Interlobular artery

Neighboring nephrons also communicate with one another. Experiments performed by Holstein-Rathlou show how nephrons that share a common interlobular artery tend to adjust their TGF mediated pressure oscillations so as to produce a state of in-phase synchronization [7]. Holstein-Rathlou also demonstrated how microperfusion of one nephron (with artificial tubular fluid) affects the amplitude of the pressure oscillation in a neighboring nephron. This provides a method to determine the strength of the nephron-nephron interaction. 

As illustrated in Fig. 12.14 the nephrons are arranged in a tree-like structure with their afferent arterioles branching off from a common interlobular artery [29]. This... 

Fig. 12.19 Left sketch of a vascular-coupled nephron tree including the interlobular artery, the afferent arterioles and the glomeruli. Right oscillation amplitudes as function of the arterial pressure and the position of the branching point along the vascular tree.

Blood flow to the two kidneys is approximately 22-25% of the cardiac output. The kidneys are supplied by the renal artery which enters the kidneys through the hilum and then branches progressively to form the interlobar arteries, arcuate arteries, interlobular arteries (also called radial arteries), and afferent arterioles, which lead to the glomerular capillaries. The distal ends of each glomerulus coalesce to form the efferent arteriole, which leads to a secondary capillary network, the peritubular capillaries which surround the renal tubules. The cortex receives approximately 90% of the blood flow compared to the medulla or papillae so blood-borne toxic molecules reaching the kidneys have a more toxic effect on the cortex, as compared to the medulla or renal papillae. The interstitial space is occupied by the fenestrated peritubular capillaries and a small number of fibroblast-like cells. Increase in thickness of interstitial space in pathological conditions is due to edema, proliferation of fibrous tissue, or infiltration of inflammatory cells (Guyton and Hall, 2006). 

In the porta hepatis, the proper hepatic artery divides into the right branch (from which the cystic artery emerges) and the left branch (from which a middle hepatic artery occasionally emerges). The branches of the hepatic artery run close to the portal veins and may even (rarely) coil round them in places. An arterial sphincter is located prior to the further division of the hepatic artery into smaller branches. There are anastomoses between the arterial branches and the hepatic vein. By way of an arteriolar sphincter (46), the interlobular arteries branch into intralobular arterioles, supplying the lobules of the liver with arterial blood. The arterial blood enters the sinusoids either through terminal branches or through arterioportal anastomoses and mixes with the portal blood. The pressure in the hepatic arterioles is 30-40 mm Hg. (36, 46, 61)... 

The effect of acetylcholine, dopamine, and bradyki-nin on vascular tone has been examined in interlobular arteries and superficial afferent and efferent arterioles isolated from rabbit kidney [141]. Acetylcholine caused a dose-dependent relaxation of norepinephrine-induced tone in all three vessel types. Significant relaxation was observed with 10(-8) M acetylcholine and higher concentrations caused complete relaxation. In afferent and efferent arterioles dopamine caused a dose-dependent relaxation that was indistinguishable from the one caused by acetylcholine. Dopamine was much less effective on interlobular arteries. In afferent arterioles atropine blocked the effect of acetylcholine, and metoclopramide selectively inhibited dopamine-induced relaxation. Bradykinin caused a dose-dependent relaxation of norepinephrine- induced tone only in efferent arterioles. Bradykinin, either in the bath or lumen, had no effect on the preglomerular microves-... 

Blood vessels, arcuate or interlobular arteries, and arterioles are affected in the form of intimal sclerosis and thickening of lamina elastica interna. In addihon, the blood vessels are compressed and torsioned [79]. 

A second form of cyclosporine-induced nephrotoxicity is acute thrombotic microangiopathy. The mechanism for induction of this toxicity is unclear but may be due to a direct toxic effect of cyclosporine on renal arterioles and glomerular capillaries. Histologically, arterioles exhibit protein deposits while glomeruli show thrombosis and endothelial cell damage. These effects are similar in nature to transplant rejection thrombotic microangiopathy, but arcuate and interlobular arteries rather than arterioles are primarily affected with transplant rejection. 

The second model is usually known as the hydro-nephrotic rat kidney model, and was developed for in vivo visualization of the microcirculation by Steinhausen [96] and involves 60 min renal artery occlusion combined with 3 weeks of ligation of the ureter. Atrophy of tubular structures leaves the cortical vasculature relatively intact and visualizable using planar microscopy in an illuminated observation chamber with nerve and blood supply left intact. Absolute and relative changes in lumen diameter of the major resistance vessels-interlobular arteries, afferent and efferent arterioles can be monitored in response to vasoactive stimuli. This model was adapted for in vitro perfusion by Loutzenhiser et al [97], removing systemic neurohumoral influences. 

Extracapillary glomerulonephritis with renal vasculitis is also been reported as a rare complication of D-penidllamine therapy [117,126,156]. Necrosis of interlobular arteries with glomerular crescent [117] and necrotic and ocduded periglomerular arterioles [156] have been reported. Aggressive treatment with pulse steroid, anticoagulants, and antiplatelet agents may be beneficial. The two patients with renal vasculitis, whose outcome was known, died from bacterial infection within ten months after the onset of the disease [117,... 

The renal arteries originate from the aorta at the L2 level. A third of the population has multiple renal arteries. The main renal arteries are 5 to 6 mm in diameter and typically bifurcate into anterior and posterior divisions. There is further subdivision into segmental, interlobar, arcuate, and interlobular arteries before termination in glomeruli. Capsular and adrenal arteries take their origin from the main renal arteries. 

The intrarenal veins accompany the arteries. There are two types of interlobular veins draining the cortex. One type originates at the surface of the kidney as stellate veins draining the most superficial parts of the renal cortex. Most interlobular veins are of the second type, which originates in the cortex as a result of the joining of venules from the peritubular plexus. Both types accompany interlobular arteries... 

Renal blood flow originates from the renal arteries, which are direct branches off of the aorta. Renal arteries progressively branch to form interlobar arteries, arcuate arteries, interlobular arteries, and afferent arterioles, the latter of which provide blood to the glomerulus. The kidney receives up to 20-25% of cardiac output, with the cortex receiving the majority (90%) of the blood flow, and the medulla (6-10%) and papilla (1-2%) receiving considerably less direct blood flow (Schnellmann, 2008). Thus, blood-bome toxicants are delivered in higher amounts to the cortex, whereas the medulla and papilla... 

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