BRADYKININ BK2 RECEPTORS CONTRIBUTE TO REFLEX CARDIOVASCULAR-RESPONSES DURING BRIEF ABDOMINAL ISCHEMIA

Ischemically sensitive visceral sympathetic nerve fibers, which are th ought to represent the afferent limb of a strong cardiovascular presse r reflex, can be stimulated by exogenously applied bradykinin (BK). Du ring ischemia, BK also is known to be produced locally and to serve as an endogenous stimulus for activation of ischemically sensitive nerve endings. It is unclear however, whether ischemically induced BK produ ction is sufficient to elicit a reflex cardiovascular response. Accord ingly, femoral arterial and venous catheters were positioned in anesth etized cats, and the superior mesenteric and celiac arteries were isol ated for placement of snare occluders. After dual occlusion of these a rteries (20 min), one of two chemically dissimilar specific kinin B-2 (BK2) receptor antagonists, HOE-140 (30-40 mu g/kg iv, n = 8) or NPC-1 7731 (30-40 mu g/kg iv, n = 11), was administered and dual occlusion w as repeated. The reflex rise of mean arterial blood pressure (BP) of 1 6 +/- 3.7% was significantly (P < 0.05) reduced by HOE-140 to 8.4 +/- 2.0%. NPC-17731 similarly attenuated the reflex BP increment from 13 /- 1.2 to 6.2 +/- 1.6% (P < 0.05). In a separate set of control animal s the first and second periods of ischemia induced reflex BP increment s that did not differ significantly (16 +/- 2.7 and 16 +/- 5.7%, respe ctively). Qualitatively similar decrements of the BP response were pro duced by the BK2 receptor antagonists in two additional groups in whic h blood flow to the superior mesenteric and celiac arteries was divert ed to a venous reservoir to eliminate the initial transient (mechanica lly induced) rise in BP associated with artery ligation that is known not to be associated with the reflex response. These results indicate that the stimulation of BK2 receptors on visceral afferent nerves by B K is responsible, at least in part, for the reflex cardiovascular resp onse during visceral ischemia.