Renal blood supply

Dopamine is found in every sympathetic neuron and ganglion in the CNS. As a drug, and in addition to stimulation of dopaminergic receptors, dopamine indirectly stimulates both a- and )3-adrenoreceptors. Dopamine also causes a release of endogenous norepinephrine. The mechanism of action is based on the excitatory effect on )3-adrenoreceptors (in low and moderate doses), as well as on a-adrenoreceptors (in large doses). It has a positive inotropic effect on the heart, increases blood supply, selectively widens renal and mesenteric blood vessels, does not elevate blood pressure, and slightly increases the frequency of heartbeats. 

Each kidney receives its blood supply from a renal artery, two of which branch from the abdominal aorta. Upon entering the hilum of the kidney, the renal artery divides into smaller arteries which in turn give off still smaller branches. Branching off these are the afferent arterioles supplying the glomerular capillaries, which drain into efferent arterioles. Efferent arterioles divide into peritubular capillaries that provide an extensive blood supply to the renal cortex. Blood from these capillaries collects in renal venules and leaves the kidney via the renal vein. Blood supply is intimately linked to blood pressure. 

Figure 29.1. Sagittal section of a human kidney, showing major gross anatomical features and renal blood supply.

Hepatorenal syndrome is characterized by pronounced vasoconstriction of the renal cortex with tortuosity and narrowing of the interlobular and arcuate arteries. The blood supply to the renal cortex may be almost totally interrupted and, at the same time, the blood flow is diverted into areas containing cortical vessels... 

The second model is usually known as the hydrone-phrotic rat kidney model, and was developed for in vivo visualization of the microcirculation [275] 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-inter-lobular arteries, afferent and efferent arterioles can be monitored in reponse to vasoactive stimuli. This model was adapted for in vitro perfusion by Loutzenhiser et al [276], removing systemic neurohumoral influences. 

Hepatorenal syndrome, functional renal failure in the setting of cirrhosis in the absence of intrinsic renal disease, occurs in patients with cirrhosis as a result of intense vasoconstriction within the renal cortical vasculature. It is common and develops in approximately 40% of patients with cirrhosis and ascites within 5 years. The resultant reduction in blood supply to the kidneys causes avid sodium retention and oliguria. The vasoconstriction that occurs in the kidneys is in stark contrast to the state of systemic vasodilation that is characteristic of chronic liver failure. The pathophysiologic mechanism responsible for these effects is unknown, but is linked to the systemic vasodilation, hypovolemia, and hyperkinetic circulation seen in chronic liver failure. ... 

If the GFR falls due to restriction of the renal blood supply, or as a result of destruction of nephrons by renal disease, there is retention of the waste products of metabolism in the blood. In chronic disease, a new steady state is reached w ith a constant elevation in the serum concentration of substances such as urea and creatinine. As the renal di.sease progresses, urea and creatinine concentrations may increase slowly over many months. 

Renal tissue metabolism and transport mechanisms play important roles in the excretion and detoxification of xenobiotics (and/or their metabolites). Although the kidneys play an important part in the detoxification of xenobiotics, renal tissue may produce or increase the amounts of toxic metabolites received via the renal blood supply by metabolism (e.g., mixed-function oxidase reactions or concentrating effects within the nephron) (Piperno 1981 Commandeur and Vermeulen 1990 Goldstein 1994 Diamond and Zalups 1998 Endou 1998 Tarloff and Lash 2004). 

Proximal tubular injury due to nephrotoxicants occurs more frequently than other nephrotoxic effects, and this probably reflects a combination of the proportion of the total renal blood supply received by the renal cortex and the number of xenobiotics reabsorbed and excreted within the proximal tubule. Xenobiotics can alter or inhibit the transport processes of passive diffusion and/or carrier transporters for both anionic/base and cationic molecules. 

While Rowachol is used as a measure against gallstones and biliary tract stones, Rowatinex is used in the treatment of renal stones. The mechanism of action is not known, but is thought to involve an improved renal blood supply thereby stimulating an increased urine secretion, and an antispas modic effect to allow passage of the calculi. 

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