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)

To examine the pathophysiological mechanisms in transgenic rats carrying the murine Ren-2d renin gene, we studied atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) gene expression and secretion in 12-week-old hypertensive TGR(mREN-2)27 and normotensive Sprague-Dawley rats. Hypertension and marked left ventricular hypertrophy in TGR(mREN-2)27 rats were associated with high baseline plasma levels of immunoreactive ANP (148 +/- 18 versus 34 +/- 3 pmol/L, hypertensive versus normotensive rats; P < .001), whereas plasma immunoreactive BNP levels did not differ significantly between the strains (19 +/- 4 versus 12 +/- 3 pmol/L, P = .06). ANP mRNA and immunoreactive ANP levels in the left ventricular endocardial and epicardial layers in TGR(mREN-2)27 rats were about 20 to 40 times higher (P < .001) than those in normotensive rats. There were no statistically significant differences between atrial and ventricular BNP mRNA levels, but left ventricular immunoreactive BNP concentrations were twofold higher in hypertensive TGR(mREN-2)27 than in normotensive rats. Infusion of [Arg8]-vasopressin (0.05 microgram/kg per minute IV, for 2 hours) in normotensive rats produced rapid increases (twofold, P < .05 to .01) in left ventricular BNP mRNA and immunoreactive BNP levels, whereas ventricular BNP mRNA and peptide levels did not change significantly in hypertensive rats. The increase in left atrial BNP mRNA levels in response to acute pressure overload was also significantly smaller in the hypertensive than normotensive rats (3.5-fold versus 5.2-fold, P < .01). Furthermore, the proportional but not absolute (in picomoles per liter) increase in plasma immunoreactive ANP was smaller in transgenic rats in response to acute saline and [Arg8]-vasopressin infusions (0.9% NaCl: 1.9-fold increase versus 4.4-fold increase in normotensive rats, P < .001; [Arg8]-vasopressin: 2.2-fold versus 4.8-fold increase, P < .001). These results show that baseline and cardiac overload-induced increases in BNP synthesis are markedly attenuated in transgenic rats carrying the murine Ren-2d renin gene. In addition, acute volume and pressure overload produced a smaller proportional increase in ANP secretion in hypertensive rats than normotensive rats. These alterations in the natriuretic peptide system may contribute to the pathogenesis of hypertension and cardiovascular complications in the TGR(mREN-2)27 rat.
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PMID:Synthesis and secretion of natriuretic peptides in the hypertensive TGR(mREN-2)27 transgenic rat. 895 88

Cardiodilatin/atrial natriuretic peptide (CDD/ ANP) is a hormone system of great clinical importance. The prohormone CDD/ANP-1-126 is a peptide synthesized in the heart and cleaved during exocytosis into the circulating form CDD/ANP-99-126. Urodilatin (CDD/ ANP-95-126) is a homologue natriuretic peptide that differs from CDD/ANP-99-126 by four amino acids. Whereas CDD/ANP-99-126 circulates in blood plasma and is not excreted into the urine, urodilatin is detected only in urine. Urodilatin exerts its renal effects in a paracrine fashion. After its secretion from cells in the distal tubule, it interacts with luminally located receptors in the collecting duct, resulting in increased diuresis and natriuresis. Results suggest that urodilatin plays an important role in the physiologic regulation of fluid-balance and sodium homeostasis. Pharmacology studies reveal significant differences when urodilatin and CDD/ANP-99-126 are given intravenously, showing that stronger diuresis and natriuresis are induced by urodilatin as compared with those induced by CDD/ANP-99-126. Clinical studies indicate the prophylactic and therapeutic effect of urodilatin in patients suffering from acute renal failure following heart and liver transplantation. A significant reduction in requirements for hemodialysis/hemofiltration can be achieved using urodilatin. Postobstructive diuresis and natriuresis is probably due to a defective urinary concentrating mechanism and is usually resistant to treatment with antidiuretic hormone. The distal tubule and collecting duct have often been considered to be the site of altered sodium and water excretion following relief of obstruction. Since circulating CDD/ANP-99-126 levels are markedly elevated during obstruction and decrease upon relief of the obstruction, natriuretic peptides may play an important role in this clinical feature. On the basis of recent findings attributing an important role in sodium homeostasis to urodilatin in contrast to CDD/ANP-99-126, future studies have to clarify whether urodilatin, not CDD/ANP-99-126, might be responsible for the altered renal sodium excretion observed in postobstructive diuresis. In the past decade a considerable amount of research has led to the identification and characterization of hormones of the natriuretic peptide family [13]. These peptides are involved in the regulation of salt and water homeostasis. The prototype of the natriuretic hormones is cardiodilatin/atrial natriuretic peptide (CDD/ANP), or A-type natriuretic peptide. CDD/ANP is primarily produced in the heart [6]. It is synthesized as a precursor molecule, CDD/ ANP-1-126, in specific granules in atrial myoendocrine cells [15]. The prohormone, upon appropriate stimuli for release, is cleaved into the C-terminus CDD/ANP-99-126 and excreted into the circulation via exocytosis [16]. Further members of the natriuretic peptide family are brain natriuretic peptide (BNP, or B-type natriuretic peptide) [45] and C-type natriuretic peptide (CNP) [46]. All the members of this family share many common features, including tissue distribution of gene expression, biosynthetic pathways, and pharmacologic effects in target organs [13,26]. The main biologic effects of these hormones are natriuresis, diuresis, and vasodilation [5, 6, 14, 22], but these vary among the individual peptides. Natriuretic effects such as increased glomerular filtration, inhibition of aldosterone production, and secretion result from direct inhibition of sodium absorption in the collecting duct. Urodilatin (INN: Ularitide) is a member of the natriuretic peptide family, discovered in 1988 by Schulz-Knappe et al. [43]. This hormone is presumably synthesized in the kidney and exerts potential paracrine renal effects [17]. Results of clinical phase I-II trials suggest a potent therapeutic effect of urodilatin in the treatment of acute renal failure in patients following organ transplantation [4, 27, 33].
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PMID:The renal paracrine peptide system--possible urologic implications of urodilatin. 898 39

Brain natriuretic peptide (BNP) messenger RNA was measured with a semiquantitative method from heart auricles and ventricles of vasopressin-deficient Brattleboro rats (DI) and from desmopressin treated Brattleboro rats (DI + DDAVP). Desmopressin had been injected peripherally and Long-Evans rats (LE) served as controls. The 3-day substitution treatment had shifted the fluid balance of DI almost to that of LE. In the present study, the amount of BNP mRNA, normalized to the glyceraldehyde-3-phosphate dehydrogenase mRNA content, was constant in all three groups in the right auricle. No changes were when the right auricular and left auricular mRNA levels were compared within each group. In the left auricle, desmopressin treatment increased significantly (P < 0.05) the amount of BNP mRNA compared with that of LE rats (from 1.09 +/- 0.21, n = 7 to 1.72 +/- 0.17, n = 8, arbitrary units). In all groups, the left ventricle had significantly (P < 0.05) higher mRNA content than the right ventricle (LE: 2.24 +/- 0.23 vs. 0.67 +/- 0.13, n = 6; DI: 2.30 +/- 0.60 vs. 0.33 +/- 0.05, n = 8; DI + DDAVP: 2.36 +/- 0.29 vs. 0.37 +/- 0.07, n = 10). In the right ventricle, both DI and DI + DDAVP rats had significantly (P < 0.05) lower mRNA content than LE rats (0.33 +/- 0.5 vs. 0.67 +/- 0.13 and 0.37 +/- 0.07 vs. 0.67 +/- 0.13, respectively). To conclude, these findings suggest that brain natriuretic peptide gene expression dissociates from, or rapidly adapts to, the chronic effects of peripheral desmopressin treatment which have shifted the fluid balance to almost normal in Brattleboro rats. The left ventricular pressure appears to regulate the brain natriuretic peptide gene expression.
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PMID:Brain natriuretic peptide (BNP) gene expression in the heart of vasopressin-deficient Brattleboro rats. 907 57

Changes in the redox state of liver mitochondria were investigated by measuring the arterial ketone body ratio (acetoacetate/3-hydroxybutyrate: AKBR) in nine healthy volunteers (eight males and one female, mean age 38.4 +/- 5.0 years) during exercise. The correlation between the changes in AKBR and levels of various hormones controlling energy metabolism was also investigated. Subjects participated in symptom-limited exercise test using the ramping bicycle ergometer with expired gas analysis, blood pressure and 12 lead electrocardiogram monitoring. Anaerobic threshold by gas exchange parameters (ATge) was determined from the expired gas data with the v-slope method. AKBR, glucose, non-esterified fatty acid (NEFA) and lactate were measured in arterial plasma samples. Catecholamines (epinephrine, norepinephrine, dopamine), insulin, glucagon, antidiuretic hormone (ADH), growth hormone (GH), thyroid-stimulating hormone (TSH), triiodothyronine (T3), thyroxine (T4), human-atrial natriuretic peptide (hANP) and brain natriuretic peptide (BNP) were measured in venous plasma samples. AKBR was gradually decreased by exercise from the resting value of 1.82 +/- 0.20. AKBR reduction was potentiated after ATge to 0.93 +/- 0.18 (p < 0.01 vs rest) at peak exercise. AKBR was further decreased during recovery to the minimum value of 0.70 +/- 0.06 (p < 0.01) at 6 min in the recovery phase. AKBR then began to increase and reached 0.95 +/- 0.07 30 min after peak exercise. Epinephrine increased from 45.9 +/- 11.0 to 210 +/- 75 pg/ml (p < 0.01), norepinephrine increased from 348 +/- 52 to 1,277 +/- 111 pg/ml (p < 0.01), and dopamine increased from 13.0 +/- 1.9 to 25.0 +/- 2.5 pg/ml (p < 0.01) between rest and peak exercise, respectively. Insulin decreased from 22.0 +/- 3.5 to 14.2 +/- 2.1 pg/ml (p < 0.05). No significant change was observed in glucagon, ADH, GH, TSH, T3, T4, hANP or BNP. Glucose decreased from 124 +/- 9 to 84 +/- 8 mg/dl (p < 0.05), whereas NEFA increased from 94 +/- 10 to 190 +/- 66 mg/dl (p < 0.05). A negative correlation was observed between AKBR and lactate (r = -0.41, p < 0.001). These results indicate that hepatic adenosine triphosphate production is promoted as energy demand increases by exercise, and maximizes early in the recovery phase when hepatic energy demand is maximum due to active gluconeogenesis. The levels of catecholamines, insulin and lactate contribute to the control of liver energy metabolism.
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PMID:[Evaluation of changes in hepatic energy metabolism during exercise by ketone body ratio in humans]. 912 Jul 98

The levels of adrenomedullin (ADM), a newly discovered vasodilating and natriuretic peptide, are elevated in plasma and ventricular myocardium in human congestive heart failure suggesting that cardiac synthesis may contribute to the plasma concentrations of ADM. To examine the time course of induction and mechanisms regulating cardiac ADM gene expression, we determined the effect of acute and short-term cardiac overload on ventricular ADM mRNA and immunoreactive ADM (ir-ADM) levels in conscious rats. Acute pressure overload was produced by infusion of arginine8-vasopressin (AVP, 0.05 microg/kg/min, i.v.) for 2 h into 12-week-old hypertensive TGR(mREN-2)27 rats and normotensive Sprague-Dawley (SD) rats. Hypertension and marked left ventricular hypertrophy were associated with 2.2-times higher ir-ADM levels in the left ventricular epicardial layer (178 +/- 36 vs. 81 +/- 23 fmol/g, P<0.05) and 2.6-times higher ir-ADM levels in the left ventricular endocardial layer (213 +/- 23 vs. 83 +/- 22 fmol/g, P<0.01). The infusion of AVP for 2 h in normotensive rats produced rapid increases in the levels of left ventricular ADM mRNA (epicardial layer: 1.6-fold, P<0.05) and ir-ADM (endocardial layer: from 83 +/- 22 to 140 +/- 12 fmol/g, P<0.05), whereas ventricular ADM mRNA and ir-ADM levels did not change significantly in hypertensive rats. Short-term cardiac overload, induced by administration of angiotensin II (33.3 microg/kg/h, s.c., osmotic minipumps) for two weeks in normotensive SD rats resulted in left ventricular hypertrophy (3.05 +/- 0.17 vs. 2.75 +/- 0.3 mg/g, P<0.05) and a 1.5-fold increase (P<0.05) in ventricular ADM mRNA levels. In conclusion, the present results show that pressure overload acutely stimulated ventricular ADM gene expression in conscious normotensive rats suggesting a potential beneficial role for endogenous ADM production in the heart against cardiac overload. Since pressure overload-induced increase in ADM synthesis was attenuated in hypertensive rats, alterations in the ADM system may contribute to the pathogenesis of hypertension in the TGR(mREN-2)27 rat.
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PMID:Adrenomedullin gene expression in the rat heart is stimulated by acute pressure overload: blunted effect in experimental hypertension. 916 59

Central administration of C-type natriuretic peptide (CNP) affects various neuroendocrine systems. In the present study, we examined whether CNP acts directly on arginine-vasopressin (AVP) secretion from rat supraoptic nucleus (SON) neurons, using acute dissociated cell preparations. CNP inhibited the basal secretion of AVP in a dose-dependent manner (10(-11)-10(-6) M). A- type natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) also suppressed the basal secretion of AVP, however, the effects were two-orders of magnitude less potent than CNP. CNP also suppressed All-induced AVP secretion, however, the inhibitory effect of CNP was less than that of ANP or BNP. These findings suggest that CNP inhibits the basal secretion of AVP through natriuretic peptide receptor (NPR)-B and has a role in the body water and electrolyte homeostasis in the central nervous system.
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PMID:C-type natriuretic peptide suppresses arginine-vasopressin secretion from dissociated magnocellular neurons in newborn rat supraoptic nucleus. 922

The mechanism of acidification in the cortical distal tubule of mammalian kidney was analysed by "in vivo" microperfusion and using MDCK cells in culture, by electrophysiological and by cell pH microfluorescence techniques. An electrogenic effect of the vacuolar H(+)-ATPase, which has been localized to the intercalated cells of the cortical distal tubule (connecting segment and initial collecting duct) was only observed after blocking Cl- channels by NPPB. In MDCK cells, the recovery of cell pH after an acid pulse in Na(+)-free medium was also depressed by NPPB, indicating that Cl- ions have an important role in the function of H+ ATPase. The regulation by hormonal agents of distal H+ transport due to Na+/H+ exchange and to vacuolar H+ ATPase, was also studied by microperfusion and cell pH techniques. Angiotensin and vasopressin at picomolar concentrations stimulated both transport mechanisms in late distal tubule, and only Na+/H+ exchange in the early segment. In MDCK cells, cell pH recovery in the presence of Na+ was stimulated by picomolar concentrations of angiotensin and vasopressin, and inhibited by micromolar levels, both effects being reverted by micromolar ANP. Studies with specific antagonists suggest that the luminal effect of angiotensin is mediated by AT1 receptors, and of vasopressin by V1 receptors. There is evidence that cell Ca2+ may have an important regulatory role in the action of these hormones.
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PMID:Mechanisms and regulation of H+ transport in distal tubule epithelial cells. 926 82

Hyponatremia after pituitary surgery is presumed to be due to antidiuresis; however, detailed prospective investigations of water balance that would define its pathophysiology and true incidence have not been established. In this prospective study, the authors documented water balance in patients for 10 days after surgery, monitored any sodium dysregulation, further characterized the pathophysiology of hyponatremia, and correlated the degree of intraoperative stalk and posterior pituitary damage with water balance dysfunction. Ninety-two patients who underwent transsphenoidal pituitary surgery were studied. To evaluate posterior pituitary damage, a questionnaire was completed immediately after surgery in 61 patients. To examine the osmotic regulation of vasopressin secretion in normonatremic patients, water loads were administered 7 days after surgery. Patients were categorized on the basis of postoperative plasma sodium patterns. After pituitary surgery, 25% of the patients developed spontaneous isolated hyponatremia (Day 7 +/- 0.4). Twenty percent of the patients developed diabetes insipidus and 46% remained normonatremic. Plasma arginine vasopressin (AVP) was not suppressed in hyponatremic patients during hypoosmolality or in two-thirds of the normonatremic patients after water-load testing. Only one-third of the normonatremic patients excreted the water load and suppressed AVP normally. Hyponatremic patients were more natriuretic, had lower dietary sodium intake, and had similar fluid intake and cortisol and atrial natriuretic peptide (ANP) levels compared with normonatremic patients. Normnonatremia, hyponatremia, and diabetes insipidus were associated with increasing degrees of surgical manipulation of the posterior lobe and pituitary stalk during surgery. The pathophysiology of hyponatremia after transsphenoidal surgery is complex. It is initiated by pituitary damage that produces AVP secretion and dysfunctional osmoregulation in most surgically treated patients. Additional events that act together to promote the clinical expression of hyponatremia include nonatrial natriuretic peptide-related excess natriuresis, inappropriately normal fluid intake and thirst, as well as low dietary sodium intake. Patients should be monitored closely for plasma sodium, plentiful dietary sodium replacement, mild fluid restriction, and attention to symptoms of hyponatremia during the first 2 weeks after transsphenoidal surgery.
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PMID:Pathophysiology of hyponatremia after transsphenoidal pituitary surgery. 932 39

The explosion of new knowledge about the complex mechanisms mediating high blood pressure is providing new targets for drug therapy of hypertension and other cardiovascular disorders. This article reviews the current status of several new approaches in the management of hypertension, including vasopressin antagonists, natriuretic peptide clearance inhibitors, endothelin antagonists, renin inhibitors, angiotensin receptor antagonists, and selective T-type calcium ion channel antagonists.
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PMID:New developments in drug therapy of hypertension. 935 4

Ouabain can cause increased secretion of atrial natriuretic peptide (ANP) from atrial cardiocyte culture, but the effects of digitalis in a therapeutic range on the secretion of cardiac natriuretic peptide including ANP and brain natriuretic peptide (BNP), mainly from the ventricle, in patients with congestive heart failure remain to be investigated. Therefore we studied the acute effects of intravenous infusion of a relatively low dose of digitalis or placebo on hemodynamics and neurohumoral factors including the plasma levels of ANP and BNP and cyclic guanosine monophosphate, a second messenger of cardiac natriuretic peptide, in 13 patients with severe congestive heart failure. No significant change in the hemodynamic parameters or neurohumoral factors was observed with placebo. After 1 hour of intravenous administration of deslanoside (0.01 mg/kg), there was a significant decrease of plasma renin activity and angiotensin II, aldosterone, and norepinephrine levels but no significant change of plasma levels of vasopressin and a significant decrease of the pulmonary capillary wedge pressure but no significant change in cardiac index. In addition, plasma levels of ANP (217 +/- 47 vs 281 +/- 70 pg/ml, p < 0.05), BNP (628 +/- 116 vs 689 +/- 132 pg/ml, p < 0.05), and cyclic guanosine monophosphate (9.7 +/- 1.1 vs 10.9 +/- 1.5 pmol/ml, p < 0.05) increased despite the decrease of pulmonary capillary wedge pressure (19.7 +/- 2.3 vs 16.8 +/- 2.3 mm Hg, p < 0.05). These results indicate the acute intravenous low dose of digitalis resulted in a significant increase in plasma levels of ANP, BNP, and cyclic guanosine monophosphate concomitant with the significant decrease of pulmonary capillary wedge pressure, suggesting the acute direct action of digitalis on the cardiac natriuretic peptides released from the heart in patients with severe congestive heart failure.
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PMID:Digitalis increases brain natriuretic peptide in patients with severe congestive heart failure. 939 3


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