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Scientia Pharmaceutica is published by MDPI from Volume 84 Issue 3 (2015). Articles in this Issue were published by another publisher in Open Access under a CC-BY (or CC-BY-NC-ND) licence. Articles are hosted by MDPI on mdpi.com as a courtesy and upon agreement with Austrian Pharmaceutical Society (Österreichische Pharmazeutische Gesellschaft, ÖPhG).
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Sci. Pharm. 2013, 81(3), 749-762; https://doi.org/10.3797/scipharm.1305-13 (registering DOI)

Pharmacological Analysis of the Rat Femoral Artery Response to Bradykinin

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Received: 7 May 2013 / Accepted: 4 June 2013 / Published: 4 June 2013
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Abstract

Bradykinin (BK) plays an important role in different physiological processes including the general preservation and modulation of vascular systems. The present study was designed in order to examine the effect of BK on isolated rat femoral artery rings and to investigate the participation of intact endothelium, cyclooxygenase products, Ca2+ channels, Na+/K+–ATPase, and B2 kinin receptors in BK-induced action. Circular artery segments were placed in organ baths. The endothelium was mechanically removed from some arteries. Concentration–contraction curves for BK were obtained in the rings previously equilibrated at the basal tone. BK produced a concentration–dependent contraction, which was reduced by endothelial denudation. The BK–induced effect was almost completely inhibited by indomethacin (cyclooxygenase inhibitor) or OKY–046 (thromboxane A2–synthase inhibitor). Nifedipine (Ca2+ channel blocker), ouabain (Na+/K+–ATPase inhibitor), or HOE–140 (selective B2 kinin receptor antagonist) significantly reduced the BK–evoked effect. In conclusion, it can be proposed that BK produces concentration– and endothelium–dependent contractions of the isolated rat femoral artery, which is for the most part a consequence of B2 kinin receptor activation. Cyclooxygenase contractile products, especially thromboxane A2, play a significant role in this course of action. The transduction mechanism involved in the process of BK–induced femoral artery contraction include the activation of voltage–gated Ca2+ channels, and in a smaller extent Na+/K+–ATPase as well.
Keywords: Bradykinin; Femoral artery; Endothelium; Ca2+ channels; Thromboxane A2Introduction Bradykinin; Femoral artery; Endothelium; Ca2+ channels; Thromboxane A2Introduction
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RADENKOVIĆ, M.; STOJANOVIĆ, M.; SKORUPAN, N.; PROSTRAN, M. Pharmacological Analysis of the Rat Femoral Artery Response to Bradykinin. Sci. Pharm. 2013, 81, 749-762.

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