Disease relevance of BDKRB1

• Mechanisms of kinin B1-receptor-induced hypotension in the anesthetized dog [1].

High impact information on BDKRB1

• In conclusion, canine prostates express functional B2 receptors, with no apparent B1 receptor subtypes [2].
• The selective B1 receptor antagonist [des-Arg9, Leu8]-bradykinin, (10(-7) to 10(-5) M) had no significant effect on bradykinin-induced contractions [3].
• The dog renal artery without endothelium was also used as a BK1 receptor system [4].
• Superfusion of the epicardium with a selective B1-receptor antagonist, des-Arg9-[Leu8]BK (50-100 micrograms/min) had no effect on reflex responses to epicardial BK (0.03-0.1 microgram) [5].
• Experiments were carried out on rabbit isolated aortae (a B1 receptor system) or rabbit jugular veins and dog carotid arteries (two B2 receptor systems) [6].

Biological context of BDKRB1

• The different mechanisms underlying the BK-induced vasodilatation are summarized in Fig. 3. Three mechanisms are at least involved; 1) EDRF-release from endothelial cells which may not be mediated by B1 receptor, but presumably by B2 receptor, 2) PGI2-release from endothelial cells, 3) PGI2-release from smooth muscle (subendothelial) cells [7].

Associations of BDKRB1 with chemical compounds

• The PGI2-release may be mediated by B1 receptor [7].
• The new potent B2-receptor antagonist, HOE 140 (100 micrograms), significantly blocked the BK-induced chronotropic effect, whereas desArg9-BK, a B1-receptor agonist, was without effect [8].

References