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Ca²⁺ influx in the endothelial cells is required for the bradykinin-induced endothelium-dependent contraction in the porcine interlobar renal artery

Eikichi Ihara, Dmitry N. Derkach, Katsuya Hirano, Junji Nishimura, Hajime Nawata * and Hideo Kanaide

1. To determine the mechanism of bradykinin-induced production of endothelium-derived contracting factors, we monitored the changes in cytosolic Ca²⁺ concentration ([Ca²⁺]_i) in in situ endothelial cells in porcine aortic valvular strips and the changes in [Ca²⁺]_i of smooth muscle cells and force in porcine interlobar renal arterial strips using front-surface fluorometry of fura-2.
2. In the presence of N-nitro-L-arginine methyl ester, bradykinin caused an endothelium-dependent transient elevation of [Ca²⁺]_i and contraction in smooth muscle in the interlobar renal artery. This contraction was completely inhibited by a prostaglandin H₂/thromboxane A₂ receptor antagonist.
3. In the absence of extracellular Ca²⁺, bradykinin failed to induce contraction. However, replenishing extracellular Ca²⁺ to 0.75 mM and higher induced an instantaneous contraction. However, replenishing Ca²⁺ per se did not induce any contraction in the absence of bradykinin. Pretreatment with either 10^-5 M 1-(-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenethyl)-1H-imidazole hydrochloride (SKF96365) or 0.2 mM Ni²⁺ abolished the contraction induced by bradykinin in the presence of extracellular Ca²⁺.
4. Treatment with 10^-5 M indomethacin completely inhibited the contractile response induced by Ca²⁺ replenishment, regardless of the timing of its application, before or after the application of bradykinin.
5. In endothelial cells in the valvular strips, bradykinin caused a transient [Ca²⁺]_i elevation in the presence of 1.25 mM extracellular Ca²⁺, but [Ca²⁺]_i returned to the resting level within 10 min. Neither 10^-5 M SKF96365 nor 0.2 mM Ni²⁺ had any effect on the peak [Ca²⁺]_i elevation, but decreased [Ca²⁺]_i in the declining phase. In the absence of extracellular Ca²⁺, bradykinin induced a transient [Ca²⁺]_i elevation to a level similar to that seen in the presence of 1.25 mM extracellular Ca²⁺. However, [Ca²⁺]_i then rapidly returned to the prestimulation level within 5 min. Subsequent Ca²⁺ replenishment to 0.75 mM and higher in the presence of bradykinin elevated [Ca²⁺]_i to significantly higher levels than the resting level seen in the media containing 1.25 mM Ca²⁺.
6. In conclusion, Ca²⁺ influx in the endothelial cells is essential for bradykinin to induce endothelium-dependent contraction in the porcine interlobar renal artery.