Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:Q92565 (GFR)
 4,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tubuloglomerular feedback (TGF) is an important intrarenal regulatory mechanism, which acts to stabilize renal blood flow, GFR, and the tubular flow rate. The anatomical basis for this negative feedback system is the Juxtaglomerular Apparatus (JGA). This is located at the point of contact between the thick ascending limb of the loop of Henle (TAL) and the vascular pole of the glomerulus. The JGA includes the macula densa, a specialized plaque of cells in the TAL thought to be responsible for the sensing step in the feedback mechanism; the mesangial cells, a cushion of cells separating the macula densa from the vascular pole of the glomerulus; and the afferent arteriole, the main effector site for the TGF. An increase in the NaCl concentration at the macula densa elicits a response in the smooth muscle cells of the afferent arteriole increasing the hemodynamic resistance of the preglomerular vasculature. These changes will, through decreases in the GFR and the tubular flow rate, cause a decrease in the NaCl concentration at the macula densa. Thus, the system acts to stabilize the NaCl concentration at the macula densa. The purpose of the present study was to describe the dynamic characteristics of the TGF, and to use this knowledge in elucidating the role of the TGF system in the autoregulation of renal blood flow. Further, by comparing the dynamic characteristics of TGF between hypertensive and normotensive rats, to identify possible alterations in renal function that could play a role in the etiology and pathogenesis of hypertension. Anesthesia and surgery are unavoidable complications in experimental work in animals. It is shown that the anesthetics commonly used in micropuncture experiments in rats have different effects on various aspects of renal function, e.g. GFR, sodium excretion, proximal tubular compliance, and TGF function. It is concluded that the thiobarbiturate inactin, the most used anesthetic, has more detrimental effects on renal function than halothane and other barbiturates. In halothane anesthetized rats, the proximal tubular pressure oscillates with a frequency of 30-50 mHz. The pressure oscillations are associated with oscillations in tubular flow, and the early distal tubular Cl- activity. The possible mechanisms behind the oscillations are discussed. It is concluded that the oscillations appear because of the operation of the TGF system. Although it seems unlikely, it cannot be excluded that a vascular pacemaker is involved in the underlying oscillatory mechanism. To test the hypothesis that the oscillations are caused by the TGF system, a series of dynamic mathematical models of the TGF system have been developed.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Dynamic aspects of the tubuloglomerular feedback mechanism. 161 20

The effects of acidosis on renal function and morphology were examined in the isolated perfused rat kidney (IPK). Kidneys were perfused with oxygenated Krebs-Henseleit-albumin medium for 60 minutes at pH 7.4 or pH 7.0. At the lower pH, GFR was reduced by 25%, TRNa by 32% and oxygen consumption by 41% as compared to perfusion at pH 7.4 (all P less than 0.05). In addition, the usual hypoxic injury observed in the medullary thick ascending limb of the Loop of Henle (TAL) in the IPK at pH 7.4 (consisting of nuclear pyknosis and focal fragmentation necrosis) was reduced by acidosis from 62% to 14% of tubules involved (P less than 0.005). This cytoprotection was not the result of improved oxygenation since O2 delivery was actually slighty reduced at pH 7.0 compared to pH 7.4. Furthermore, acidosis was protective even after perfusion with non-oxygenated media (42% tubules damaged at pH 7.0 vs. 95% of tubules damaged at pH 7.4; P less than 0.01), making it very unlikely that the effect of acidosis is to improve TAL oxygenation. Since previous studies indicate that the TAL lesion is transport dependent and prevented in the non-filtering kidney, it was possible that the decrease in GFR associated with acidosis could account for decreased injury. The GFR was manipulated by alterations in perfusion pressure or albumin concentration, and no consistent relationship between the extent of injury and GFR could be shown at either pH over a wide range of GFR values. Therefore, acidosis protected the TAL from hypoxic injury by a mechanism apparently independent of oxygen or solute delivery.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Acidosis and hypoxic medullary injury in the isolated perfused kidney. 321 May 40