Rho-kinase Contributes to Pressure-induced Constriction ofRenal Microvessels
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- Homma Koichiro
- Departments of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan Emergency Medicine, School of Medicine, Keio University, Tokyo, Japan
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- Hayashi Koichi
- Departments of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan
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- Wakino Shu
- Departments of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan
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- Tokuyama Hirobumi
- Departments of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan
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- Kanda Takeshi
- Departments of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan
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- Tatematsu Satoru
- Departments of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan
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- Hasegawa Kazuhiro
- Departments of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan
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- Fujishima Seitaro
- Emergency Medicine, School of Medicine, Keio University, Tokyo, Japan
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- Hori Shingo
- Emergency Medicine, School of Medicine, Keio University, Tokyo, Japan
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- Saruta Takao
- Departments of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan
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- Itoh Hiroshi
- Departments of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan
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抄録
Renal afferent arterioles (AFF) regulate glomerular capillary pressure through two main mechanisms: the myogenic response (MYO) and tubuloglomerular feedback (TGF). Because Rho-kinase and nitric oxide synthase (NOS) are established factors that modulate vascular tone, we examined the role of these factors in pressure-induced AFF tone in Wistar-Kyoto rats and in spontaneously hypertensive rats (SHR) using an intravital CCD camera. Elevated renal perfusion pressure elicited marked AFF constriction that was partially inhibited by gadolinium, furosemide and fasudil, which inhibit MYO, TGF and Rho-kinase, respectively; however, this AFF constriction was completely blocked by combined treatment with fasudil+gadolinium or fasudil+furosemide. S-methyl-L-thiocitrulline (SMTC) partially reversed the fasudil-induced inhibition of TGF-mediated, but not that of MYO-mediated, AFF constriction. In SHR, the pressure-induced AFF response was enhanced, and MYO- and TGF-induced constriction were exaggerated. In the presence of gadolinium, SMTC partially mitigated the fasudil-induced inhibition of TGF-mediated AFF constriction. Immunoblot analyses demonstrated that both Rho-kinase activity and neuronal NOS were augmented in SHR kidneys. In conclusion, Rho-kinase contributes to MYO- and TGF-mediated AFF responses, and these responses are enhanced in SHR. Furthermore, neuronal NOS-induced nitric oxide modulates the TGF mechanism. This mechanism constitutes a target for Rho-kinase in TGF-mediated AFF constriction.
収録刊行物
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- Ｔｈｅ Ｋｅｉｏ Ｊｏｕｒｎａｌ ｏｆ Ｍｅｄｉｃｉｎｅ
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Ｔｈｅ Ｋｅｉｏ Ｊｏｕｒｎａｌ ｏｆ Ｍｅｄｉｃｉｎｅ 63 (1), 1-12, 2014
The Keio Journal of Medicine