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Renin (etymology and pronunciation), also known as an angiotensinogenase, is an aspartic protease protein and enzyme secreted by the kidneys that participates in the body's renin-angiotensin-aldosterone system (RAAS)—also known as the renin-angiotensin-aldosterone axis—that increases the volume of extracellular fluid (blood plasma, lymph, and interstitial fluid) and causes arterial ...
The kidney is responsible for about half of the total gluconeogenesis in fasting humans. The regulation of glucose production in the kidney is achieved by action of insulin, catecholamines and other hormones. [14] Renal gluconeogenesis takes place in the renal cortex. The renal medulla is incapable of producing glucose due to absence of ...
One cause of this can be increased renin production due to narrowing of the renal artery, or a juxtaglomerular cell tumor that produces renin. These will lead to secondary hyperaldosteronism, which will cause hypertension, high blood sodium, low blood potassium, and metabolic alkalosis. [citation needed]
When renal blood flow is reduced, juxtaglomerular cells in the kidneys convert the precursor prorenin (already present in the blood) into renin and secrete it directly into the circulation. Plasma renin then carries out the conversion of angiotensinogen, released by the liver, to a decapeptide called angiotensin I, which has no biological ...
In the kidney, the macula densa is an area of closely packed specialized cells lining the wall of the distal tubule where it touches the glomerulus.Specifically, the macula densa is found in the terminal portion of the distal straight tubule (thick ascending limb of the loop of Henle), after which the distal convoluted tubule begins.
Furosemide blocks NaCl reabsorption mediated by the NKCC2 at the ascending loop of henle, which leads to increased renin release. Excluding loop diuretic use, the usual situation that causes a reduction in reabsorption of NaCl via the NKCC2 at the macula densa (DCT) is a low tubular lumen concentration of NaCl due to low GFR.
Renal glucose reabsorption is the part of kidney (renal) physiology that deals with the retrieval of filtered glucose, preventing it from disappearing from the body through the urine. If glucose is not reabsorbed by the kidney, it appears in the urine, in a condition known as glycosuria. This is associated with diabetes mellitus. [1]
Abnormal kidney function may cause too much or too little urine to be produced. The ability of the kidneys to filter protein is often measured, as urine albumin or urine protein levels, [ 2 ] measured either at a single instance or, because of variation throughout the day, as 24-hour urine tests.