Direct visualization of effects of endothelin on the renal microvasculature

Rodger Loutzenhiser, Murray Epstein, Koichi Hayashi, Charles Horton

研究成果: Article

124 引用 (Scopus)

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The renal microvascular and hemodynamic actions of endothelin were assessed directly in isolated perfused hydronephrotic (HYD) and normal kidneys, respectively. In HYD kidneys endothelin was a potent vasoconstrictor of the afferent arteriole (AA), eliciting a threshold vasoconstrictor response at 0.01 nM (P < 0.05). At 0.1 and 0.3 nM, endothelin reduced AA diameter by 22 ± 6 (P < 0.025) and 41 ± 4% (P < 0.001), respectively. Furthermore, endothelin provoked oscillatory vasomotion in the AA. In contrast, endothelin had less effect on the efferent arteriole (EA), reducing EA diameter by only 7 ± 4 (P > 0.20) and 13 ± 4% (P < 0.05), at 0.1 and 0.3 nM, respectively. In normal kidneys endothelin elicited a long-lasting vasoconstriction with a dose dependency similar to that observed in the AA of HYD kidneys. Furthermore, endothelin reduced glomerular filtration rate (GFR) from 0.58 ± 0.04 to 0.09 ± 0.05 ml·min-1· g-1 (P < 0.001) in this model. Both the AA vasoconstriction and reduction in GFR were completely reversed by nifedipine. These findings indicate that endothelin is a potent renal vasoconstrictor that decreases GFR by a predominant vasoconstriction of the AA. Our observations are consistent with the postulate that endothelin elicits renal vasoconstriction via a mechanism involving dihydropyridine-sensitive calcium channels and that such calcium channels play a prominent role in the activation of the AA.

元の言語English
ジャーナルAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
258
発行部数1 27-1
出版物ステータスPublished - 1990

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Endothelins
Microvessels
Arterioles
Kidney
Vasoconstriction
Vasoconstrictor Agents
Glomerular Filtration Rate
Calcium Channels
Nifedipine
Hemodynamics

ASJC Scopus subject areas

  • Physiology

これを引用

Direct visualization of effects of endothelin on the renal microvasculature. / Loutzenhiser, Rodger; Epstein, Murray; Hayashi, Koichi; Horton, Charles.

:: American Journal of Physiology - Renal Fluid and Electrolyte Physiology, 巻 258, 番号 1 27-1, 1990.

研究成果: Article

Loutzenhiser, Rodger ; Epstein, Murray ; Hayashi, Koichi ; Horton, Charles. / Direct visualization of effects of endothelin on the renal microvasculature. :: American Journal of Physiology - Renal Fluid and Electrolyte Physiology. 1990 ; 巻 258, 番号 1 27-1.
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abstract = "The renal microvascular and hemodynamic actions of endothelin were assessed directly in isolated perfused hydronephrotic (HYD) and normal kidneys, respectively. In HYD kidneys endothelin was a potent vasoconstrictor of the afferent arteriole (AA), eliciting a threshold vasoconstrictor response at 0.01 nM (P < 0.05). At 0.1 and 0.3 nM, endothelin reduced AA diameter by 22 ± 6 (P < 0.025) and 41 ± 4{\%} (P < 0.001), respectively. Furthermore, endothelin provoked oscillatory vasomotion in the AA. In contrast, endothelin had less effect on the efferent arteriole (EA), reducing EA diameter by only 7 ± 4 (P > 0.20) and 13 ± 4{\%} (P < 0.05), at 0.1 and 0.3 nM, respectively. In normal kidneys endothelin elicited a long-lasting vasoconstriction with a dose dependency similar to that observed in the AA of HYD kidneys. Furthermore, endothelin reduced glomerular filtration rate (GFR) from 0.58 ± 0.04 to 0.09 ± 0.05 ml·min-1· g-1 (P < 0.001) in this model. Both the AA vasoconstriction and reduction in GFR were completely reversed by nifedipine. These findings indicate that endothelin is a potent renal vasoconstrictor that decreases GFR by a predominant vasoconstriction of the AA. Our observations are consistent with the postulate that endothelin elicits renal vasoconstriction via a mechanism involving dihydropyridine-sensitive calcium channels and that such calcium channels play a prominent role in the activation of the AA.",
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N2 - The renal microvascular and hemodynamic actions of endothelin were assessed directly in isolated perfused hydronephrotic (HYD) and normal kidneys, respectively. In HYD kidneys endothelin was a potent vasoconstrictor of the afferent arteriole (AA), eliciting a threshold vasoconstrictor response at 0.01 nM (P < 0.05). At 0.1 and 0.3 nM, endothelin reduced AA diameter by 22 ± 6 (P < 0.025) and 41 ± 4% (P < 0.001), respectively. Furthermore, endothelin provoked oscillatory vasomotion in the AA. In contrast, endothelin had less effect on the efferent arteriole (EA), reducing EA diameter by only 7 ± 4 (P > 0.20) and 13 ± 4% (P < 0.05), at 0.1 and 0.3 nM, respectively. In normal kidneys endothelin elicited a long-lasting vasoconstriction with a dose dependency similar to that observed in the AA of HYD kidneys. Furthermore, endothelin reduced glomerular filtration rate (GFR) from 0.58 ± 0.04 to 0.09 ± 0.05 ml·min-1· g-1 (P < 0.001) in this model. Both the AA vasoconstriction and reduction in GFR were completely reversed by nifedipine. These findings indicate that endothelin is a potent renal vasoconstrictor that decreases GFR by a predominant vasoconstriction of the AA. Our observations are consistent with the postulate that endothelin elicits renal vasoconstriction via a mechanism involving dihydropyridine-sensitive calcium channels and that such calcium channels play a prominent role in the activation of the AA.

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