Combined oral contraceptive-induced hypertension is accompanied by endothelial dysfunction and upregulated intrarenal angiotensin II type 1 receptor gene expression

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dc.contributor.authorOlatunji, L.A.
dc.contributor.authorSeok, Y.
dc.contributor.authorIgunnu, Adedoyin
dc.contributor.authorKang, S.
dc.contributor.authorKim, I.
dc.date.accessioned2020-05-29T15:40:58Z
dc.date.available2020-05-29T15:40:58Z
dc.date.issued2016
dc.description.abstractCombined oral contraceptive (COC) use is associated with increased risk of developing hypertension. Activation of the intrarenal renin-angiotensin system (RAS) and endothelial dysfunction play an important role in the development of hypertension.We tested the hypothesis that COC causes hypertension that is associated with endothelial dysfunction and upregulation of intrarenal angiotensin-converting enzyme 1 (Ace1) and angiotensin II type 1 receptor (At1r). Female Sprague-Dawley rats aged 12 weeks received (p.o.) olive oil (control) and a combination of 0.1 μg ethinyl estradiol and 1.0 μg norgestrel (low COC) or 1.0μg ethinyl estradiol and 10.0 μg norgestrel (high COC) daily for 6 weeks. Blood pressure was recorded by tail cuff plethysmography. Expression of genes in kidney cortex was determined by quantitative real time polymerase chain reaction. COC treatment led to increased blood pressure, circulating uric acid, C-reactive protein and plasminogen activator inhibitor-1, renal uric acid, and expression of renal Ace1 and At1r. COC treatment resulted in increased contractile responses to phenylephrine in endothelium-denuded aortic rings. Endothelium-dependent relaxation responses to acetylcholine, but not endothelium independent relaxation responses to nitric oxide (NO) donation by sodium nitroprusside, were attenuated in COC-exposed rings. Impaired relaxation responses to acetylcholine were masked by the presence of NO synthase inhibitor (L-NAME) in the COC-exposed rings, whereas the responses to acetylcholine in the presence of selective cyclooxygenase-2 inhibitor (NS-398) were enhanced. These findings indicate that COC induces hypertension that is accompanied by endothelial dysfunction, upregulated intrarenal Ace1 and At1r expression, and elevated proinflammatory biomarkers.en_US
dc.description.sponsorshipThis research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF)(2013R1A1A2058145,and2013K2A4A1044932),fundedbythe Ministry of Education, Science and Technology; the Korean Health Technology R&D Project; Ministry of Health and Welfare, Republic of Korea (HI13C1527); and Kyungpook National University Research Fund, 2014.en_US
dc.identifier.urihttps://www.ncbi.nlm.nih.gov/pubmed/27447455
dc.identifier.urihttp://hdl.handle.net/123456789/4132
dc.language.isoenen_US
dc.publisherSpringeren_US
dc.relation.ispartofseriesNaunyn-Schmiedeberg's Arch Pharmacol;389:1147–1157
dc.subjectGene expressionen_US
dc.subjectInflammationen_US
dc.subjectNitricoxideen_US
dc.subjectRenal angiotensin receptoren_US
dc.subjectUric aciden_US
dc.subjectVascular endotheliumen_US
dc.titleCombined oral contraceptive-induced hypertension is accompanied by endothelial dysfunction and upregulated intrarenal angiotensin II type 1 receptor gene expressionen_US
dc.typeArticleen_US

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