Kidney blood flow

Under normal conditions, ca 25% of the resting cardiac output passes through the kidney. Blood flowing through the renal artery and the afferent... 

Decreases kidney blood flow Antidiuretic, releases ACTH Increases sodium chloride and urea excretion... 

Kidney Blood flow f Adaptation to salt load lack of H2O... 

Some joined companies that manufacture polymers (plastics). One is working on the development of membranes for desalination of seawater (fresh water pa.sses through, salt is kept out) and for gas separations (hydrogen passes through and hydrocarbons are kept out, or vice versa) another is developing membranes to be used in hollow-tube artificial kidneys (blood flows from the patient s body through thin-walled tubes metabolic wastes in the blood pass through the tube walls but proteins and other important body chemicals remain in the blood, and the purified blood is returned to the body). 

Iodine isotopes are used in many ways. Iodine-123 is used in studies of the brain, kidneys, and thyroid. Iodine-125 is used in studies of the pancreas, blood flow, thyroid, liver, take-up of minerals in bones, and loss of proteins in the body. And iodine-131 is used in studies of the liver, kidneys, blood flow, lungs, brain, pancreas, and thyroid. 

Juxtaglomerular cells function as a baroreceptor-sensing device. Decreased renal artery pressure and kidney blood flow are sensed by these cells and stimulate secretion of renin. The juxtaglomerular apparatus also includes a group of specialized distal tubule cells... 

Cardiac Flushing, a rapid heart rate, wide pulse pressure, and an increase in cardiac output may be seen initially. This may be followed by a reduction in cardiac output, blood pressure, and liver and kidney blood flow. 

The first successful drug treatments for hypertension were introduced after World War II. By that time, researchers had learnt that blocking the sympathetic nervous system could lower blood pressure. In 1946, tetraethyl-ammonium, a drug known for 30 years to block nerve impulses, was introduced as a treatment for hypertension. Hexamethonium, an improved version of tetraethylammo-nium, was available for use by 1951. Another effective blood pressure-lowering drug, hydralazine, resulting from the search for antimalarial compounds, was diverted to the treatment of hypertension when it was found to have no antimalarial activity, but to lower blood pressure and increase kidney blood flow. 

As an example, let us consider a simple one-compartment model for the prescription of treatment protocols for dialysis by an artificial kidney device (Fig. 1.1). While fire blood irrea concentration (BUN) in the normal individual is usually 15 mg% (mg% = milligrams of the substance per 100 mL of blood), the BUN in irremic patients could teach SO mg%. The purpose of the dialysis is to bring the BUN level closer to the normal. In the artificial kidney, blood flows on one side of the dialyzer membrane and dialysate fluid flows on the other side. Mass transfer across the dialyzer membrane occurs by diffusion due to concentration difference across the membrane. Dilysate fluid is a makeup solution consisting of saline, ions, and the essential nutrients that maintains zero concentration difference for these essential materials across the membrane. However, during the dialysis, some hormones also diffuse out of the dialyzer membrane along with the urea molecule. Too-rapid dialysis often leads to depression in the individual because of the rapid loss of hormones. On the other hand, too-slow dialysis may lead to unreasonable time required at the hospital. 

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. 

Methyldopa. Methyldopa reduces arterial blood pressure by decreasing adrenergic outflow and decreasing total peripheral resistance and heart rate having no change in cardiac output. Blood flow to the kidneys is not changed and that to the heart is increased. It causes regression of myocardial hypertrophy. 

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. 

Levy, M.N. (1959). Oxygen consumption and blood flow in the hypothermic perfused kidney. Am. J. Physiol. 197, 1111. 

Activation of both the RAAS and the SNS also contribute to vasoconstriction in an attempt to redistribute blood flow from peripheral organs such as the kidneys to coronary and cerebral circulation.7 However, arterial vasoconstriction leads to impaired forward ejection of blood from the heart due to an increase in afterload. This results in a decrease in CO and continued stimulation of compensatory responses, creating a vicious cycle of neurohormonal activation. 

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. 

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