Renal system cortex

The renal system consists of the kidneys and their vasculature and innervation, the kidneys each draining through a ureter into a single median urinary bladder, and the latter draining to the exterior via a single duct, the urethra. The kidney has three major anatomical areas the cortex, the medulla, and the papilla. 

The renal system is composed of functional units called nephrons. Nephrons have two portions, the cortex (i.e., glomerulus. Bowman capsule, and proximal and distal tubules) and the medulla (i.e., the loop of Henle and the collecting tubules). The nephron also contains two primary sections ... 

Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) are members of a family of so-called natriuretic peptides, synthesized predominantly in the cardiac atrium, ventricle, and vascular endothelial cells, respectively (G13, Y2). ANP is a 28-amino-acid polypeptide hormone released into the circulation in response to atrial stretch (L3). ANP acts (Fig. 8) on the kidney to increase sodium excretion and glomerular filtration rate (GFR), to antagonize renal vasoconstriction, and to inhibit renin secretion (Ml). In the cardiovascular system, ANP antagonizes vasoconstriction and shifts fluid from the intravascular to the interstitial compartment (G14). In the adrenal cortex, ANP is a powerful inhibitor of aldosterone synthesis (E6, N3). At the hypothalamic level, ANP inhibits vasopressin secretion (S3). It has been shown that some of the effects of ANP are mediated via a newly discovered hormone, called adreno-medullin, controlling fluid and electrolyte homeostasis (S8). The diuretic and blood pressure-lowering effect of ANP may be partially due to adrenomedullin (V5). 

The dominant mercury pool in the body is the kidney [23, 31]. The kidneys contained over 85% of the body burden of mercury 15 days or more after a single injection of mercuric chloride into rats [32]. Maximum levels in the rat kidney were attained in less than a day after doses of mercuric chloride [33], The renal cortex contained the highest levels [34-36], the maximum concentrations being found in the proximal tubular system, while mercury was close to background levels in the glomeruli and collecting ducts. 

Dopamine is an intermediate product in the biosynthesis of noradrenaline. Furthermore it is an active transmitter by itself in basal ganglia (caudate nucleus), the nucleus accumbens, the olfactory tubercle, the central nucleus of the amygdala, the median eminence and some areas in the frontal cortex. It is functionally important, for example in the extra-pyramidal system and the central regulation of emesis. In the periphery specific dopamine receptors (Di-receptors) can be found in the upper gastrointestinal tract, in which a reduction of motility is mediated, and on vascular smooth muscle cells of splanchnic and renal arteries. Beside its effect on specific D-receptors, dopamine activates, at higher concentrations, a- and -adrenoceptors as well. Since its clinical profile is different from adrenaline and noradrenaline there are particular indications for dopamine, like situations of circulatory shock with a reduced kidney perfusion. Dopamine can dose-dependently induce nausea, vomiting, tachyarrhythmia and peripheral vasoconstriction. Dopamine can worsen cardiac ischaemia. 

Mineralocorticoids are involved in controlling electtolyte and fluid levels.9,44 The primary mineralo-corticoid produced by the adrenal cortex is aldosterone. Aldosterone increases the reabsorption of sodium from the renal tubules. By increasing sodium reabsorption, aldosterone facilitates the reabsorption of water. Aldosterone also inhibits the renal reabsorption of potassium, thus increasing potassium excretion. Mineralocorticoid release is regulated by fluid and electrolyte levels in the body and by other hormones, such as the renin-angiotensin system. 

The papilla is the smallest anatomical portion of the kidney. Papillary tissue consists primarily of terminal portions of the collecting duct system and the vasa recta. Papillary blood flow is low relative to cortex and medulla less than 1% of total renal blood flow reaches the papilla. However, tubular fluid is maximally concentrated and the volume of luminal fluid is maximally reduced within the papilla. Potential toxicants trapped in tubular lumens may attain extremely high concentrations within the papilla during the process of urinary concentration. High intraluminal concentrations of potential toxicants may result in diffusion of these chemicals into papillary tubular epithelial and/or interstitial cells, leading to cellular injury. 

The transport mechanisms of the organic ion transport systems have been characterized at both membrane sides of proximal tubule, mainly by studies in brush-border and basolateral membranes purified from homogenates of renal cortex. Since a detailed review and a critical discussion of the present knowledge in this field was pubfished by Pritchard [44], only the main conclusions are summarized here. 

The hydronephrotic kidney was developed for in vivo visuahzation of the glomerular microcirculation, the vas afferens and the vas efferens [138]. This preparation utihzes postischemic hydronephrosis (PIH) to destroy the renal tubular system while preserving a portion of the cortex. In this preparation, glomeruli and... 

Superoxide generated by xanthine oxidase or in the redox cycling of paraquat can cause the reductive release of F3 from ferritin, a process that is dependent on the activity of microsomal NADPH-cytochrome P-450 reductase [119]. Iron appears to be an essential component in the formation of reactive species such as superoxide and hydroxyl radical via redox cycling of cephaloridine. Addition of EDTA or of the specific iron chelator desferrioxamine to an incubation system containing renal cortex microsomes and cephaloridine depressed cephaloridine-induced peroxidation of microsomal lipids significantly EDTA showed a weaker effect than desferrioxamine at equimolar concentrations. By chelating F3 preferentially [120], desferrioxamine reduced the availability of F2 produced by the iron redox cycle and decreased cephaloridine-stimu-lated peroxidation of membrane lipids [36, 37]. 

Kishi et al. (169)evaluated the acute toxicity of Lipiodol infusion into the hepatic arteries (HAD of beagles and found the influence of Lipiodol HAI to be dose dependent. The infused Lipiodol first passed through an arterioportal communication and distributed through the hepatic sinusoids to pulmonary capillaries and thence into systemic blood circulation. The circulation and embolization of oil droplets were found in the renal tubular cells of supracapsular cortex, the choroid plexus, the vascular endothelium, and the pancreatic duct epithelium, showing a process of intracellular collection of Lipiodol from the systemic blood circulation and of further metabolism-provoking cellular reactions. 

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