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 present studies examined whether vasopressin increases prostaglandin biosynthesis in isolated rabbit cortical collecting tubules (CCT) and whether endogenous prostaglandin biosynthesis plays a role in modulating the response of this nephron segment to vasopressin. Three groups of studies were performed. In the first group, CCT and proximal straight tubules (PST) were incubated with [(3)H]arachidonic acid, and metabolites were separated and identified using silica gel thin-layer chromatography. CCT were capable of producing all of the major prostaglandins (PG) (PGE(2) > thromboxane B(2)[TxB(2)] > PGF(2alpha) > PGI(2)). PST produced significantly lesser quantities of these lipids. In the second group, radiolabeled arachidonic acid was incorporated into the phospholipid pool of both CCT and PST, vasopressin was added to the incubation medium, and metabolities were separated and identified as above. Vasopressin stimulated the release of all of the major prostaglandins in CCT but had no effect on PST. PGE release into the incubation medium, as assessed by a radioreceptor assay, increased 108%, and a vasopressin analogue, 1-desamino-8-d-arginine vasopressin, had a quantitatively similar effect. In the third group, a submaximal dose of vasopressin was administered to isolated, perfused CCT studied in the presence and absence of indomethacin to assess whether endogenous prostaglandins play a role in modulating the antidiuretic response to vasopressin. Studies were performed in rabbits on a normal diet and in desoxycorticosterone acetate (DOCA)- or KCl-loaded animals. In the state of mineralocorticoid excess, basal prostaglandin synthesis was 63% lower, and vasopressin-stimulated prostaglandin synthesis 76% lower, than the synthesis observed in rabbits on a normal diet. Cyclooxygenase inhibition exposed a significant hydroosmotic response to a submaximal dose of vasopressin in CCT from DOCA- or KCl-loaded animals. With arachidonic acid in the bath, the same dose of vasopressin failed to elicit a hydroosmotic response in CCT from rabbits on a normal diet even in the presence of a cyclooxygenase inhibitor. However, removal of exogenous arachidonic acid, with a consequently lower rate of prostaglandin synthesis, allowed the cyclooxygenase inhibitor to enhance the hydroosmotic response to vasopressin in these tubules.We conclude from these studies that the rabbit CCT has the capacity to synthesize all of the major prostaglandins and that the rate of synthesis of these lipids is enhanced by vasopessin. Prostaglandin synthesis by the CCT is postulated to modulate the antidiuretic action of vasopressin via a closed feedback loop. The effectiveness of this feedback regulation is dependent upon the mineralocorticoid status of the animal, which determines the level of basal and vasopressin-stimulated prostaglandin synthesis by the CCT.
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PMID:Regulation of vasopressin action by prostaglandins. Evidence for prostaglandin synthesis in the rabbit cortical collecting tubule. 717 90

Cellular calcium modulates enzyme activity, cell proliferation, and differentiation. In vascular smooth muscle cells (VSMC), calcium may contribute to increased vascular contractility and structural alterations in both hypertension and atherosclerosis. We investigated the role of calcium in angiotensin II (AII)-induced prostaglandin release and DNA synthesis in VSMC. Prostaglandin levels were determined by radioimmunoassay, and DNA synthesis was determined by the incorporation of [3H]thymidine. AII dose-dependently stimulated the release of prostaglandin E2 and prostaglandin I2, and this effect was synergistically enhanced by the Ca2+ ionophore A23187. Conversely, the AII response was inhibited by EGTA, a chelator of Ca2+ ions and by verapamil and nifedipine, two Ca2+ channel blockers or by incubation of the cells without exogenous Ca2+. TMB-8, an inhibitor of calcium mobilization, also strongly reduced angiotensin response. Similar results were obtained for angiotensin III (AIII) and vasopressin, two other agonists of prostaglandin production. AII- or serum-stimulated DNA synthesis was almost abolished by EGTA, whereas TMB-8, verapamil, and nifedipine had little or no effect. The production of prostaglandins triggered by angiotensins and vasopressin in VSMC is dependent on both intracellular and extracellular calcium, with calcium entering through L-type Ca2+ channels. Extracellular calcium is important for AII and serum mitogenic activity, but L-type Ca2+ channels do not appear to be implicated.
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PMID:Role of calcium in angiotensin II-induced prostaglandin release and DNA synthesis in rat vascular smooth muscle cells. 872 Apr 17

This review describes recent advances in our knowledge about the pathogenesis and therapeutic approaches to human gastric dysrhythmias. A number of clinical conditions has been found to be associated with gastric slow-wave rhythm disturbances that may relate to the induction of nausea and vomiting. Human and animal studies indicate that multiple neurohumoral factors are involved in the generation of gastric dysrhythmias. Antral distension and increased intestinal delivery of lipids may cause slow-wave disruption and development of nausea. This may be mediated by cholinergic and serotonergic pathways. Similarly, progesterone and estrogen may also disrupt gastric slow-wave rhythm in susceptible individuals. Prostaglandin overproduction in gastric smooth muscle appears to mediate slow-wave disruption in diabetes and with tobacco smoking. On the other hand, central cholinergic pathways play an important role in the genesis of gastric dysrhythmias associated with motion sickness. This may be mediated by vasopressin released from the pituitary. Although it is difficult to ascribe with certainty a causative role of slow-wave rhythm disturbances in the genesis of nausea and vomiting, the search has begun for novel antiemetic therapies based on their abilities to ablate or prevent gastric dysrhythmia formation. This includes the use of prostaglandin synthesis inhibitors, central muscarinic receptor antagonists, and dopamine receptor antagonists. Finally direct gastric electrical stimulation using a surgically implanted neurostimulator has shown promise in reducing emesis in patients with gastroparesis and gastric dysrhythmias.
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PMID:Physiology and pathophysiology of the interstitial cells of Cajal: from bench to bedside. VI. Pathogenesis and therapeutic approaches to human gastric dysrhythmias. 1206 86

This review of the physiology of ovarian contractility cites the functions of FSH and LH and the contribution of chorionic gonadotropin (HCG) to follicular swelling and rupture. Endogenous estrogen priming seems to be needed for this response. Luteninizing hormone releasing hormone (LHRH) administered during the ovulatory phase also causes changes to occur in ovaries treated with smooth muscle stimulants. A contractile response may be induced by alpha-adrenergic receptors, which confirms the finding of smooth muscle fibers in the ovaries. Spontaneous contractions have also been observed in ovaries removed from animals at estrus. Estrogen activate, progesterone inhibits ovarian contractility. In rabbits and guinea pigs spontaneous activity of the ovary is increased during early pregnancy. Treatment with nor- epinephrine inhibits this. Quiescent ovaries show marked activation with nor-adrenergic compounds such as nor-epinephrine and phenilephrine. Pretreatment with alpha-adrenergic blocking agents such as progranolol reverses this effect. Prostaglandin F-2-alpha is a more powerful stimulant on ovarian motility than vasopressin or oxytocin. The role of ovarian contractions in the reproductive function is still unknown. Further studies may provide ways of interfering with reproduction at the ovarian level.
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PMID:Ovarian contractility and ovulation. 1225 6

As first observed in rat adrenal glomerulosa cells, cytoplasmic Ca(2+) signal, induced by K(+), angiotensin II or vasopressin, evokes an increase in the level of reduced mitochondrial pyridine nucleotides, NADH and NADPH. Prostaglandin F(2)alpha and extracellular ATP exert similar effects in rat ovarian luteal cells. This coupling of cytoplasmic Ca(2+) concentration and mitochondrial metabolism occurs also when the stimuli are applied at physiological concentration and under conditions when no formation of high-Ca(2+) perimitochondrial microdomains may be presumed. We present evidence that low submicromolar Ca(2+) signals in the cytoplasm can increase mitochondrial Ca(2+) concentration and activate mitochondrial dehydrogenation processes. Several observations support the assumption that intramitochondrial Ca(2+) signals play a significant role in the stimulation of steroid hormone production.
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PMID:The effect of cytoplasmic Ca2+ signal on the redox state of mitochondrial pyridine nucleotides. 1502 83


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