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 role of histamine (H) and prostaglandins (PGs) in the renal vasoconstriction prompted by a 10-min intrarenal infusion of norepinephrine (NE, 0.2 micrograms), antidiuretic hormone (ADH, 10 mU), or angiotensin II (ANG II, 0.05 micrograms) was evaluated in anesthetized dogs (amounts are per min per kg). Renal blood flow (RBF, flow probe) decreased four- to fivefold during the 1st min of infusion with each agonist but then gradually returned toward base line. This "escape" was greatest with ADH, less with NE, and small with ANG II. There was a postinfusion reactive hyperemia (RH) only after NE; NE-RH was 4.26 +/- 0.75 (SE) ml/g. Meclofenamate (MFA) reduced NE-RH to 60 +/- 11% of control and decreased NE escape. The H1-receptor antagonist, chlorpheniramine (CP), decreased NE-RH to 24 +/- 5% of control and reduced NE escape. MFA slowed, but did not block, ADH escape and had little effect on ANG II escape. CP did not affect ADH or ANG II escape. The histidine decarboxylase inhibitor, p-toluenesulfonohydrazine, did not affect NE escape but decreased NE-RH to 22 +/- 6% of control. Bolus injections of ADH during a constant infusion of the hormone were not vasoactive, indicating a tachyphylaxis-like phenomenon; this was not found with ANG II or NE. Finally, the excretion of histamine-like material increased from a control value of 0.69 +/- 0.08 to 1.28 +/- 0.28 micrograms/min during NE-RH. These results indicate that NE releases histamine and PGs from the kidney and that PGs account, primarily, for NE escape, whereas histamine accounts, primarily, for NE-RH.
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PMID:Vasoconstrictor-induced changes in renal blood flow: role of prostaglandins and histamine. 335 83

The role of prostaglandins in the regulation of sodium and water excretion has been widely studied, but little is known about the influence of prostaglandins (PGs) on the tubular handling of calcium, magnesium or phosphorus. Recent observations have suggested that PGE2 and vasopressin may interact and influence reabsorption of calcium and phosphorus in the cortical collecting duct. The present study investigated the effect of meclofenamate (2 mg/kg), and inhibitor of PG synthesis, on the excretion of calcium, magnesium and phosphorus. Experiments were performed in antidiuretic and water diuretic rats to examine potential PG-vasopressin interactions on the reabsorption of these ions by renal tubules. In antidiuretic rats given meclofenamate, urine osmolality increased whereas urine flow and the fractional excretion of water, urea, sodium, calcium and magnesium decreased by 30 to 50%. In water diuretic animals, urine osmolality and urea excretion were unaltered after meclofenamate administration. Fractional excretion of sodium, water, calcium and magnesium declined approximately 50% in water diuretic rats given meclofenamate. Urinary excretion of PGE2 was not significantly different in water diuretic and antidiuretic rats averaging 262 +/- 78 vs. 167 +/- 35 pg/min, respectively. Meclofenamate significantly reduced urinary excretion of PGE2 in both groups. The results indicate that renal PGs modulate renal tubular reabsorption of calcium and magnesium, as well as sodium and water.
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PMID:Prostaglandin-vasopressin interactions on the renal handling of calcium and magnesium. 658 91

To evaluate roles of prostaglandins (PGs) in vasopressin (AVP) secretion elicited by stimulating alpha-adrenergic and dopaminergic receptors in the periventricular region, we examined in conscious rats the effects of intracerebroventricular (i.c.v.) injections of a cyclooxygenase inhibitor meclofenamate on the plasma AVP responses to i.c.v. applications of angiotensin II (ANG II), phenylephrine and dopamine. I.c.v. injections of 58 pmol ANG II produced, 5 and 15 min later, augmentations of plasma AVP accompanied by elevations of arterial pressure and tendencies of reduction in heart rate. Similarly, the administrations of 0.53 mumol phenylephrine or dopamine enhanced plasma AVP 5 min later, without altering arterial pressure and heart rate significantly. Meclofenamate (0.31 mumol) applied i.c.v. 30 min prior to the administrations of ANG II remarkably inhibited the AVP and pressor responses to this peptide. However, the responses of plasma AVP, arterial pressure and heart rate to phenylephrine or dopamine were not affected by the i.c.v. administrations of 0.31 mumol meclofenamate. The injections of meclofenamate followed by the administrations of a vehicle for ANG II and the catecholamines were without effect on plasma AVP and the cardiovascular parameters. Plasma osmolality, sodium, potassium and chloride in all the groups mentioned above were not significantly changed during experiments. These results suggest that PGs generated in the periventricular region, despite their probable stimulatory roles in the ANG II-evoked AVP secretion, may not participate in the AVP-releasing mechanisms activated by dopaminergic and alpha-adrenergic receptors, supporting the view that PGs and the catecholamines may facilitate AVP release via separate pathways.
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PMID:Evaluation for roles of brain prostaglandins in the catecholamine-induced vasopressin secretion in conscious rats. 838 72

This study explored the roles of prostaglandins in the anteroventral third ventricular region, a cerebral osmoreceptor site, in the osmoregulation mechanism of vasopressin release. We injected (1 microliter) prostaglandin E2 (12.8 nmol) or meclofenamate (78.3 nmol), an inhibitor of prostaglandin biosynthesis, into the brain region or the lateral cerebral ventricle of conscious rats, examining their effects on plasma vasopressin and its controlling factors in the presence or absence of an osmotic stimulus. The injection of prostaglandin E2 into the anteroventral third ventricular region augmented plasma vasopressin and arterial pressure after 5 min and 15 min, without influencing plasma osmolality, sodium, potassium, or chloride. In contrast, intraventricular injection of prostaglandin E2 did not cause any significant effect on those variables. The i.v. infusion (0.1 ml.kg-1.min-1) of hypertonic saline (2.5 mol/l) enhanced plasma vasopressin after 15 min and 30 min; this was accompanied by increased plasma osmolality, sodium, and chloride, and by unaltered or elevated arterial pressure. Meclofenamate given into the anteroventral third ventricular region 30 min before starting the hypertonic saline infusion abolished the osmotic vasopressin response without significantly changing the responses of the other variables. Histological analysis showed that the injection sites of meclofenamate in these rats were close to those of prostaglandin E2 in the anteroventral third ventricular region and included the organum vasculosum of the lamina terminalis and the surrounding area, the medial preoptic area, and periventricular and median preoptic nuclei. When injection cannulae for meclofenamate deviated from those areas incidentally or when the drug was expressly administered into the cerebral ventricle, the osmotic vasopressin response was not inhibited. Plasma vasopressin and the other variables observed during the i.v. infusion of isotonic saline (0.15 mol/l) were not affected significantly by meclofenamate administration into the anteroventral third ventricular region or the cerebral ventricle. On the basis of these results, we concluded that prostaglandins synthesized in and/or near the anteroventral third ventricular region might contribute to the facilitation of vasopressin release in the hyperosmotic state.
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PMID:Possible roles of prostaglandins in the anteroventral third ventricular region in the hyperosmolality-evoked vasopressin secretion of conscious rats. 906 12

To compare the coronary effects of endothelin-1 and vasopressin, as well as the role of nitric oxide (NO) and prostanoids in these effects, blood flow in the left circumflex (73 animals) or left anterior descending (19 animals) coronary artery (coronary flow) was electromagnetically measured, and both peptides were intracoronarily injected in anesthetized goats under control conditions and after intravenous administration of the inhibitor of NO synthesis NW-nitro-L-arginine methyl ester (L-NAME, 47 mg/kg, nine animals) or the inhibitor of cyclooxygenase meclofenamate (6-8 mg/kg, seven animals). In every animal, both endothelin-1 and vasopressin reduced coronary flow in a dose-dependent way, but these reductions by 0.03, 0.1 and 0.3 nmol of endothelin-1 (16%, 33% and 66%, respectively) were significantly higher than those by the equimolar doses of vasopressin (11%, 22% and 35%, respectively). After L-NAME treatment, the reductions of coronary flow by both peptides were augmented, and this augmentation was about two times higher for endothelin-1 than for vasopressin. Meclofenamate treatment did not affect the reductions of coronary flow caused by both peptides. Therefore, we suggest that endothelin-1 is more effective than vasopressin for producing coronary vasoconstriction, but vasopressin also produces remarkable coronary vasoconstriction. Also, it is suggested that NO may play a more relevant role for modulating the coronary vasoconstriction by endothelin-1 than by vasopressin, and that cyclooxygenase products may not be involved in the coronary effects of these two peptides.
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PMID:Comparison of the in vivo coronary action of endothelin-1 and vasopressin role of nitric oxide and prostanoids. 1525 91