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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies have demonstrated that prostaglandin E2 (PGE2) inhibits arginine vasopressin-(AVP)dependent adenosine 3',5'-cyclic monophosphate (cAMP) accumulation in microdissected rat outer medullary collecting tubules (OMCD), by a mechanism unrelated to the inhibition of cAMP synthesis. The potential role of the activation of protein kinase C (PKC) to explain the negative regulation elicited by PGE2 was investigated in this study. Single OMCD samples were pre-incubated (10 min, 30 degrees C) in the presence or absence of either activators of PKC, phorbol 12-myristate 13-acetate (PMA), 1-oleoyl-2-acetyl-glycerol (OAG), dioctanoylglycerol (DOG) or an inhibitor of PKC, staurosporine (SSP). These compounds were present also with the agonists tested during the incubation period (4 min, 35 degrees C). In contrast to PGE2, activators of PKC did not decrease AVP-dependent cAMP accumulation (mean +/- SEM): 1 nM AVP = 47.1 +/- 6.8 fmol.mm-1 x 4 min-1; AVP+0.3 microM PGE2 = 20.1 +/- 2.7, P < 0.01 versus AVP; AVP + 10 nM PMA = 42.0 +/- 4.7, NS versus AVP; AVP + 50 micrograms/ml OAG = 44.1 +/- 4.8. NS versus AVP, N = 5 experiments. However, 10 nM PMA prevented PGE2-induced inhibition: AVP + PGE2 = 44.2 +/- 3.5% of the response to AVP and 90.3 +/- 3.2% without and with PMA respectively, N = 16. Similar results were obtained with either 50 micrograms/ml OAG or 25 micrograms/ml DOG (AVP + PGE2 + OAG = 92.9 +/- 6.6% of the response to AVP, N = 8; AVP + PGE2 + DOG = 94.1 +/- 5.3%, N = 7).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The activation of protein kinase C prevents PGE2-induced inhibition of AVP-dependent cAMP accumulation in the rat outer medullary collecting tubule. 790 84

To characterize the short-term ACTH secretion pattern and to investigate factors regulating it, pituitary venous (PV) blood was collected using our nonsurgical method from 8 unperturbed horses every 20 or 30 s for approximately 1 h. In all but 1 horse, sampling occurred during the broad circadian maximum in plasma cortisol concentrations. Concentrations of corticotropin-releasing hormone (CRH; n = 7 horses), arginine vasopressin (AVP), ACTH and cortisol were measured by radioimmunoassay. In all horses, CRH, AVP and ACTH secretion patterns appeared irregular in time and amplitude. The mean (+/- SEM) numbers of peaks per hour detected by the cluster program were 2.8 +/- 1.2, 10.1 +/- 1.9 and 10.2 +/- 1.4 for CRH, AVP and ACTH, respectively. However, when 2- and 5-min sampling frequencies were simulated by meaning consecutive values, significantly fewer peaks were detected in each hormone. There was no correlation between the prevailing cortisol concentration and peak frequencies of CRH, AVP or ACTH. Secretion patterns of ACTH and AVP were closely related in all horses as assessed by cross correlation analysis and coincidence of peaks, although the ratio between PV ACTH and AVP concentrations fluctuated markedly within each horse. In contrast, the relationship between CRH and ACTH secretion was variable. Bivariate spectral analysis showed only a modest degree of underlying periodicity in CRH, AVP and ACTH secretion during the very short term studied. Nevertheless, distinct peaks exceeding the 95% confidence limits of white noise were observed at periods between 2 and 30 min in 5 of 7 CRH, 6 of 8 AVP and 5 of 8 ACTH spectra. Furthermore, the slope of the regression line through each spectrum did not become indistinguishable from zero, i.e. the flat white noise continuum, until mean (+/- SEM) periods of 2.6 +/- 0.8, 1.6 +/- 0.2, and 2.0 +/- 0.2 min, for CRH, AVP and ACTH spectra, respectively. At the ACTH spectral maximum, the coherence coefficient, which is analogous to the squared correlation coefficient, exceeded 0.5 in comparisons of all ACTH and AVP spectra and of 5 of 7 ACTH and CRH spectra.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Short-term secretion patterns of corticotropin-releasing hormone, arginine vasopressin and ACTH as shown by intensive sampling of pituitary venous blood from horses. 796 80

To see if arginine vasopressin (AVP) influenced fetal sodium balance, we infused AVP i.v. (45 mU h-1 kg-1) into two groups of chronically catheterized fetal sheep. One group had urinary osmolalities of 147 +/- 23 mosm kg-1 (SEM, n = 6) and the other group had higher urinary osmolalities (339 +/- 3 mosm kg-1, n = 4, P < 0.001). The group with high urinary osmolalities had higher systolic pressures (P < 0.05), higher glomerular filtration rates (GFR; P < 0.05), and higher urinary electrolyte excretion rates (P < 0.05), but lower membrane blood flows (P < 0.05) and lower fractional reabsorption of sodium by the proximal tubule (P < 0.01). In the group with low urinary osmolalities, AVP caused a rise in arterial blood pressure (P < 0.001), a fall in heart rate (P < 0.001), a fall in membrane blood flow (P < 0.02), but no change in placental or renal blood flow. Renal sodium excretion increased (P < 0.001) because GFR rose (P < 0.001) and proximal fractional sodium reabsorption fell (P < 0.001). Distal fractional sodium reabsorption increased (P < 0.001), but not enough to compensate for the fall in proximal fractional reabsorption. Lung liquid flow decreased (P = 0.006), as did lung liquid sodium excretion (P = 0.002). There were no changes in fetal plasma sodium, blood volume or haematocrit. The effects of AVP infusion were similar in the group with high urinary osmolalities. This study shows that high levels of AVP, such as occur in fetal "stress", have widespread effects on fetal cardiovascular, renal and lung functions. The characteristic profile of the fetuses with high urinary osmolalities prior to AVP infusion could be entirely explained by high endogenous AVP levels and AVP could possibly be a sole mediator of these widespread effects of fetal "stress". Furthermore, although during infusion of AVP sodium excretion increased, blood volumes did not change. Therefore, the fetuses must have accessed additional sodium from either their extracellular fluids, the amniotic and/or allantoic cavities or across the placenta.
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PMID:The roles of arginine vasopressin in fetal sodium balance and as a mediator of the effects of fetal "stress". 808 38

The accumulation of cyclic adenosine 3',5'-phosphate (cAMP) elicited by antidiuretic hormone (arginine vasopressin, AVP) in the medullary collecting tubule (OMCD) microdissected from the rat kidney is inhibited by different factors: the A1 agonist of adenosine (-)-N6-(R-phenylisopropyl) adenosine (PIA), an alpha 2-adrenergic agonist clonidine (CLO), and prostaglandin E2 (PGE2). The negative regulation elicited by PGE2 was further characterized by measuring summation of inhibition with other inhibitors, by testing the effect of pertussis toxin and by studying the part played by extracellular calcium. Inhibitors were used at concentrations inducing maximum effects. The simultaneous addition of 0.3 microM PGE2 with either 0.1 microM PIA or 1 microM CLO led to an inhibition of the response to AVP (80.0 +/- 3.5%, SEM, N = 7 and 92.6 +/- 0.8%, N = 5, respectively) greater than those elicited by each agent alone. In contrast, PIA and CLO added together induced an inhibition similar to that due to CLO alone. The action of PGE2 in combination with either PIA or CLO corresponded to a partial summation fitting with the values calculated by assuming a cumulative inhibition. Preincubation of OMCD samples with pertussis toxin (100 ng/ml or 1 micrograms/ml) relieved the inhibitory effects of CLO and PIA but did not affect the action of PGE2. PGE2-induced inhibition was prevented in a calcium-free medium [0 Ca2+ + 0.1 mM [ethylene-bis (oxyethylene-nitrilo)] tetraacetate (EGTA)]: values were 67.0 +/- 2.1% and 5.8 +/- 8.7% (+/- SEM) in 2 mM Ca2+ and 0 Ca2+ medium, respectively, N = 7.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:PGE2-induced inhibition of AVP-dependent cAMP accumulation in the OMCD of the rat kidney is cumulative with respect to the effects of alpha 2-adrenergic and alpha 1-adenosine agonists, insensitive to pertussis toxin and dependent on extracellular calcium. 810 83

Aging is frequently associated with changes in physiological and cognitive processes. Among these changes is a distinct dysregulation of the hypothalamic-pituitary-adrenal axis. In the current experiments, aspects of hypothalamic-pituitary-adrenal axis function were compared in young (3- to 4-month-old) and aged (21- to 24-month-old) Fisher 344/N male rats. Basal ACTH and corticosterone levels during the circadian trough were elevated in aged compared to young rats. During the evening peak of the circadian cycle, plasma ACTH levels in the young and aged rats were comparable; however, aged rats had significantly lower corticosterone levels than young rats. Stimulus-induced secretion of pituitary-adrenal hormones was attenuated in aged rats. The ACTH response to hemorrhage in the aged group was only 45 +/- 3% of the hemorrhage response in young rats. Pituitary responsiveness to an iv CRF challenge was 58 +/- 6% of that in the young population. These changes were associated with a 38 +/- 5% loss of anterior pituitary CRF receptor number in the aged population. Changes in the hypothalamic regulation of pituitary-adrenal function were also evident in the aged rats. Hypophysial-portal blood concentrations of CRF were significantly greater in aged (56 +/- 6 pM) compared to young rats (37 +/- 4 pM; P < 0.02, by two-tailed unpaired t test; n = 8/group), whereas portal levels of arginine vasopressin were significantly reduced in aged (0.56 +/- 0.01 nM) compared to young rats (0.89 +/- 0.01 nM; P < 0.01, by two-tailed unpaired t test; mean +/- SEM; n = 8/group). Portal CRF responses to hemorrhage were significantly (P < 0.01) greater in aged rats, whereas hemorrhage-stimulated increases in portal AVP levels were significantly (P < 0.01) reduced in the aged group compared to those in the young rats. Finally, regional assay of CRF content demonstrated significant reductions in the median eminence and frontal cortex of aged rats compared to young rats, whereas in situ hybridization analysis failed to reveal age-related differences in paraventricular CRF mRNA levels. Overall, these observations are consonant with the hypothesis that senescence is associated with hypothalamic CRF hypersecretion and a consequent down-regulation of corticotrope CRF receptor.
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PMID:Age-related alterations of hypothalamic-pituitary-adrenal axis function in male Fischer 344 rats. 811 95

It is well known that arginine vasopressin (AVP) exerts a stimulatory effect on adrenocorticotrophic hormone (ACTH) secretion. Moreover, there is consistent evidence that the hypothalamic AVP-secreting neurons are involved in the neuroregulation of ACTH secretion. With the aim to throw further light on the interaction between AVP and corticotrophin-releasing hormone (CRH) in the neuroregulation of ACTH secretion, in this study we compared the ACTH and cortisol responses to human CRH (100 micrograms iv as a bolus) in 18 normal subjects (15 females and three males, age 22-35 years) and seven patients with central isolated diabetes insipidus (six females and one male, age 16-40 years). Two patients were newly diagnosed and five had discontinued substitution therapy with desamino-D-AVP 24 h before testing. All had free access to water before and during the test period. The ACTH and cortisol responses to CRH were higher in subjects with diabetes insipidus than in controls, either when evaluated as peak values (ACTH, mean +/- SEM: 17.0 +/- 1.2 vs 7.7 +/- 0.7 pmol/l, p = 0.0003; cortisol: 611.3 +/- 59.4 vs 450.7 +/- 21.2 nmol/l, p = 0.01) or area under curve values (ACTH: 672.5 +/- 75.7 vs 364.0 +/- 33.6 pmol.l-1 x h-1, p = 0.002; cortisol: 29158.0 +/- 2937.0 vs 23236.7 +/- 1052.1 nmol.l-1 x h-1, p = 0.03). These results show that patients with diabetes insipidus have an exaggerated pituitary-adrenal response to CRH. This may be due to the fact that in diabetes insipidus AVP secretion from parvocellular neurons of the paraventricular nucleus in the hypophysial portal system is not impaired.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enhanced adrenocorticotrophic hormone and cortisol responses to corticotrophin-releasing hormone in central idiopathic diabetes insipidus. 813 Aug 84

Factors regulating the secretion of atrial natriuretic hormone (ANH) and arginine vasopressin (AVP) have not been elucidated fully. In several studies the release of these peptides has been studied by inducing both increased atrial pressure and atrial distension. A few studies employ cardiac tamponade, allowing the effect of atrial pressure and atrial stretch to be studied separately. In eleven dogs with spontaneous cardiac tamponade the effect of pericardiocentesis on circulating concentrations of ANP and AVP was studied. Pericardiocentesis was followed by a prompt rise in (non-elevated) plasma ANH concentrations from 21.6 +/- 7.3 to 65.4 +/- 17.1 pmol/l (mean +/- SEM). The initially slightly elevated AVP concentration of 5.5 +/- 1.5 pmol/l declined following pericardiocentesis to 2.1 +/- 0.5 pmol/l. In three dogs the systolic arterial pressure was measured indirectly and the central venous pressure was measured with a fluid-filled catheter. Before and after pericardiocentesis arterial pressure readings did not change significantly. Central venous pressure values showed an immediate very steep significant decrease after centesis. It is concluded that ANH release is primarily regulated by stretch and not by atrial pressure, that plasma AVP concentrations are moderately elevated in cardiac tamponade and that in cardiac tamponade pericardiocentesis causes a rapid decline in plasma AVP concentration.
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PMID:Effect of pericardiocentesis on circulating concentrations of atrial natriuretic hormone and arginine vasopressin in dogs with spontaneous pericardial effusion. 816 64

To investigate the possible role of atrial and brain natriuretic peptides (ANP and BNP) in the renal effects of mechanical ventilation with positive end-expiratory pressure (PEEP), we measured changes in plasma ANP and BNP levels during PEEP in patients undergoing subtotal esophagectomy. Application of 15 cm of H2O PEEP for 1 h decreased the levels of plasma ANP and BNP from 24.4 +/- 5.5 (mean +/- SEM) and 19.0 +/- 3.5 fmol/mL to 14.4 +/- 2.1 and 15.3 +/- 3.0 fmol/mL, respectively (P < 0.05). The level of plasma cyclic guanosine monophosphate, an intracellular second messenger of ANP and BNP, also decreased from 8.4 +/- 1.5 to 5.7 +/- 0.8 pmol/mL (P < 0.05). PEEP increased the levels of plasma arginine vasopressin from 2.0 +/- 0.5 to 4.2 +/- 1.2 pg/mL, aldosterone from 36.1 +/- 4.9 to 65.3 +/- 12.7 pg/mL, and plasma renin activity from 1.4 +/- 0.5 to 2.7 +/- 0.7 ng.mL-1.h-1. During PEEP ventilation, urine output, urinary sodium and potassium excretion, osmolar clearance, and cardiac index all decreased. PEEP increased free water clearance, right atrial pressure, pulmonary arterial pressure, and pulmonary capillary wedge pressure. The level of plasma endothelin, mean blood pressure, and heart rate did not change significantly. These results suggest that not only hemodynamics and the vasopressin and renin-angiotensin-aldosterone system, but also the natriuretic peptide system (ANP and BNP), are involved in the renal effects of PEEP.
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PMID:Positive end-expiratory pressure ventilation decreases plasma atrial and brain natriuretic peptide levels in humans. 825 Mar

The ultrastructure of the early chick embryo was investigated, using scanning (SEM) and transmission electron microscopy (TEM). Eggs were obtained from the shell gland by injecting hens intravenously with a synthetic prostaglandin or arginine vasopressin. Embryos were examined during late cleavage (stages IV-VI, Eyal-Giladi and Kochav, '76), formation of the area pellucida (stages VII-XI), and formation of the hypoblast (stages X-XIV). SEM highlighted the reduction in cell number at the underside of the embryo during formation of the area pellucida although it became apparent that the thickness of the embryo is not reduced to a single layer of cells at stage X. In addition, blastomeres at the perimeter of embryos (stages V-VI) project filopodial extensions onto a smooth membrane that separates the sub-embryonic cavity from the yolk. During hypoblast formation, epiblast cells generate stellate projections at their basal aspect, thus providing a meshwork for the advancing secondary hypoblast cells. By stage XII the epiblast was one cell thick and reminiscent of a columnar epithelium when viewed transversely. Cells of the deep portion of the posterior marginal zone were distinguished morphologically in the stage XII embryo by their many cell surface projections and ruffled appearance. Blastomeres at the perimeter of stage V-VI embryos projected filopodial extensions onto a smooth membrane which separates the sub-embryonic cavity from the yolk. This membrane is presumed to be confluent with the cytolemma. Evidence is presented demonstrating the presence of intracellular membrane-bound droplets which are hypothesised to contain sub-embryonic fluid.
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PMID:Early development of the chick embryo. 844 61

The aim of this study was to determine platelet intracellular free calcium with respect to age, sex, race, and agonist stimulation in patients with essential hypertension compared with normotensive subjects. Intracellular free calcium was measured, using Fura-2-AM, in 42 normotensive and 52 patients with untreated essential hypertension. Of these, 22 pairs were age, sex, and race matched. The intracellular free calcium response to agonist stimulation was measured in the presence of 1 mumol/L arginine vasopressin (AVP). Intracellular calcium was significantly raised in patients with hypertension in both the matched and unmatched groups with values (means +/- SEM) in the matched group of 68.4 +/- 2.6 nmol/L for the hypertensives and 60.2 +/- 2.1 nmol/L for the normotensives (n = 22; P < or = .02) and in the unmatched group of 63.3 +/- 1.8 nmol/L (n = 52) and 57.6 +/- 1.4 nmol/L (n = 42, P < or = .02), respectively. There was no sex difference but intracellular calcium was significantly lower in black hypertensives compared with white hypertensives (P < .005). A significant correlation with blood pressure was only observed in the combined normotensive and hypertensive group (r = 0.23; P = .030). There was no significant correlation with age in any group (even when excluding the black individuals), but in the hypertensive group there was a significant correlation with serum cholesterol (r = 0.34, P = .02; n = 46).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Determinants of platelet intracellular free calcium in essential hypertension and effect of stimulation by arginine vasopressin. 846 8


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