Transient receptor potential channels in rat renal microcirculation: Actions of angiotensin II

Tsuneo Takenaka, Hiromichi Suzuki, Hirokazu Okada, Tsutomu Inoue, Yoshihiko Kanno, Yuri Ozawa, Koichi Hayashi, Takao Saruta

Research output: Contribution to journalArticle

39 Citations (Scopus)

Abstract

Background. This study assessed the calcium-activating mechanisms mediating glomerular arteriolar constriction by angiotensin II (Ang II). Methods. Immunohistochemical and physiological studies were carried out, using antibody against transient receptor potential (TRP)-1 and an isolated perfused kidney model. Results. Immunohistochemical experiments demonstrated that TRP-1 proteins were transcribed on both afferent and efferent arteriolar myocytes. In the first series of physiological experiments, Ang II (0.3 nmol/L) considerably constricted afferent (20.2 ± 0.9 to 14.9 ± 0.7 μm) and efferent arterioles (18.4 ± 0.7 to 14.0 ± 0.7 μm). The addition of nifedipine (1 μmol/L) restored decrements in afferent (to 20.0 ± 0.8 μm) but not efferent arteriolar diameters. Further administration of SKF-96365 (100 μmol/L), a TRP channel blocker, reversed efferent arteriolar constriction (to 16.2 ± 0.8 μmol/L). In the second group, although 2-aminoethoxydiphenyl borate (100 μmol/L), an inhibitor of inositol trisphosphate-induced calcium release (IP3CR), did not alter glomerular arteriolar diameters, it prevented Ang II-induced afferent arteriolar constriction and attenuated efferent arteriolar constriction (18.8 ± 0.8 to 16.9 ± μm). Subsequent removal of extracellular calcium abolished residual efferent arteriolar constriction (to 19.1 ± 0.8 μm). Conclusions. Our data provide evidence that Ang II elicits IP3CR, possibly inducing a cellular response that activates voltage-dependent calcium channels on afferent arterioles. The present results suggest that Ang II-induced efferent arteriolar constriction involves IP3CR and calcium influx sensitive to SKF-96365.

Original languageEnglish
Pages (from-to)558-565
Number of pages8
JournalKidney International
Volume62
Issue number2
DOIs
Publication statusPublished - 2002

Fingerprint

Transient Receptor Potential Channels
Microcirculation
Constriction
Angiotensin II
1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole
Kidney
Calcium
Arterioles
Inositol
Calcium Channels
Nifedipine
Muscle Cells
Antibodies
Proteins

Keywords

  • Arteriolar constriction
  • Calcium release
  • Cardiovascular disease
  • Cell signaling
  • Receptor-activated calcium channel
  • SKF-96365
  • Voltage-dependent calcium channel

ASJC Scopus subject areas

  • Nephrology

Cite this

Takenaka, T., Suzuki, H., Okada, H., Inoue, T., Kanno, Y., Ozawa, Y., ... Saruta, T. (2002). Transient receptor potential channels in rat renal microcirculation: Actions of angiotensin II. Kidney International, 62(2), 558-565. https://doi.org/10.1046/j.1523-1755.2002.00484.x

Transient receptor potential channels in rat renal microcirculation : Actions of angiotensin II. / Takenaka, Tsuneo; Suzuki, Hiromichi; Okada, Hirokazu; Inoue, Tsutomu; Kanno, Yoshihiko; Ozawa, Yuri; Hayashi, Koichi; Saruta, Takao.

In: Kidney International, Vol. 62, No. 2, 2002, p. 558-565.

Research output: Contribution to journalArticle

Takenaka, T, Suzuki, H, Okada, H, Inoue, T, Kanno, Y, Ozawa, Y, Hayashi, K & Saruta, T 2002, 'Transient receptor potential channels in rat renal microcirculation: Actions of angiotensin II', Kidney International, vol. 62, no. 2, pp. 558-565. https://doi.org/10.1046/j.1523-1755.2002.00484.x
Takenaka, Tsuneo ; Suzuki, Hiromichi ; Okada, Hirokazu ; Inoue, Tsutomu ; Kanno, Yoshihiko ; Ozawa, Yuri ; Hayashi, Koichi ; Saruta, Takao. / Transient receptor potential channels in rat renal microcirculation : Actions of angiotensin II. In: Kidney International. 2002 ; Vol. 62, No. 2. pp. 558-565.
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AU - Inoue, Tsutomu

AU - Kanno, Yoshihiko

AU - Ozawa, Yuri

AU - Hayashi, Koichi

AU - Saruta, Takao

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N2 - Background. This study assessed the calcium-activating mechanisms mediating glomerular arteriolar constriction by angiotensin II (Ang II). Methods. Immunohistochemical and physiological studies were carried out, using antibody against transient receptor potential (TRP)-1 and an isolated perfused kidney model. Results. Immunohistochemical experiments demonstrated that TRP-1 proteins were transcribed on both afferent and efferent arteriolar myocytes. In the first series of physiological experiments, Ang II (0.3 nmol/L) considerably constricted afferent (20.2 ± 0.9 to 14.9 ± 0.7 μm) and efferent arterioles (18.4 ± 0.7 to 14.0 ± 0.7 μm). The addition of nifedipine (1 μmol/L) restored decrements in afferent (to 20.0 ± 0.8 μm) but not efferent arteriolar diameters. Further administration of SKF-96365 (100 μmol/L), a TRP channel blocker, reversed efferent arteriolar constriction (to 16.2 ± 0.8 μmol/L). In the second group, although 2-aminoethoxydiphenyl borate (100 μmol/L), an inhibitor of inositol trisphosphate-induced calcium release (IP3CR), did not alter glomerular arteriolar diameters, it prevented Ang II-induced afferent arteriolar constriction and attenuated efferent arteriolar constriction (18.8 ± 0.8 to 16.9 ± μm). Subsequent removal of extracellular calcium abolished residual efferent arteriolar constriction (to 19.1 ± 0.8 μm). Conclusions. Our data provide evidence that Ang II elicits IP3CR, possibly inducing a cellular response that activates voltage-dependent calcium channels on afferent arterioles. The present results suggest that Ang II-induced efferent arteriolar constriction involves IP3CR and calcium influx sensitive to SKF-96365.

AB - Background. This study assessed the calcium-activating mechanisms mediating glomerular arteriolar constriction by angiotensin II (Ang II). Methods. Immunohistochemical and physiological studies were carried out, using antibody against transient receptor potential (TRP)-1 and an isolated perfused kidney model. Results. Immunohistochemical experiments demonstrated that TRP-1 proteins were transcribed on both afferent and efferent arteriolar myocytes. In the first series of physiological experiments, Ang II (0.3 nmol/L) considerably constricted afferent (20.2 ± 0.9 to 14.9 ± 0.7 μm) and efferent arterioles (18.4 ± 0.7 to 14.0 ± 0.7 μm). The addition of nifedipine (1 μmol/L) restored decrements in afferent (to 20.0 ± 0.8 μm) but not efferent arteriolar diameters. Further administration of SKF-96365 (100 μmol/L), a TRP channel blocker, reversed efferent arteriolar constriction (to 16.2 ± 0.8 μmol/L). In the second group, although 2-aminoethoxydiphenyl borate (100 μmol/L), an inhibitor of inositol trisphosphate-induced calcium release (IP3CR), did not alter glomerular arteriolar diameters, it prevented Ang II-induced afferent arteriolar constriction and attenuated efferent arteriolar constriction (18.8 ± 0.8 to 16.9 ± μm). Subsequent removal of extracellular calcium abolished residual efferent arteriolar constriction (to 19.1 ± 0.8 μm). Conclusions. Our data provide evidence that Ang II elicits IP3CR, possibly inducing a cellular response that activates voltage-dependent calcium channels on afferent arterioles. The present results suggest that Ang II-induced efferent arteriolar constriction involves IP3CR and calcium influx sensitive to SKF-96365.

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KW - Calcium release

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KW - Cell signaling

KW - Receptor-activated calcium channel

KW - SKF-96365

KW - Voltage-dependent calcium channel

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