β-Adrenoceptor antagonist propranolol potentiates hypotensive action of natriuretic peptides

Takanobu Yoshimoto, Mitsuhide Naruse, Kaoru Ire, Akiyo Tanabe, Toshirou Seki, Masami Tanaka, Toshihiro Imaki, Kiyoko Naruse, Takamura Muraki, Yuzuru Matsuda, Hiroshi Demura

研究成果: Article査読

17 被引用数 (Scopus)

抄録

β-Adrenoceptor antagonists are known to increase plasma atrial natriuretic peptide (ANP) levels despite their hypotensive action. The aim of the present study was to examine the role of the ANP system in the antihypertensive effects of a β-adrenoceptor antagonist. We investigated the effects of propranolol (75 mg kg-1 day-1, p.o., 4 weeks) on the ANP system in stroke-prone spontaneously hypertensive rats. Plasma ANP levels were significantly higher in the propranolol group than in the control group. Both receptor densities and mRNA levels of ANP(C) receptor were significantly decreased in the lung as the major site of ANP clearance from the circulation. In contrast, both central venous pressure and ANP mRNA levels in the heart were not significantly different between the two groups. Under both basal and ANP-stimulated conditions, the cGMP content in the aorta was significantly greater in the propranolol group than in the control group, whereas the basal and stimulated cGMP content of the kidney was similar in the two groups. Inhibition of endogenous ANP action by a specific ANP receptor antagonist, HS-142-1, produced a greater increase of blood pressure in the propranolol group than in the control group. These results suggest potentiation of natriuretic peptide activity as a new antihypertensive mechanism of the β-adrenoceptor antagonist propranolol.

本文言語English
ページ(範囲)61-66
ページ数6
ジャーナルEuropean journal of pharmacology
351
1
DOI
出版ステータスPublished - 1998 6 12

ASJC Scopus subject areas

  • 薬理学

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