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 prostaglandins (PG) has been evoked in the mechanism of action of indapamide. Indeed, PG can act in the regulation of the blood pressure (BP) at different levels: vasodilatation, diuretic, natriuretic, antagonism of angiotensin II and vasopressin (VP), action on adrenergic system. To confirm this hypothesis, we studied the action of certain eicosanoids inhibitors on the antihypertensive action of indapamide in the SHR rat, anaesthetized with pentobarbital (40 mg/kg i.p.). Indapamide (3 mg/kg i.p.) induces significant decrease on BP over 60 min. Mepacrine (5 mg/kg i.p.), phospholipase A2 inhibitor, indomethacin (5 mg/kg i.p), cyclo-oxygenase inhibitor, and tranylcypromine (0,1 mg/kg i.p.), prostacyclin synthase inhibitor, antagonize the antihypertensive action of indapamide. In order to eliminate the importance of VP, we used Brattleboro rats (genetically depleted in VP): indapamide (3 mg/kg i.p.) maintains its hypotensive activity. To eliminate the role of kidney in PG synthesis, we have used cyclo-oxygenase extrarenal inhibitor (sulindac) and the bilateral nephrectomy. Sulindac (1,25 mg/kg i.p.) and the bilateral nephrectomy do not remove the hypotensive action of indapamide. These results, demonstrating the PG extrarenal role and probably that of PGI2, localized in the vascular wall, could explain part of the antihypertensive mechanism of indapamide.
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PMID:[Role of prostaglandins in the mechanism of action of indapamide]. 212 58

The modulation of the production of prostacyclin and thromboxane from cat and cat aortic tissue slices by different vasoactive agents has been studied in order to reveal whether the release of these main two vasoactive prostanoids goes in parallel or may be controlled independently. Norepinephrine, isoproterenol, phentolamine, propranolol, angiotensin II, vasopressin, bradykinin, thrombin, verapamil, gallopamil, dopamine or methionin enkephalin were added to the incubation medium and 6-keto-PGF1 alpha (the stable metabolite of prostacyclin) and TxB2 (the stable metabolite of thromboxane) were determined in the supernatant by radioimmunoassay. The ratio of the release of prostacyclin and thromboxane was computed. Norepinephrine increased both prostacyclin and thromboxane release. Isoproterenol increased the ratio of prostacyclin and thromboxane released in cat aortic tissue slices. Phentolamine and propranolol had no effects. Angiotensin II induced a slight but statistically insignificant increase in the ratio of the two prostanoids released. Vasopressin increased thromboxane release only. Bradykinin stimulated the prostacyclin while thrombin stimulated the thromboxane release. Verapamil decreased both prostacyclin and thromboxane production. Gallopamil decreased prostacyclin release and increased thromboxane release from vessel wall slices in a certain concentration range causing a characteristic dose dependent minimum in the ratio of prostacyclin and thromboxane release. Dopamine separately increased prostacyclin release while enkephalin had no significant effect. The data obtained show that in vascular tissue some unidentified yet cytophysiological mechanisms might exist which specifically control the activities of the prostacyclin synthase and thromboxane synthase enzymes.
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PMID:Prostacyclin and thromboxane production of rat and cat arterial tissue is altered independently by several vasoactive substances. 890 22

Mesangial cells play an important role in glomerular function. They are an important source of cyclooxygenase (COX)-derived arachidonic acid metabolites, including prostaglandin E(2) and prostacyclin. Prostacyclin receptor (IP) mRNA was amplified from cultured mesangial cell total RNA by RT-PCR. While the prostaglandin E(2) receptor subtype EP(2) was not detected, EP(1,3,4) mRNA was amplified. Also, IP protein was noted in mesangial cells, proximal tubules, inner medullary collecting ducts, and the inner and outer medulla. But no protein was detected in whole cortex preparations. Prostacyclin analogues: cicaprost and iloprost, increased cAMP levels in mesangial cells. On the other hand, arginine-vasopressin and angiotensin II increased intracellular calcium in mesangial cells, but cicaprost, iloprost and prostaglandin E(2) had no effect. Moreover, a 50% inhibition of cicaprost- and iloprost-cAMP stimulation was observed upon mesangial cell exposure to 25 and 35 mM glucose for 5 days. But no change in IP mRNA was observed at any glucose concentration or time exposure. Although 25 mM glucose had no effect on COX-1 protein levels, COX-2 was increased up to 50%. In contrast, PGIS levels were reduced by 50%. Thus, we conclude that the prostacyclin/IP system is present in cultured rat mesangial cells, coupling to a cAMP stimulatory pathway. High glucose altered both enzymes in the PGI(2) synthesis pathway, increasing COX-2 but reducing PGIS. In addition, glucose diminished the cAMP response to prostacyclin analogues. Therefore, glucose attenuates the PGI(2)/IP system in cultured rat mesangial cells.
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PMID:Characterization of the PGI2/IP system in cultured rat mesangial cells. 1506 48