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)

Current evidence suggests that the antidiuretic hormone (ADH) and changes in sodium balance influence renal prostaglandins (PGs). To separate these two mechanisms, the effect of sodium loading on the urinary excretion of PGE2 and PGF2 alpha was studied in female Brattleboro rats with diabetes insipidus (DIHO) and compared with that in female, age matched, heterozygous Long Evans controls (LEHE). Ten DIHO and ten LEHE rats had a normal sodium intake. In ten DIHO rats a 0.16% NaCl solution was supplied instead of drinking water for either 8 days (n = 5) or 14 days (n = 5). In two groups of LEHE rats, sodium loading was obtained with a 0.80% NaCl solution for the same study periods. Urine PGs were measured by radioimmunoassay in three 24 h urine collections for each rat. Urine PGs were significantly increased in the 8 day loaded but not in the 14 day loaded LEHE rats. In DIHO rats, a non-significant increase in both PGE2 and PGF2 alpha was present after 8 days of sodium loading, while PGE2 and the E/F ratio were decreased after 14 days of salt loading. The findings suggest that the natriuresis induced by sodium loading in the rat may be mediated in part by increased production of PGs. In addition, it seems that ADH plays a role in this response.
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PMID:Effect of sodium loading on the urinary excretion of prostaglandins E2 and F2 alpha in rats with hereditary diabetes insipidus (Brattleboro rats). 385 54

Vasopressin stimulates renal prostaglandin (PGE2) production at several loci and in turn PGE2 modulates the antidiuresis. We have found the time courses of increased urinary PGE2 in subjects with central diabetes insipidus (DI) parallel the antidiuretic responses to AVP and dDAVP. The antidiuretic response to 4 micrograms dDAVP in these subjects was far greater than the response to 5 U (12.5 micrograms) AVP, but the PGE2 response to the dDAVP was only marginally greater than that which followed the AVP. Therefore, dDAVP disproportionately stimulates antidiuresis in relation to PGE2 production, whereas the reverse holds for AVP. In subjects with nephrogenic DI 12.5 micrograms AVP caused no antidiuresis but stimulated PGE2 excretion as well as in subjects with central DI. There was an intermediate relationship between antidiuresis and PGE2 excretion in subjects with central DI given AVP and subjects with nephrogenic DI injected with dDAVP. In summary, 1) the normal PGE2 response to AVP in subjects with nephrogenic DI is consistent with other evidence that non-antidiuretic actions of vasopressin are not impaired in these subjects. 2) The limited capability of dDAVP to stimulate PGE2 may be a factor in the augmented antidiuretic response to dDAVP in subjects with central DI. 3) Antidiuretic and PGE2 responses to vasopressin can be dissociated, thus allowing further consideration of mechanisms by which each may be independently controlled and interrelated.
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PMID:Antidiuretic and PGE2 responses to AVP and dDAVP in subjects with central and nephrogenic diabetes insipidus. 385 99

In order to assess the relative roles played by potassium (K) and the antidiuretic hormone (ADH) on the renal production of prostaglandins (PG) E2 and F2 alpha, the 24 hour urinary excretion of these substances was measured in Brattleboro rats (devoid of ADH) and in control Long Evans heterozygote rats. Rats of each strain received either a normal K intake or a K load for 8 days. Urinary PGE2 and PGF2 alpha were measured by radioimmunoassay in three consecutive 24 h urine collections obtained after the above periods. K loading induced an increase in PGF2 alpha (p less than 0.01), PGE2 showing a non significant trend to decrease. The E/F ratio was decreased in K loaded animals. The changes were qualitatively similar in presence or absence of ADH, but animals with diabetes insipidus had lower levels of PGs than control animals. The results suggest the possibility that K loading induces an increase in the activity of the renal enzyme PGE2-9-ketoreductase. The resulting increase in PGF2 alpha could play a role in K excretion and this response is probably independent of ADH.
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PMID:Effect of potassium loading on prostaglandin E2 and F2 alpha excretion in the Brattleboro rat. 386 68

The purpose of the study was to clarify the mechanism(s) of glucocorticoid-induced hypertension. Hypertension was induced in rats by single i.m. injection of methylprednisolone (MP) 20 mg/kg. In normal Wistar rats, systolic blood pressure (SBP) increased by 30 mmHg from days 2 to 10 after MP. Urinary sodium excretion increased transiently and sodium balance was negative. Plasma volume (PV; ml/100 g body weight) increased on day 5, but was unchanged on day 2 after MP, at a time when SBP had already increased. In rats with chronic renal failure (CRF) and low sodium intake, SBP increased more than in control rats (48 versus 22 mmHg on day 10). Hypertension was not accompanied by a significant drop in urinary excretion of prostaglandin E2 (PGE2; measured by radio-immunoassay). In normal MP-injected rats, PGE2 excretion decreased slightly and then increased; in CRF rats, basal PGE2 excretion was too low to evaluate the effect of MP. In homozygous Brattleboro rats lacking antidiuretic hormone (ADH), MP increased SBP by 28 mmHg (day 10). Similar changes were obtained in heterozygous Brattleboro rats. The changes in PV were identical to those found in Wistar rats. We conclude that increase in PV, change in PGE2 and vasopressin do not play a key role in MP hypertension. Direct effect of glucocorticoid on vascular receptors is likely to be involved in this model.
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PMID:Methylprednisolone-induced hypertension in the rat: evidence against the role of plasma volume changes, vasopressin and renal prostaglandin E2. 386 57

Tubal segments of the ascending uterine arteries and of intramyometrial arteries were obtained from 18 women who underwent hysterectomy at various phases of the menstrual cycle. Ring preparations of the vessels were mounted in organ baths and isometric tension was recorded. In extramyometrial arteries (outer diameter 2-3 mm) prostaglandin (PG) F2 alpha most potently, but also PGE2 caused concentration-related contractions. In contrast, the contractant effects of both PGs on intramyometrial arteries (outer diameter 0.5-0.6 mm) were negligible. Both extra- and intramyometrial vessels were relaxed to a moderate degree (10-25%) by low concentrations of PGF2 alpha and PGE2. No significant differences between the responses to vasopressin and noradrenaline were found between the vessel preparations. Thus human uterine arteries seem to change their responses to PGF2 alpha and PGE2 as they enter the myometrium and decrease in diameter, and the results raise doubt about the view that direct vasoconstrictor effects of these PGs contribute to the regulation of myometrial blood flow. Such effects of vasopressin and noradrenaline cannot be excluded.
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PMID:Different responses to prostaglandin F2 alpha and E2 in human extra- and intramyometrial arteries. 386 62

This study was designed to investigate relationships between dietary potassium and the renal prostaglandin system in rats. The potassium content of the diet was 0.162 mmol/g during the control period and 0.004, 0.162, 1.351, or 2.702 mmol/g during the experimental period. Relative to control data in rats fed a 0.162 mmol/g potassium diet, the urinary excretion of 6-keto-PGF1 alpha was not affected by high potassium intake but increased (P less than 0.05) by 25% in rats fed a low potassium diet for 13 days and was associated with reduction of plasma potassium and with elevation of both plasma renin and net release of 6-keto-PGF1 alpha from renal inner medulla slices incubated in Krebs solution. The excretion of PGF2 alpha was not affected by low potassium intake but increased (P less than 0.05) by about twofold in rats fed a potassium-rich diet (1.351 and 2.702 mmol/g) for 13 days and was associated with elevation of plasma potassium concentration, renal prostaglandin 9-keto-reductase activity, and urinary excretion of kallikrein and vasopressin. The urinary excretion of PGE2 was not altered in rats fed either low or high potassium diets. Altogether, these results indicate selective influence of dietary potassium on the urinary excretion of prostaglandins in the rat.
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PMID:High potassium intake selectively increases urinary PGF2 alpha excretion in the rat. 388 12

Sodium nitroprusside (SNP) is a potent, effective and readily reversible vasodilating agent frequently used in anaesthesia for deliberate hypotension. Moderate hypotension induced by SNP activated catecholamine and vasopressin secretions, and the renin-angiotensin system, resulting in partial antagonism of the hypotensive response to SNP. Furthermore, this increase in renin release was involved in the hypertensive rebound after SNP withdrawal. This activation of vasoconstrictor systems led to pharmacological associations aimed at reducing the risk of cyanide poisoning. The physiological interrelationship between prostaglandins and renin secretion has now been well established but, as far as we know, no paper existed concerning prostaglandins during SNP-induced hypotension. In such hypotension (Pa: -30%), monitored by invasive and non invasive haemodynamic techniques (pulsed Doppler), the variations in plasma renin activity (PRA) and in venous and arterial plasma PGE2 concentrations (V PGE2 and A PGE2), determined by radioimmunoassay, were studied in anaesthetized dogs. Invasive haemodynamic data were similar to previous reports. Common carotid diameter increased (p less than 0.05), with a constant common carotid blood flow. PRA (p less than 0.05), V PGE2 (p less than 0.05) and A PGE2 (p less than 0.05) increased. PRA and V PGE2 were highly correlated before and after SNP. SNP resulted in hypotension with reflex sympathetic activation and dilatation of large arteries. Carotid blood flow autoregulation was maintained. Whilst pulmonary removal of PGE2 remained unchanged, an increase in A PGE2 may have been involved in the vasodilator mechanisms.
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PMID:[Plasma renin activity and prostaglandin E2 in hypotension induced by sodium nitroprusside]. 388

We compared the effects of three vasoactive peptides (angiotensin II, vasopressin, and bradykinin) and norepinephrine on the production of prostaglandin I2 [prostacyclin (PGI2)] and PGE2 by isolated rat adipocytes. Angiotensin II, vasopressin, and bradykinin stimulated PGI2 production but had minimal or no effect on PGE2 production or triglyceride lipolysis in isolated rat adipocytes, while norepinephrine stimulated PGI2 production, PGE2 production, and triglyceride lipolysis. The arachidonic acid that serves as substrate for PGI2 production in adipocytes in response to the vasoactive peptides appears to be derived from the cellular phospholipids rather than the triglycerides in these triglyceride-laden cells. The adipocyte contains two separate mechanisms for PG production: 1) a catecholamine-stimulated mechanism for the production of PGI2 and PGE2 that is activated concomitantly with triglyceride lipolysis, and 2) a mechanism activated by vasoactive peptides for the stimulation of PGI2 production independent of triglyceride lipolysis and PGE2 production. These mechanisms may have distinct functions.
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PMID:Stimulation of prostacyclin production in isolated rat adipocytes by angiotensin II, vasopressin, and bradykinin: evidence for two separate mechanisms of prostaglandin synthesis. 388 13

Prostaglandin E2 (PGE2) inhibits the action of the antidiuretic hormone (ADH) in isolated collecting tubules. A negative feedback loop has been postulated whereby ADH stimulates PGE2 synthesis. Furthermore, lysyl-bradykinin (LBK) inhibits the antidiuretic effect of ADH, probably via PGE2. Enhanced PGE2 synthesis has also been implicated as contributing to the inability to maximally concentrate urine during the neonatal period. We investigated PGE2 synthesis in microdissected cortical (CCT), medullary (MCT), and branched cortical (BCT) collecting tubules from adult and in corticomedullary collecting tubules (CT) from newborn rabbits. Isolated BCT produced significantly less PGE2 (12 +/- 2 pg X mm-1 X 20 min-1) than CCT (65 +/- 9) or MCT (76 +/- 8) from kidneys of adult rabbits. CT from newborn rabbits produced only 19 +/- 3 pg/mm, significantly less than either CCT or MCT from adults. A large variability in basal PGE2 production and hormonal response was observed from tubule to tubule. Under either basal conditions or in the presence of 2 microM arachidonic acid, LBK enhanced PGE2 synthesis in CCT and MCT from adults. ADH enhanced PGE2 production in MCT under basal conditions and in CCT in the presence of arachidonic acid. Neither LBK nor ADH stimulated PGE2 synthesis in neonatal CT. A23187 consistently stimulated PGE2 synthesis in CCT and MCT from adults and, to a lesser extent, in CT from newborn rabbits. Our results support the hypothesis that ADH and LBK enhance PGE2 synthesis in the collecting tubule. This response is, however, subject to large variations from tubule to tubule and depends on the in vitro incubation conditions.
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PMID:Synthesis of prostaglandin E2 in different segments of isolated collecting tubules from adult and neonatal rabbits. 391 55

Various agonists induced sustained contractions of estrogen-dominated rat uterine smooth muscle in Ca-free salt solution containing 0.2 mM EGTA after incubation of the muscle with 3 mM EGTA for 1 hr. The magnitudes of contraction varied with agonists. (bradykinin greater than oxytocin greater than or equal to vasopressin greater than PGF2 alpha greater than angiotensin II greater than acetylcholine greater than or equal to PGE2 greater than or equal to 5-hydroxytryptamine. Addition of 10(-4) Ca ion reduced the tension developed: Ca ion inhibited these contractions when they were sufficiently large (marked inhibition on bradykinin-, oxytocin-, and vasopressin-induced contractions; definite one on PGF2 alpha-induced contraction), as observed previously with oxytocin-induced contraction under the same conditions and named "Ca Reversal".
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PMID:Calcium reversal: inhibition by Ca ion of sustained contraction in Ca-free medium induced by various agonists in rat uterine smooth muscle. 392 49


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