Tissue Kallikrein–Kinin System

Abstract

The sections in this article are: Historical Perspectives Kallikrein–Kinin Systems Plasma Kallikrein–Kinin System Tissue Kallikrein–Kinin System Components of the Tissue Kallikrein–Kinin System Tissue Kallikrein Kallikrein Inhibitors: Kallistatin Kininogens Kinins and Peptidase Metabolism Kinin Receptors Tissue Kallikrein–Kinin System and Electrolyte and Water Balance in the Kidney Localization of Kallikrein–Kinin System Components Interrelationship of Renin–Angiotensin and Kallikrein–Kinin Systems Regulatory and Mediatory Factors Kinins and Electrolyte Transport Prostaglandins and Other Intracellular Mediators Tissue Kallikrein–Kinin System and Electrolyte Transport in Other Tissues Colon and Intestinal Epithelia Other Epithelia Overview

Differential action of bradykinin on intrarenal regional perfusion in the rat: waning effect in the cortex and major impact in the medulla

“…in the cells of the renal connecting or distal tubule (Vio et al . 1992; Clements, 2000). An appropriate alternative to renal artery infusions is administration of agents into the renal cortical interstitium.…”

“…2000) and considering the postulated role of the renal medulla in this control (Mattson, 2003; Bergström & Evans, 2004; Cowley, 2008), during the past two decades attention was focused on Bk effects on perfusion of the renal medulla (Navar et al . 1996; Clements, 2000; Tornel et al . 2000).…”

“…Thus, infusions directly into the tissue (interstitium) may be thought to better mimick Bk diffusion from the major sites of synthesis, e.g. in the cells of the renal connecting or distal tubule (Vio et al 1992;Clements, 2000). An appropriate alternative to renal artery infusions is administration of agents into the renal cortical interstitium.…”

“…Due to the increasing interest in the potential contribution of kinins to the control of arterial pressure (Katori & Majima, 1996;Navar et al 1996;Nafz et al 1998;Tornel et al 2000) and considering the postulated role of the renal medulla in this control (Mattson, 2003;Bergström & Evans, 2004;Cowley, 2008), during the past two decades attention was focused on Bk effects on perfusion of the renal medulla (Navar et al 1996;Clements, 2000;Tornel et al 2000). However, there is ample evidence indicating that kinins may affect vessel tone throughout the kidney.…”

“…Bradykinin (Bk), a major and functionally most important member of the kinin family, has two sources: it is both a paracrine agent generated by the tissue kallikrein–kinin system and a product of plasma kallikrein. Under most conditions it acts by stimulation of widely distributed constitutive B 2 receptors, which leads to activation of mediating systems, mostly of the NO cascade and the still elusive endothelium‐derived hyperpolarizing factor (EDHF) (Clements, 2000; Imig, 2005; Moreau et al 2005; Fleming & Busse, 2006). In the kidney, Bk modifies tubular transport and causes intrarenal vasodilatation (Vio et al .…”