Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/13271
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dc.contributor.authorBurrell, Louise Men
dc.contributor.authorPhillips, P Aen
dc.contributor.authorStephenson, J Men
dc.contributor.authorRisvanis, Johnen
dc.contributor.authorRolls, K Aen
dc.contributor.authorJohnston, Colin Ien
dc.date.accessioned2015-05-16T03:05:37Z
dc.date.available2015-05-16T03:05:37Z
dc.date.issued1994-06-01en
dc.identifier.citationHypertension; 23(6 Pt 1): 737-43en
dc.identifier.govdoc8206571en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/13271en
dc.description.abstractWe studied the contribution of vasopressin to the maintenance of high blood pressure in deoxycorticosterone acetate (DOCA)-salt hypertension in the rat using the nonpeptide orally effective vasopressin V1 receptor antagonist OPC-21268. Binding kinetic studies demonstrated that oral OPC-21268 (30 mg/kg) acted as a competitive antagonist at the vasopressin V1 receptor in DOCA-salt and salt control rats. Basal mean intra-arterial blood pressure was 140 +/- 4 mm Hg (n = 12) in DOCA-salt rats compared with 111 +/- 2 mm Hg in salt control rats (n = 18). Acute oral OPC-21268 (30 mg/kg) significantly (P < .01) reduced mean intra-arterial pressure in DOCA-salt hypertension, with an average maximal decrease of 24 +/- 3 mm Hg occurring at 2.5 +/- 0.7 hours after dosing. Systolic blood pressure (tail-cuff) in DOCA-salt rats was 178 +/- 2 mm Hg. Chronic oral OPC-21268 (30 mg/kg) twice daily for 7 days significantly (P < .01) reduced systolic blood pressure in DOCA-salt hypertension, with an average maximal decrease of 27 +/- 5 mm Hg. The antihypertensive effect was reversed 5 days after treatment with OPC-21268 was stopped. In water control rats basal systolic pressure (120 +/- 1 mm Hg, n = 20) was unchanged by chronic oral OPC-21268 (30 mg/kg twice daily for 7 days), and this was confirmed by direct measurement of mean intra-arterial pressure. After chronic oral OPC-21268 (30 mg/kg twice daily for 7 days) hepatic V1 receptor binding was significantly reduced for up to 10 hours (P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)en
dc.language.isoenen
dc.subject.otherAdministration, Oralen
dc.subject.otherAnimalsen
dc.subject.otherAntidiuretic Hormone Receptor Antagonistsen
dc.subject.otherArginine Vasopressin.metabolismen
dc.subject.otherBinding Sitesen
dc.subject.otherBlood Pressure.drug effectsen
dc.subject.otherDesoxycorticosteroneen
dc.subject.otherFemaleen
dc.subject.otherHypertension.chemically induced.physiopathologyen
dc.subject.otherKineticsen
dc.subject.otherMesenteric Arteries.drug effectsen
dc.subject.otherPiperidines.pharmacologyen
dc.subject.otherQuinolones.pharmacologyen
dc.subject.otherRatsen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherReceptors, Vasopressin.classificationen
dc.subject.otherSodium Chlorideen
dc.subject.otherSystoleen
dc.subject.otherVascular Resistance.drug effectsen
dc.titleBlood pressure-lowering effect of an orally active vasopressin V1 receptor antagonist in mineralocorticoid hypertension in the rat.en
dc.typeJournal Articleen
dc.identifier.journaltitleHypertensionen
dc.identifier.affiliationUniversity of Melbourne, Austin Hospital, Heidelberg, Victoria, Australiaen
dc.description.pages737-43en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/8206571en
dc.type.austinJournal Articleen
item.languageiso639-1en-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeJournal Article-
item.grantfulltextnone-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
crisitem.author.deptCardiology-
crisitem.author.deptGeneral Medicine-
crisitem.author.deptMedicine (University of Melbourne)-
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