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)

Synergistic interaction between ADP, adrenaline, 5-hydroxytryptamine (5HT) and [8-arginine]vasopressin is not observed for the aggregatory response of aspirin-treated human platelets when this response is estimated directly from the decrease in the number of single platelets in the suspension. This finding is in marked contrast with prior reports of synergistic interaction between these agonists when the rate and extent of the aggregometer response is estimated from the increase in the light transmittance of the suspension, using a platelet aggregometer. We propose that the apparent synergistic response detected using the aggregometer results from the inability of this instrument to respond during the initial phase of aggregation. Significant synergistic interaction is observed for the increase in cytosolic [Ca2+] induced by addition of the ADP/5HT and, to a lesser extent, of the ADP/vasopressin agonist pairs as compared with that caused by addition of the individual agonists. This effect is not, however, typical of the system since increases in cytosolic [Ca2+] induced by addition of the ADP/thrombin or 5HT/vasopressin agonist pairs are no greater than the sum of the responses to these agonists added separately. Addition of collagen prior to ADP or 11,9-epoxymethanoprostaglandin H2 (U46619) fails to enhance the increase in cytosolic [Ca2+] induced by these latter agonists. Adrenaline, when added prior to non-saturating concentrations of U46619, thrombin, vasopressin or ADP, significantly enhances the increase in cytosolic [Ca2+] induced by these agonists in platelets suspended in media containing less than 0.1 microM or 1 mM Ca2+. However, adrenaline fails to enhance the increase in cytosolic [Ca2+] induced by the divalent cation ionophore, ionomycin. Enhancement by adrenaline of Ca2+ influx induced by U46619, thrombin and ADP has been shown by using Mn2+ as probe. Adrenaline also enhances the extent of [3H]5HT secretion induced by U46619, thrombin and vasopressin but fails to increase that induced by ADP in this aspirin-treated preparation. These results are in part consistent with the postulate that adrenaline, acting via an alpha 2-adrenoceptor, modulates receptor--phospholipase-C coupling. However, such modulation does not appear to involve inhibition of adenylate cyclase.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Synergistic responses in human platelets. Comparison between aggregation, secretion and cytosolic Ca2+ concentration. 349 Sep 77

The effects of compounds affecting gastric acid secretion were studied on the formation of inositol phosphates after prelabelling with [3H]-inositol in enriched gastric parietal cells of the rat, prepared by isopycnic centrifugation with Percoll. In cell preparations with 60 to 70% parietal cells, carbachol (10(-6)-10(-2) M) enhanced the accumulation of [3H]-inositol monophosphate ([3H]-IP1), [3H]-inositol bisphosphate ([3H]-IP2) and [3H]-inositol trisphosphate ([3H]-IP3) in a concentration-dependent manner, an effect which was antagonized by 10(-8) M atropine. Li+ (0.5-30 mM) enhanced the basal and carbachol-induced accumulation of all three [3H]-inositol phosphates, the formation of [3H]-IP1 being more sensitive to Li+ than those of [3H]-IP2 and [3H]-IP3. The concentration of Ca2+ in the incubation medium did not affect the relative stimulation of the accumulation of [3H]-inositol phosphates by carbachol, although the basal formation was higher in the presence of Ca2+ in the medium. In the absence of added Ca2+, the incorporation of [3H]-inositol into phospholipids was increased--an effect which was further enhanced by the addition of EGTA to the medium. Gastrin and pentagastrin (10(-8)-10(-5) M) enhanced the formation of [3H]-inositol phosphates, although they were clearly less effective than carbachol. Histamine (10(-6)-10(-3) M) had no effect of its own, but slightly attenuated the effect of carbachol. Cholecystokinin octapeptide (10(-9)-10(-6) M) slightly increased the formation of [3H]-inositol phosphates. Indomethacin (10(-4) M) had no consistent effect on the basal and carbachol-induced accumulation of [3H]-inositol phosphates, nor did prostaglandin E2 (10(-5) M) modify it. Adrenaline (10(-3) M), 5-hydroxytryptamine (10(-3) M), forskolin (10(-5) M), vasopressin (10(-5) M), angiotensin II (10(-5) M) and bombesin (10(-9)-10(-6) M) were all without effect. We suggest that the hydrolysis of inositol phospholipids may be involved in the signal transduction mechanism by which the activation of the muscarinic and gastrin receptors on the parietal cells leads to Ca2+ mobilization and the stimulation of hydrogen ion secretion.
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PMID:Effect of gastric secretagogues on the formation of inositol phosphates in isolated gastric cells of the rat. 356 57

Seven male volunteers were given apomorphine (14-20 micrograms/kg) subcutaneously on a total of ten occasions. Nausea was experienced on six occasions and on four occasions there was no effect. Venous samples were taken before injection, at peak nausea and 20 min later for assay of factor VIII coagulant activity (FVIIIC), von Willebrand factor antigen (vWFAg), the ristocetin cofactor (FVIIIRiCof), euglobulin clot lysis time (ECLT), fibrinopeptide A (FPA), FPA generation time, activated partial thromboplastin time (APTT), vasopressin (aVP) and adrenaline. During nausea plasma aVP concentrations rose from median values of 0.4 pg/ml (at time 0) to 76 pg/ml at peak nausea and fell to 32 pg/ml 20 min later. Adrenaline rose from 0.36 to 0.91 nmol/l (P less than 0.05) before falling to 0.55 nmol/l. During nausea, FVIIIC rose from 100% to 143% (P less than 0.05) and to 214% (P less than 0.05) 20 min later. FVIIIRiCof and vWFAg showed similar changes. Plasminogen activator activity (10(6)/ECLT2) rose from 23 units at time 0 to 592 units during nausea and 1135 units (P less than 0.05) after 20 min. The APTT fell from 49 s to 44 s during the study, plasma FPA levels and the FPA generation time both remained unchanged. On the four occasions nausea was not experienced, there were no changes in vasopressin and catecholamine concentrations nor in haemostatic function. During the study, plasma aVP concentrations rose to levels previously shown to influence haemostatic function. This provides further support for the view that aVP has a secondary role as a mediator of acute changes in haemostasis, and during nausea contributes with adrenaline to an abrupt change in factor VIII and fibrinolytic activator activity.
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PMID:Vasopressin and catecholamine secretion during apomorphine-induced nausea mediate acute changes in haemostatic function in man. 376 10

The mechanism of impaired water excretion in adrenalectomized mammals is unclear. Previous workers have suggested that one cause might be increased water permeability of the distal nephron, allowing back diffusion of water from tubular fluid diluted by the ascending limb. Evidence to support this mechanism in previous studies has been confounded by simultaneous changes in steroid and antidiuretic hormone levels. We compared osmotic and diffusional water permeability of the surface late distal tubule in vivo in intact and adrenalectomized Brattleboro rats, which are free of antidiuretic hormone. The adrenalectomized rats were demonstrated to have impaired diluting capacity in clearance studies. Adrenalectomized rats had a sixfold increase in osmotic permeability and a 1.5-fold increase in diffusional permeability over intact controls. Adrenal steroids have a specific action on water permeability of the distal nephron, independent of antidiuretic hormone.
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PMID:Effect of adrenalectomy on distal tubule water permeability of the Brattleboro rat. 377 16

Descending projections from the paraventricular nucleus of the hypothalamus (PVN) either terminate in the dorsal medulla or pass through the ventrolateral medulla to terminate in the intermediolateral column of the spinal cord. We sought to determine whether a cardiovascular function is subserved by these pathways. Electrical stimulation of the PVN in urethan-anesthetized rats produced increases in blood pressure and mesenteric and renal vascular resistances while hindquarter resistance decreased. This integrated cardiovascular response appeared to be neurogenically mediated because it was virtually abolished by ganglionic blockade and unaffected by blockade of peripheral vascular vasopressin receptors. Adrenal catecholamines appeared to contribute since adrenalectomy reduced the response, especially the hindquarter vasodilation. Interruption with a knife cut of the PVN-dorsal medullary pathway did not affect the response to PVN stimulation except for hindquarter vasodilation, which was reduced significantly. Interruption of the PVN-ventrolateral medullary pathway by local microinjection of lidocaine blocked the pressor and vasoconstrictor responses to PVN stimulation but enhanced the hindquarter vasodilation. These data suggest that fibers descending from the PVN responsible for skeletal muscle vasodilation pass to or through the dorsal medulla, whereas efferent vasoconstrictor pathways from the PVN appear to course through, or synapse in, the ventrolateral medulla.
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PMID:Neural projections from paraventricular nucleus that subserve vasomotor functions. 388 13

A modification of the rat isolated seminal vesicle preparation is described, emphasizing the necessity to use younger animals (40-50 days old and weighing between 125 and 150 g) and to expel thoroughly all vesicular contents. Under the experimental conditions used (tissues suspended under a resting tension of 350 mg in a continuous flow of a modified Krebs solution run at the rate of 15 ml/min, maintained at 32 degrees C, and bubbled with 5% CO2 in O2), the preparation was quite sensitive, but only to a few selected agonists, and remained viable for over 4-6 hr. Adrenaline, noradrenaline, dopamine, and acetylcholine all produced concentration-dependent and reproducible contractions. However, histaminergic, serotoninergic, purinergic, and opioid agonists were inactive as were prostaglandins of the E and F series and the polypeptides angiotensin, vasopressin, and oxytocin. In general, the tissue was rather insensitive to relaxant drugs, with only papaverine and sodium nitrite producing some relaxation in tissues previously contracted by carbachol. Advantages of the preparation include marked responsiveness, but only to a few selected agonists, and suitability for use as a paired tissue. It is suggested that employed under suitable experimental conditions, the preparation deserves a more frequent consideration for use during pharmacological investigations concerned with postsynaptic aspects of noradrenergic or cholinergic transmission.
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PMID:Pharmacological evaluation of the isolated rat seminal vesicle preparation. 395 Dec 38

Hypothalamic extract, containing the releasing factors for anterior pituitary hormones, within minutes stimulated adenyl cyclase activity and adenosine 3':5'-cyclic phosphate (cyAMP) concentrations in rat anterior pituitary in vitro. Cerebral cortical extract was ineffective and hypothalamic extract had no effect on these parameters in posterior pituitary or thyroid. Prostaglandin E(1) also increased adenyl cyclase activity and cyAMP levels in anterior pituitary tissue. Although NaF augmented adenyl cyclase activity, it did not elevate cyAMP. Epinephrine, norepinephrine, histamine, serotonin, dopamine, and vasopressin did not increase either adenyl cyclase or cyAMP. The increased adenyl cyclase and cyAMP produced by hypothalamic extract was associated with greater luteinizing hormone release from anterior pituitary in vitro.
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PMID:Stimulation of anterior pituitary adenyl cyclase activity and adenosine 3':5'-cyclic phosphate by hypothalamic extract and prostaglandin E1. 431 May 17

1. Hepatic volume was recorded by a plethysmographic technique in cats anaesthetized with pentobarbitone; the hepatic artery and portal vein remained intact. Dose-response curves were obtained for intravenous infusions of adrenaline, noradrenaline, angiotensin, vasopressin and histamine.2. Adrenaline and noradrenaline decreased hepatic blood volume and did not differ significantly in potency. Up to 40% of the hepatic blood volume was expelled by doses within the range secreted by the adrenal medullae.3. Isoprenaline, infused into the hepatic artery, had no significant effect on hepatic blood volume in doses which caused maximal vasodilatation of the hepatic arterial bed. Relaxation of hepatic capacitance vessels mediated by beta-adrenoceptors did not occur.4. Angiotensin infusions in doses previously shown to cause intestinal and splenic vasoconstriction, decreased hepatic blood volume and on a molar or microgramme basis, angiotensin was the most potent of the agents tested. Doses within the probable physiological range of endogenous production decreased hepatic blood volume by up to 20%. The responses were not significantly different when the hepatic nerves were intact or sectioned.5. Vasopressin infusions produced only small decreases in hepatic blood volume. Doses within the range secreted by the posterior pituitary which constrict the intestinal and splenic resistance vessels, did not decrease hepatic blood volume by more than 10%.6. Histamine produced no change in hepatic blood volume in doses which readily produce outflow block in dogs. Either the specific hepatic venous smooth muscle involved in outflow block is absent in the cat or it has no histamine receptors.7. After the rapid change in hepatic blood volume at the onset of the infusion, hepatic volume remained steady for the duration of each infusion. There was no evidence that these agents caused net transsinusoidal fluid movements.
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PMID:Effects of infusions of catecholamines, angiotensin, vasopressin and histamine on hepatic blood volume in the anaesthetized cat. 435 9

Literature on the effects of hormones on human myometrial activity is reviewed. The effects of estrogens, gestagens, and prostaglandins on myometrial activity in pregnant and nonpregnant women, and those of maternal and fetal corticosteroids, biogenic amines, and oxytocin and vasopressin are discussed. Estrogens produce small, frequent, local, and nonpropagated contractions of the myometrium, while gestagens produce contractions of higher amplitude, longer duration, and lower frequency. Maternal and fetal corticosteroids have some importance for myometrial activity of pregnancy in some animals, but their role in humans remains obscure. Epinephrine and norepinephrine stimulate myometrial activity in humans, though their physiologic and therapeutic importance is doubtful. The same holds for serotonin. Oxytocin in large doses stimulates myometrial activity during the proliferative stage of the cycle, but is without effect in smaller doses. During pregnancy, oxytocin progressively stimulates myometrial activity, particularly toward the end of pregnancy. Oxytocin is often used to initiate and stimulate labor. Vasopressin, on the other hand, stimulates myometrial activity during the secretory phase of the cycle, especially around the onset of menstruation. Vasopressin has a less marked effect during pregnancy than oxytocin, and its effects are not enhanced as pregnancy comes to term. The fetus is known to produce considerable amounts of oxytocin and vasopressin during labor, though the significance of this contribution remains to be elucidated. Prostaglandins have a potent stimulatory effect on myometrial activity in both pregnant and nonpregnant women. The possibility that prostaglandins play a physiologic role in the onset of myometrial activity remains to be determined.
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PMID:Hormonal effects on human myometrial activity. 462 Mar 76

The hypothalamic-pituitary-adrenocortical system is a complex negative feed-back control mechanism. Under non-stress conditions it functions to maintain a circadian rhythm of adrenal steroid production which is secondary to a circadian fluctuation in the sensitivity to suppression of acth by hydrocortisone. Any stressful stimulus causes an augmentation of steroid production which is due in part to a decrease in sensitivity of acth to suppression. Aldosterone production is not primarily controlled by acth. The increased understanding of this system and of its pathologic alterations has led to the development of a number of pharmacologic techniques which have proved most valuable in evaluating its integrity. Hypothalamic-pituitary function can be assessed by the response to the administration of dexamethasone, methopyrapone, bacterial pyrogen and vasopressin. Adrenal cortical function can be assessed by the response to acth, dexamethasone and spironolactone.
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PMID:The hypothalamic-pituitary-adrenocortical system. Clinical evaluation by pharmacologic techniques. 534 43


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