Selective Blockade of Endothelin Receptor Subtypes on Systemic and Renal Vascular Responses to Endothelin-1 and IRL1620, a Selective Endothelin ETB-Receptor Agonist, in Anesthetized Rats.
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- Matsuura Takeshi
- Department of Pharmacology, Osaka City University Medical School
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- Yukimura Tokihito
- Department of Pharmacology, Osaka City University Medical School
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- Kim Shokei
- Department of Pharmacology, Osaka City University Medical School
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- Miura Katsuyuki
- Department of Pharmacology, Osaka City University Medical School
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- Iwao Hiroshi
- Department of Pharmacology, Osaka City University Medical School
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抄録
By using BQ-788 as a selective endothelin ETB-receptor antagonist and FR139317 as a selective endothelin ETA-receptor antagonist, we have characterized the receptor subtypes mediating the systemic and renal vascular effects of endothelin-1 and IRL1620, a selective endothelin ETB-receptor agonist (succinyl-[G1u9, A1a11.5]-endothelin-1(8-21)), in anesthetized rats. Bolus intravenous injection of endothelin-1 (0.5 nmol/kg) and IRL1620 (1.65 nmol/kg) produced a transient fall in systemic blood pressure followed by a sustained increase. The initial fall in blood pressure observed after endothelin-1 and IRL1620 administration was completely blocked by BQ-788 (0.5 μmol/kg, i.v.), whereas the pressor response was blocked by FR139317 (0.8, μmol/kg, i.v.). Renal blood flow was decreased and calculated renal vascular resistance was dramatically increased by endothelin-1 and IRL1620. The reduction of renal blood flow by endothelin-1 was significantly suppressed by FR139317 but potentiated by BQ-788. Both BQ-788 and FR139317 partially blocked the renal vasoconstriction by IRL1620. Pretreatment by BQ-788 itself decreased renal blood flow by 14.1%. These results indicate that the systemic depressor responses induced by endothelin-1 and IRL 1620 are mediated through the endothelin ETB-receptor, and the pressor responses are mediated through the endothelin ETA-receptor. In the renal vasculature of anesthetized rats, it is suggested that vasoconstriction is mediated through both endothelin ETA and ETB-receptors and that endothelin ETB-receptors may be also involved in vasodilating responses to endothelin peptides.
収録刊行物
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- Jpn.J.Pharmacol.
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Jpn.J.Pharmacol. 71 (3), 213-222, 1996
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390001204285220736
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- NII論文ID
- 10008188918
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- NII書誌ID
- AA00691188
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- COI
- 1:CAS:528:DyaK28XksFOntrg%3D
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- ISSN
- 13473506
- 00215198
- http://id.crossref.org/issn/00215198
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- PubMed
- 8854203
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可