Figure 133

Kallikrein-kinin system. Plasma and tissue kallikreins are functionally different serine protease enzymes that act on kininogens (inactive <X2 glycoproteins) to form the biologically active kinins (bradykinin and lysyl-bradykinin [kallidin]). Kidney kallikrein and kininogen are localized in the distal convoluted and cortical collecting tubules. Release of kallikrein into the tubular fluid and intersti-tium can be stimulated by prostaglandins, mineralocorticoids, angiotensin II, and diuretics. B1 and B2 are the two major bradykinin receptors that exert most of the vascular actions. Although glomerulus and distal nephron segments contain both B1 and B2 receptors, most of the renal vascular and tubular effects appear to be mediated by B2-receptor activation [16,17,43,44]. Bradykinin and kallidin elicit vasodilation and stimulate nitric oxide, prostaglandin E2 (PGE2) and I2 (PGI2), and renin release [45,46]. Kinins are inactivated by the same enzyme that converts angiotensin I to angiotensin II, angiotensin-converting enzyme (ACE). The kallikrein-kinin system is stimulated by sodium depletion, indicating it serves as a mechanism to dampen or offset the effects of enhanced angiotensin II levels [47,48]. Des Arg— bradykinin; NEP—neutral endopeptidase.

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