1. Volume 57, Issue 1, Pages 215-223 (January 2000)
Role of protein kinase C in angiotensin II-induced constriction of renal microvessels 
Takahiko Nagahama, Koichi Hayashi, Yuri Ozawa, Tsuneo Takenaka, Takao Saruta, M.D. 
Kidney International 
Volume 57, Issue 1, Pages (January 2000)
DOI: /j x
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2. Figure 1
Vasodilator action of a phospholipase C inhibitor on angiotensin II-induced afferent and efferent arteriolar constriction. NCDC, 2-nitro-4-carboxyphenyl-N,N-diphenyl-carbamate. *P < 0.01 vs. angiotensin II.
Kidney International  , DOI: ( /j x)
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3. Figure 2
Vasodilator action of pranidipine on angiotensin II-constricted afferent (▴) and efferent (○) arterioles. In contrast to marked vasodilation of afferent arterioles, efferent arterioles manifested blunted vasodilator responses to pranidipine. (A) *P < 0.01 vs. angiotensin II. (B) P < 0.05 vs. afferent arterioles.
Kidney International  , DOI: ( /j x)
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4. Figure 3
Effects of chelerythrine on angiotensin II-induced constriction of afferent (▴) and efferent (○) arterioles. Chelerythrine reversed the vasoconstriction of both afferent and efferent arterioles in a concentration-dependent manner (A). The ability of chelerythrine to inhibit angiotensin II-induced constriction was greater in the efferent arteriole than in the afferent arteriole (B). (A) *P < 0.05; **P < 0.01 vs. angiotensin II; +P < 0.05 vs. chelerythrine (1 μmol/L). (B) †P < 0.05 vs. efferent arterioles.
Kidney International  , DOI: ( /j x)
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5. Figure 4
Vasoconstrictor action of PKC stimulators on afferent (▴) and efferent (○) arterioles. Both PKC stimulators elicited afferent and efferent arteriolar constriction in a dose-dependent manner. Subsequent addition of pranidipine failed to reverse these arteriolar tones, but chelerythrine completely returned the vessel diameters. Abbreviations are: PMA, phorbol 12-myristate 13-acetate; OAG, 1-oleoyl 2-acetyl sn-glycerol. (A) *P < 0.05; **P < 0.01 vs. control; +P < 0.05 vs. PMA (1 μmol/L). (B) **P < 0.01 vs. control; +P < 0.05 vs. OAG (3 μmol/L).
Kidney International  , DOI: ( /j x)
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6. Figure 5
Summary of the role of extracellular calcium in mediating the protein kinase C (PKC)-induced microvascular constriction. Perfusion with zero calcium medium completely prevented the PKC-induced constriction of afferent (▴) and efferent (○) arterioles (A). Furthermore, PKC-induced vasoconstriction was abolished by manganese (B). Abbreviations are: PMA, phorbol 12-myristate 13-acetate; Mn, manganese. *P < 0.05 vs. PMA.
Kidney International  , DOI: ( /j x)
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7. Figure 6
Vasodilator action of thapsigargin and dantrolene on protein kinase C-induced afferent (▴) and efferent (○) arteriolar constriction. The vasodilator action of these agents was greater in the afferent arteriole than in the efferent arteriole during phorbol 12-myristate 13-acetate-induced vasoconstriction (PMA). *P < 0.05 vs. PMA.
Kidney International  , DOI: ( /j x)
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8. Figure 7
Hypothetical diagram illustrating the role of protein kinase C in angiotensin II-induced constriction of renal microvessels. In the afferent arteriole, angiotensin II (Ang II) activates phospholipase C (PLC), and produces inositol trisphosphate (IP3) and diacyl glycerol (DAG; filled arrows). The increased IP3 facilitates calcium release from intracellular stores, activates chloride channels10, and opens voltage-dependent calcium channels (VDCC)3,4,11. Although DAG stimulates protein kinase C (PKC), the Ang II-activated PKC modulates the VDCC pathway by affecting IP3 pathways (hatched arrow). In contrast, when PKC is directly activated by phorbol ester (PMA) without stimulation of IP3 pathways (open arrows), PKC stimulates nonselective cation channels (NSCC), but has no effect on VDCC. In the efferent arteriole, both IP3 and DAG elevate the intracellular calcium concentration by different mechanisms12. Although the calcium influx through NSCC constitutes a major route for the PKC-mediated calcium entry, PKC also modulates the IP3-induced calcium release, resulting in enhanced calcium releases from intracellular stores.
Kidney International  , DOI: ( /j x)
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