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Angiotensin Converting Enzyme Inhibitor Normalizes Vascular Natriuretic Peptide Type A Receptor Gene Expression via Bradykinin-Dependent Mechanism in Hypertensive Rats
Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo, 162, Japan.
Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo, 162, Japan.
Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo, 162, Japan.
Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Tokyo, 162, Japan.
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1996 (English)In: Biochemical and Biophysical Research Communications - BBRC, ISSN 0006-291X, E-ISSN 1090-2104, Vol. 218, no 1, p. 50-53Article in journal (Refereed) Published
Abstract [en]

We previously demonstrated that angiotensin converting enzyme (ACE) inhibitor normalizes the up-regulated gene expression of vascular natriuretic peptide type A (NP-A) receptor in hypertensive rats. To elucidate the mechanism, we examined the effect of angiotensin II receptor (AT1) antagonist (TCV-116) and bradykinin receptor (B2) antagonist (Hoe 140) on the NP-A receptor mRNA level in the aorta of genetically hypertensive rats (SHR-SP/Izm) using ribonuclease protection assay. The effect of ACE inhibitor on the NP-A receptor mRNA level was completely abolished by a concomitant administration of Hoe 140, while TCV-116 did not show any significant effect on the NP-A receptor mRNA level. These results suggest that bradykinin plays an important role in the regulation of the vascular NP-A receptor gene expression.

Place, publisher, year, edition, pages
Elsevier, 1996. Vol. 218, no 1, p. 50-53
National Category
Pharmacology and Toxicology
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URN: urn:nbn:se:liu:diva-150402DOI: 10.1006/bbrc.1996.0010ISI: A1996TP75400010PubMedID: 8573174Scopus ID: 2-s2.0-0030021085OAI: oai:DiVA.org:liu-150402DiVA, id: diva2:1240654
Available from: 2018-08-22 Created: 2018-08-22 Last updated: 2018-08-30Bibliographically approved

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