Kidneys renal blood flow

Kidney Function. Prostanoids influence a variety of kidney functions including renal blood flow, secretion of renin, glomerular filtration rate, and salt and water excretion. They do not have a critical role in modulating normal kidney function but play an important role when the kidney is under stress. Eor example, PGE2 and -I2 are renal vasodilators (70,71) and both are released as a result of various vasoconstrictor stimuli. They thus counterbalance the vasoconstrictor effects of the stimulus and prevent renal ischemia. The renal side effects of NSAIDS are primarily observed when normal kidney function is compromised. 

In the kidney, ANG II reduces renal blood flow and constricts preferentially the efferent arteriole of the glomerulus with the result of increased glomerular filtration pressure. ANG II further enhances renal sodium and water reabsorption at the proximal tubulus. ACE inhibitors thus increase renal blood flow and decrease sodium and water retention. Furthermore, ACE inhibitors are nephroprotective, delaying the progression of glomerulosclerosis. This also appears to be a result of reduced ANG II levels and is at least partially independent from pressure reduction. On the other hand, ACE inhibitors decrease glomerular filtration pressure due to the lack of ANG II-mediated constriction of the efferent arterioles. Thus, one important undesired effect of ACE inhibitors is impaired glomerular filtration rate and impaired kidney function. 

In the kidney, bradykinin increases renal blood flow, whereas glomerular filtration rate remains unaffected. 

Finally, poor CO may contribute to diuretic resistance. In these patients, it may become necessary to add vasodilators or inotropes to enhance perfusion to the kidneys. Care must be taken, as vasodilators can decrease renal blood flow despite increasing CO through dilation of central and peripheral vascular beds. 

A decrease in blood volume or blood pressure may result in a decrease in the blood flow to the kidney. The kidney monitors renal blood flow by way of stretch receptors in the vessel walls. A decrease in renal blood flow stimulates the release of renin. The subsequent secretion of aldosterone causes retention of sodium and water and, therefore, an increase in blood volume and blood pressure back to normal. An increase in renal blood flow tends to cause the opposite effect. 

A substance that fulfills these criteria is para-aminohippuric acid (PAH). All of the PAH not filtered at the glomerulus is secreted by the proximal tubule. The net effect is that all of the plasma flowing through the nephrons is completely cleared of PAH. It is important to note that about 10 to 15% of the total renal plasma flow supplies regions of the kidneys that are not involved with filtration or secretion. Consequently, this plasma cannot be cleared of PAH. Therefore, the plasma clearance of PAH provides a measurement of the effective renal plasma flow, that is, the volume of plasma that actually flows through the nephrons. The ERPF is normally about 625 ml/ min. (This value is based on a renal blood flow of about 1.1 1/min and a hematocrit of about 42.)... 

The kidneys receive a disproportionate fraction of cardiac output. Although the combined weight of the kidneys accounts for less than 1% of total body weight, these organs receive 20 to 25% of the cardiac output. This magnitude of blood flow, which is in profound excess to their metabolic needs, enables them to carry out their multiple homeostatic functions more efficiently. Assuming a resting cardiac output of 5 1/min, the renal blood flow (RBF) is approximately 1.1 1/min. 

Vasopressin is a potent vasoconstrictor that increases blood pressure and systemic vascular resistance. It may have several advantages over epinephrine. First, the metabolic acidosis that frequently accompanies cardiopulmonary arrest can blunt the vasoconstrictive effect of epinephrine this does not occur with vasopressin. Second, stimulation of P receptors by epinephrine can increase myocardial oxygen demand and complicate the postresuscitative phase of CPR. Vasopressin can also have a beneficial effect on renal blood flow in the kidney, causing vasodilation and increased water reabsorption. 

The complex 99mTc(V)-DMSA (64) has been used for a long time for the imaging of renal blood flow and morphology of the kidneys. The exact composition and structure of the agent is still unknown, as is the mechanism of retention. A structure of 64 (where R = COOH) has been proposed with three possible conformations, syn-endo, syn-exo, and anti, of the carboxylic acid groups with respect to the Tc = 0 core (280). 

The rate of total body clearance accounted for by the kidney. Its magnitude is determined by the net effects of glomerular filtration, tubular secretion and reabsorption, renal blood flow, and protein binding. 

Renal function impairment In hypertensive patients with normal kidneys who are treated with hydralazine, there is evidence of increased renal blood flow and a maintenance of glomerular filtration rate. Renal function may improve where control values were below normal prior to administration. Use with caution in patients with advanced renal damage. 

Renal development is also immature in both the premature and the full-term baby. At birth overall renal function is approximately 20% of the adult value, but increases rapidly up to around one year of age when it is usually the same as that of an adult (when adjusted for body size). Glomerular filtration rate in particular may increase four-fold over the first week of life. As renal blood flow, glomerular filtration rate and tubular secretion of drugs are all low in the neonate, drugs cleared by the kidney need to be given in reduced dose - particularly if the drug has a narrow therapeutic window , and the potential to produce toxicity if Cp rises too greatly. 

III.a.4.3. Changes in renal blood flow. Blood flow through the kidney is partially controlled by the production of renal vasodilatory prostaglandins. If the synthesis of these prostaglandins is inhibited (e.g. by indomethacin), the renal excretion of lithium is reduced with a subsequent rise in serum levels. The mechanism underlying this interaction is not entirely clear, as serum lithium levels are unaffected by some potent prostaglandin synthetase inhibitors (e.g. aspirin). If an NSAID is prescribed for a patient taking lithium the serum levels should be closely monitored. 

Renal elimination of foreign compounds may change dramatically with increasing age by factors such as reduced renal blood flow, reduced glomerular filtration rate, reduced tubular secretory activity, and a reduction in the number of functional nephrons. It has been estimated that in humans, beginning at age 20 years, renal function declines by about 10% for each decade of life. This decline in renal excretion is particularly important for drugs such as penicillin and digoxin, which are eliminated primarily by the kidney. 

Renal blood flow and glomerular filtration are not decreased, although renal resistance is diminished. Like a-methyldopa, it is a useful agent for hypertension complicated by renal disease. Plasma renin activity is reduced by clonidine, presumably as a result of a centrally mediated decrease in sympathetic stimulation of the juxtaglomerular cells of the kidney. 

Kidney Methylxanthines exert mild diuretic action by inhibiting tubular reabsorption of sodium and water. In addition, it increases renal blood flow and glomerular filtration rate. 

Isoflurane, like other volatile agents, causes a transient reduction in renal blood flow, glomerular filtration rate and urinary output, but there is no evidence that these changes are harmful to the healthy kidney. Similarly, there is no evidence that isoflurane has any undesirable effects on the transplanted kidney. In... 

Renal blood flow. The blood passing through the mammalian kidney represents 25% of the cardiac output, despite the fact that the kidney only represents about 1% of the body mass. Therefore, the exposure of kidney tissue to foreign compounds in the bloodstream, especially the cortex, which receives more blood than the medulla, is relatively high. 

The three protein pressor substances are renin, a prolonged pressor substance found in shock, and vasoexcitor material. Apparently they are different substances. Renin is the best understood (10). Its reaction with a globulin substrate to form hypertensin or angiotonin suggests that it is a proteolytic enzyme. Renin has been considerably concentrated, but has not been purified. The stimulus for its release by the kidney is a reduction of renal blood flow just how this comes about is unknown. 

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