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)

The status of the renin-angiotensin-aldosterone system and the time course of vasopressin levels were studied in patients with an implanted cardiostimulator. Activation of plasma renin due to renal hypoperfusion in an inadequate stimulation was demonstrated to be followed by a rise in aldosterone and vasopressin concentrations and by an increase in blood volumes. Activation of angiotensin II and vasopressin resulted in higher peripheral resistance. Altered humoral regulation of the circulation retained 6-12 months after cardiostimulator implantation, by maintaining myocardial overload with volume and resistance.
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PMID:[The role of the renin-angiotensin-aldosterone system and vasopressin in the development of heart failure during continuous electric stimulation of the heart]. 233 66

The effects of 30-min intravenous infusions of 8-arginine vasopressin (AVP) and angiotensin-(1,8)-octapeptide (ANG II) to conscious dogs were studied by measurements of systolic (SABP), mean (MABP), and diastolic arterial blood pressures, central venous pressure (CVP), heart rate (HR), and plasma concentrations of vasopressin (pAVP). Infusion of AVP at six rates (0.4-12.8 ng X min-1 X kg-1) raised mean pAVP by 5-490 pg/ml and increased CVP by 2-10 cmH2O. HR decreased and arterial pressures increased with infusion rates of 1.6-12.8 ng X min-1 X kg-1. However, the increase in SABP was only transient. ANG II increased all arterial pressures; however, it barely changed CVP and did not change HR or pAVP. It is concluded that 1) AVP can elevate MABP without changes in SABP, 2) the effects of AVP on arterial pressures are buffered within 5-15 min, 3) CVP can be increased by doses of AVP that do not affect arterial pressures, and 4) the pressor activity is independent of the presence of ANG II. The results confirm that the cardiovascular response to vasopressin is qualitatively different from that elicited by ANG II.
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PMID:Effects on intravascular pressures of vasopressin and angiotensin II in dogs. 636 39

The present study determined the plasma ACTH and corticosterone responses of the rat to acute local inflammation induced by the im injection of a small volume of turpentine. In response to tissue injury, ACTH and corticosterone concentrations rose rapidly, peaked at 1 h, and returned toward basal values by 3 h after turpentine injection. As acute inflammation developed, plasma interleukin-6 bioactivity increased significantly, and ACTH and corticosterone levels exhibited a secondary rise. These secondary responses were maximum 6-12 h after turpentine administration, persisted for 20-28 h, and were statistically significant regardless of the normal circadian variations in ACTH and corticosterone secretion. Injection of neutralizing anti-CRF antiserum 7 h after turpentine produced a complete reversal, whereas antiarginine vasopressin (anti-AVP) caused a partial (approximately 40%) inhibition, of inflammation-induced ACTH secretion. The cyclooxygenase inhibitor, ibuprofen (10 mg/kg, iv), like CRF antiserum, rapidly and completely reversed turpentine-induced ACTH secretion. In contrast, the nitric oxide synthase inhibitor, Nw-nitro-L-arginine methyl ester (30 mg/kg, iv), produced a significant enhancement of the ACTH response within 30 min of its injection. Measurement of plasma interleukin-6 bioactivity and fever showed that neither anti-CRF, anti-AVP, ibuprofen, nor Nw-nitro-L-arginine methyl ester acutely influenced the local inflammatory process itself, suggesting that these agents interacted directly with the hypothalamo-pituitary-adrenal axis. These data demonstrate that the ACTH response to local inflammation is mediated by synergistic actions of CRF and AVP, and that both stimulatory (PGs) and inhibitory (nitric oxide) intermediates regulate this response.
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PMID:Corticotropin-releasing factor, vasopressin, and prostaglandins mediate, and nitric oxide restrains, the hypothalamic-pituitary-adrenal response to acute local inflammation in the rat. 859 89

A major concern during the early postoperative period after surgical resection of optic chiasmatic gliomas is the derangement of sodium and water metabolism which may add to the morbidity of the procedure. The purpose of this study was to characterize the abnormalities of water and sodium metabolism in children with optic chiasmatic gliomas treated surgically at British Columbia's Children's Hospital and to identify therapeutic modalities which might prevent or ameliorate the development of these complications. A retrospective chart review of children with optic/chiasmatic gliomas undergoing operations on the tumor was performed and the pre- and postoperative radiographs reviewed by an independent neuroradiologist. There were 11 patients who underwent 13 operations for either resection (n = 9) or biopsy (n = 4) of their optic chiasm tumor. The extent of resection in patients undergoing more than simple biopsy ranged from 83 to 99%, and all patients with resection had exophytic tumor extending into the hypothalamus. Postoperative syndrome of inappropriate antidiuretic hormone secretion (SIADH) and/or diabetes insipidus occurred after 8 of the 9 tumor resections and was associated with significant morbidity. No disturbance of water metabolism occurred after biopsy only. In patients with SIADH, the urinary sodium level rose markedly 6-12 h prior to the development of hyponatremia, and it was concluded that this was a valuable predictor of impending hyponatremia. Replacement of urine output was noted to be the most reliable way to avoid rapid fluctuations in serum sodium and to avoid the morbidity of diabetes insipidus or SIADH and is recommended in the postsurgical patients who cannot regulate fluid intake.
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PMID:Abnormalities of water metabolism after surgery for optic/chiasmatic astrocytomas in children. 973 44

Mammalian circadian pacemaker is located in suprachiasmatic nuclei (SCN) of the hypothalamus. The pacemaker is entrained by light-dark cycle; the photic information is transmitted primarily via the retino-hypothalamic tract (RHT). The main neurotransmitter of the tract is glutamate. RHT fibers end on the ventrolateral part of the nucleus, where vasoactive intestinal peptide (VIP)-immunopositive neurons are localized. They send their axons into dorsomedial SCN, where most of the vasopressinergic (AVP) neurones are located. The AVP neurons retain the clock-like properties in vitro. Vasopressin release from the cultured neurons shows circadian rhythm peaking in the middle of subjective day. VIP induces phase-shifts of the rhythm, magnitude and direction of the shift depending on timing of the application. VIP applied 6-12 h before the peak of vasopressin rhythm induces advances, application 4-8 h after the peak induces delays. The lowest concentration required to induce the phase-shift is 30 nM, further increase of the concentration does not affect the magnitude of the shift. In contrast, glutamate has no effect on the phase of vasopressin rhythm, although in high concentrations it transiently stimulates vasopressin release. The data indicate that the vasopressinergic cells in the SCN contain circadian oscillators, whose rhythms run mutually synchronized in our cultures. VIP acts directly on the vasopressinergic cells to shift the phase of their pacemakers; glutamate has no such effect presumably because in vivo it acts through the VIP-ergic cells but the neuronal network is altered after the dissociation of the cells.
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PMID:In vitro entrainment of the circadian rhythm of vasopressin-releasing cells in suprachiasmatic nucleus by vasoactive intestinal polypeptide. 1098 51

It is extremely difficult to detect guanine nucleotide exchange or hydrolysis stimulated by receptors which couple to G(s)alpha. Furthermore, G(s)alpha is largely resistant to the GTPase-activating properties of RGS proteins. Coexpression of the vasopressin V(2) receptor with a series of chimeric G protein alpha subunits in which the C-terminal 6-12 amino acids of G(i1)alpha were replaced with the equivalent sequence of G(s)alpha allowed robust vasopressin-stimulated [(35)S]GTPgammaS binding. Vasopressin did not stimulate the GTPase activity of fusion proteins between the V(2) receptor and either G(s)alpha or G(i1)alpha. However, it produced a concentration-dependent stimulation of V(max) for a V(2) receptor-G(i1)alpha/Gs6alpha fusion protein. This construct bound [(3)H]vasopressin with high affinity and this was competed by other ligands with rank order anticipated for the V(2) receptor. RGS1 enhanced vasopressin stimulation of V(2) receptor-G(i1)alpha/G(s)6alpha in a concentration-dependent manner. RGS-GAIP was substantially less potent. Enzyme kinetic analysis demonstrated that RGS1 increased both V(max) of the GTPase activity and the observed K(m) for GTP, consistent with RGS1 accelerating the rate of GTP hydrolysis of the chimeric G protein, whereas the agonist vasopressin accelerates guanine nucleotide exchange. This approach provides a sensitive assay for V(2) receptor agonist ligands and may be amenable to many other G(s)alpha-coupled receptors.
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PMID:Engineering a V(2) vasopressin receptor agonist- and regulator of G-protein-signaling-sensitive G protein. 1177 13

Primary nocturnal enuresis (PNE) is the most common type of nocturnal enuresis in children, but its etiology remains unclear. Recent studies indicated the differences in urinary electrolytes in enuretic children, and stressed the existence of a renal tubular maturation defect. In this study, 30 children (aged 6-12 years) with PNE were investigated in comparison with 18 healthy controls. We evaluated plasma antidiuretic hormone, electrolytes, 24-h urine volume, osmolarity, and urinary electrolytes. Unlike other studies, we firstly assessed the plasma and urinary adrenomedullin (AM) and total nitrite levels, a stable product of nitric oxide (NO), and investigated their relationship with urinary electrolytes. The plasma AM and total nitrite levels were significantly lower than controls. Urine volume (24-h) and potassium excretion were higher than in controls. However, 24-h urinary osmolarity and excretion of AM were significantly lower than in controls. Our results indicate that there may be a problem in renal regulation of potassium in children with PNE. Although decreased levels of AM and total nitrite may be a compensatory response to abnormal potassium and water excretion, further investigations are required to exclude whether the renal synthesis of AM and NO are also deficient in these children.
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PMID:Adrenomedullin and nitrite levels in children with primary nocturnal enuresis. 1218 69

Traumatic brain injuries (TBI) are common occurrences in childhood, often resulting in long term, life altering consequences. Research into endocrine sequelae following injury has gained attention; however, there are few studies in children. This paper reviews the pathophysiology and current literature documenting risk for endocrine dysfunction in children suffering from TBI. Primary injury following TBI often results in disruption of the hypothalamic-pituitary-adrenal axis and antidiuretic hormone production and release, with implications for both acute management and survival. Secondary injuries, occurring hours to weeks after TBI, result in both temporary and permanent alterations in pituitary function. At five years after moderate to severe TBI, nearly 30% of children suffer from hypopituitarism. Growth hormone deficiency and disturbances in puberty are the most common; however, any part of the hypothalamic-pituitary axis can be affected. In addition, endocrine abnormalities can improve or worsen with time, having a significant impact on children's quality of life both acutely and chronically. Since primary and secondary injuries from TBI commonly result in transient or permanent hypopituitarism, we conclude that survivors should undergo serial screening for possible endocrine disturbances. High indices of suspicion for life threatening endocrine deficiencies should be maintained during acute care. Additionally, survivors of TBI should undergo endocrine surveillance by 6-12 months after injury, and then yearly, to ensure early detection of deficiencies in hormonal production that can substantially influence growth, puberty and quality of life.
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PMID:Update of Endocrine Dysfunction following Pediatric Traumatic Brain Injury. 2628 47