytes. At the genetic level, the hypertrophic response is characterized by the reprogramming of gene expression, i.e. upregulation of immediate early genes, natriuretic peptide genes and genes encoding structural proteins. In the present study, we characterized the early changes in gene expression with cDNA expression arrays in response to increase in blood pressure produced by arginine8-vasopressin infusion (0.05 microg/kg/min, i.v.) for 30 min and 4 h in conscious normotensive rats. Expression profiling revealed differential expression of 14 genes in the left ventricle, and several novel factors of immediate early genetic response to pressure overload were identified, such as growth arrest and DNA damage inducible protein 45 (GADD45alpha), epidermal fatty acid-binding protein (E-FABP) and Bcl-X. Administration of angiotensin II (Ang II) for 6 h by osmotic minipumps also increased left ventricular GADD45alpha, E-FABP and Bcl-X gene expression. Furthermore, the induction of GADD45alpha and Bcl-X gene expression by Ang II was blocked by angiotensin II type 1 receptor antagonist losartan. In summary, our analysis provided new insights into the pathogenesis of pressure overload-induced hypertrophy by suggesting the existence of novel regulators of the immediate early gene expression program.
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PMID:Early left ventricular gene expression profile in response to increase in blood pressure. 1747 29

Urocortin 1 (Ucn1) may be involved in the pathophysiology of heart failure (HF), but the impact of Ucn1 administration on progression of the disease is unknown. The aim of this study was to investigate the effects of Ucn1 in sheep from the onset of cardiac overload and during the subsequent development of HF. Eight sheep underwent two 4-day periods of HF induction by rapid left ventricular pacing (225 beats/min) in conjunction with continuous infusions of Ucn1 (0.1 microg.kg(-1).h(-1) iv) and a vehicle control (0.9% saline). Compared with control, Ucn1 attenuated the pacing-induced decline in cardiac output (2.43 +/- 0.46 vs. 3.70 +/- 0.89 l/min on day 4, P < 0.01) and increases in left atrial pressure (24.9 +/- 1.0 vs. 11.9 +/- 1.1 mmHg, P < 0.001) and peripheral resistance (38.7 +/- 9.4 vs. 25.2 +/- 6.1 mmHg.l(-1).min, P < 0.001). Ucn1 wholly prevented increases in plasma renin activity (4.02 +/- 1.17 vs. 0.87 +/- 0.1 nmol.l(-1).h(-1), P < 0.001), aldosterone (1,313 +/- 324 vs. 413 +/- 174 pmol/l, P < 0.001), endothelin-1 (3.8 +/- 0.5 vs. 2.0 +/- 0.1 pmol/l, P < 0.001), and vasopressin (10.8 +/- 4.1 vs. 1.8 +/- 0.2 pmol/l, P < 0.05) during pacing alone and blunted the progressive increases in plasma epinephrine (2,132 +/- 697 vs. 1,250 +/- 264 pmol/l, P < 0.05), norepinephrine (3.61 +/- 0.73 vs. 2.07 +/- 0.52 nmol/l, P < 0.05), and atrial (P < 0.05) and brain (P < 0.01) natriuretic peptide levels. Ucn1 administration also maintained urine sodium excretion (0.75 +/- 0.34 vs. 1.59 +/- 0.50 mmol/h on day 4, P < 0.05) and suppressed pacing-induced declines in creatinine clearance (P < 0.05). These findings indicate that Ucn1 treatment from the onset of cardiac overload has the ability to repress the ensuing hemodynamic and renal deterioration and concomitant adverse neurohumoral activation, thereby delaying the development of overt HF. These data strongly support a use for Ucn1 as a therapeutic option early in the course of the disease.
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PMID:Urocortin 1 administration from onset of rapid left ventricular pacing represses progression to overt heart failure. 1752 50


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