Angiotensin converting enzyme inhibitor normalizes vascular natriuretic peptide type A receptor gene expression via bradykinin-dependent mechanism in hypertensive rats

Takanobu Yoshimoto; Kiyoko Naruse; Kiseko Shionoya; Masami Tanaka; Toshiro Seki; Hiromi Hagiwara; Shigehisa Hirose; Lam Sau Kuen; Hiroshi Demura; Mitsuhide Naruse; Takamura Muraki

doi:10.1006/bbrc.1996.0010

Angiotensin converting enzyme inhibitor normalizes vascular natriuretic peptide type A receptor gene expression via bradykinin-dependent mechanism in hypertensive rats

Takanobu Yoshimoto, Kiyoko Naruse, Kiseko Shionoya, Masami Tanaka, Toshiro Seki, Hiromi Hagiwara, Shigehisa Hirose, Lam Sau Kuen, Hiroshi Demura, Mitsuhide Naruse, Takamura Muraki

Research output: Contribution to journal › Article › peer-review

6 Citations (Scopus)

Abstract

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.

Original language	English
Pages (from-to)	50-53
Number of pages	4
Journal	Biochemical and Biophysical Research Communications
Volume	218
Issue number	1
DOIs	https://doi.org/10.1006/bbrc.1996.0010
Publication status	Published - 1996 Jan 5
Externally published	Yes

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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10.1006/bbrc.1996.0010

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Yoshimoto, T., Naruse, K., Shionoya, K., Tanaka, M., Seki, T., Hagiwara, H., Hirose, S., Kuen, L. S., Demura, H., Naruse, M., & Muraki, T. (1996). Angiotensin converting enzyme inhibitor normalizes vascular natriuretic peptide type A receptor gene expression via bradykinin-dependent mechanism in hypertensive rats. Biochemical and Biophysical Research Communications, 218(1), 50-53. https://doi.org/10.1006/bbrc.1996.0010

Angiotensin converting enzyme inhibitor normalizes vascular natriuretic peptide type A receptor gene expression via bradykinin-dependent mechanism in hypertensive rats. / Yoshimoto, Takanobu; Naruse, Kiyoko; Shionoya, Kiseko et al.

In: Biochemical and Biophysical Research Communications, Vol. 218, No. 1, 05.01.1996, p. 50-53.

Research output: Contribution to journal › Article › peer-review

Yoshimoto, T, Naruse, K, Shionoya, K, Tanaka, M, Seki, T, Hagiwara, H, Hirose, S, Kuen, LS, Demura, H, Naruse, M & Muraki, T 1996, 'Angiotensin converting enzyme inhibitor normalizes vascular natriuretic peptide type A receptor gene expression via bradykinin-dependent mechanism in hypertensive rats', Biochemical and Biophysical Research Communications, vol. 218, no. 1, pp. 50-53. https://doi.org/10.1006/bbrc.1996.0010

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title = "Angiotensin converting enzyme inhibitor normalizes vascular natriuretic peptide type A receptor gene expression via bradykinin-dependent mechanism in hypertensive rats",

abstract = "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.",

author = "Takanobu Yoshimoto and Kiyoko Naruse and Kiseko Shionoya and Masami Tanaka and Toshiro Seki and Hiromi Hagiwara and Shigehisa Hirose and Kuen, {Lam Sau} and Hiroshi Demura and Mitsuhide Naruse and Takamura Muraki",

note = "Funding Information: We thank the Disease Model Cooperative Research Association (Kyoto, Japan) for supplying SHR-SP/Izm, Takeda Chemical Industries, Ltd. (Osaka, Japan) for the supply of derapril and TCV-116, and Hoechst AG (Frankfurt, Germany) for the supply of Hoe 140. This work was supported in part by research grants from the Japanese Ministry of Education, Science, and Culture, the Japanese Ministry of Health and Welfare “Disorders of Adrenal Hormones” Research Committee, Japan, and the Hiroto Yoshioka Memorial Medical Research Award of Tokyo Women{\textquoteright}s Medical College awarded to M. Naruse, T. Muraki, and H. Demura.",

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AU - Kuen, Lam Sau

AU - Demura, Hiroshi

AU - Naruse, Mitsuhide

AU - Muraki, Takamura

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N2 - 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.

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Angiotensin converting enzyme inhibitor normalizes vascular natriuretic peptide type A receptor gene expression via bradykinin-dependent mechanism in hypertensive rats

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