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Chapter 6I: Kinins and the kidney
| AuthorsBurton D Rose, MDTheodore W Post, MD | Section EditorBurton D Rose, MD | Deputy EditorTheodore W Post, MD |
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Kinins are another set of hormones produced in the kidney [1,2]. The process begins with the secretion of the enzyme kallikrein by the cells in the distal tubule and connecting segment (figure 1). This enzyme catalyzes the conversion of inactive kininogen (a plasma protein that might also be produced locally) into lysyl-bradykinin and then, in the presence of an aminopeptidase, into bradykinin. Kinin generation probably occurs both in the tubular lumen and, since secreted kallikrein appears to reach the vascular compartment, in the vascular space. On the other hand, filtered kinins are rapidly metabolized by kininases in the proximal tubule and therefore are not likely to have any intratubular effect [1].
The physiologic role of the renal kinins is incompletely understood. Like the prostaglandins, they are vasodilators that may act to minimize renal ischemia in hypovolemic states in which angiotensin II and norepinephrine secretion are increased [3,4]. Their site of production in the distal nephron also suggests that they may have an intraluminal effect on Na+ and water handling in the collecting tubules. Compatible with this hypothesis are the observations that kinins diminish Na+ reabsorption in the inner medulla (by closing Na+ channels in the luminal membrane) [5] and impair the ability of ADH to increase local water reabsorption [6]. The latter effect appears to be indirect, being mediated by kinin-induced prostaglandin production.
Renal kinins appear to have a significant role in the developing kidney. The expression of bradykinin receptor mRNA is elevated 10- to 30-fold in neonatal kidney as compared with adult kidney [7]. How kinins act in the maturing kidney is unknown.
The kinins are probably not important circulating hormones, since they are rapidly metabolized in the circulation by kininases, one of which is angiotensin converting enzyme. This is the same enzyme that catalyzes the conversion of angiotensin I into angiotensin II.
(See "Chapter 6J: Erythropoietin", to continue with the text).
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- Fuller PJ, Funder JW. The cellular physiology of glandular kallikrein. Kidney Int 1986; 29:953.
- Johnston PA, Bernard DB, Perrin NS, et al. Control of rat renal vascular resistance during alterations in sodium balance. Circ Res 1981; 48:728.
- Margolius, HS. Theodore Cooper Memorial Lecture. Kallikreins and kinins. Some unanswered questions about system characteristics and roles in human disease. Hypertension 1995; 26:221.
- Zeidel ML, Jabs K, Kikeri D, Silva P. Kinins inhibit conductive Na+ uptake by rabbit inner medullary collecting duct cells. Am J Physiol 1990; 258:F1584.
- Clapham, DE, Neer, EJ. New role of G-protein beta-gamma-dimers in transmembrane signalling. Nature 1993; 365:403.
- el-Dahr, SS, Figueroa, CD, Gonzalez, CB, Muller-Esterl, W. Ontogeny of bradykinin B2 receptors in the rat kidney: Implications for segmental nephron maturation. Kidney Int 1997; 51:739.
