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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science, Ltd
    Clinical and experimental pharmacology and physiology 32 (2005), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Resistance changes of the afferent and efferent arterioles determine blood flow and filtration rate in the kidney. The tone of both vessels results from the influence of nerves and humoral and paracrine factors, through a balance of constrictor and dilator systems. Angiotensin (Ang) II and nitric oxide (NO) are important factors determining vascular tone.2. In the present review, we show that, in addition to the basal production of NO, a specific and significant AngII-induced release of NO occurs in glomerular arterioles. Data from investigations of arteriolar contraction, as well as from fluorescence measurements of NO, in the presence of selective angiotensin AT1 and AT2 receptor antagonists indicate an AT1 receptor-stimulated release of NO in afferent arterioles.3. The AngII-induced liberation of NO could prevent glomerular arterioles from a marked constriction, particularly in situations of high AngII levels in the kidney.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 421 (1992), S. 466-468 
    ISSN: 1432-2013
    Keywords: Renin release ; Intraluminal pressure ; Afferent arterioles
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To evaluate the role of the proposed baroreceptor mechanism in the afferent arteriole in regulating renin release, we modified the isolated perfused tubule technique to perfuse afferent arterioles. Arterioles with attached glomeruli were isolated from rabbit kidneys and perfused using standard methods. To stop the arteriolar flow and allow perfusion pressure, as set by a mercury manometer, to be built up in the lumen of the vessel, the glomerulus was sucked into a constriction pipette. The preparation was continuously superfused with Krebs-Ringer solution in the first series of experiment, and a cell culture medium in the second series of experiment. The superfusate droplets were collected under mineral oil with 10-min collection intervals. The renin content of the samples was assayed by radioimmunoassay of the angiotensin I generated. In the two series of experiments we tested the effects of sequential changes in intraluminal pressure on renin release. In the first series of experiments (n=6) the renin release was 56.3 nGU arteriole−1 min−1 in the first 10 min of sampling. The renin release was then constant for 80 min with an average of 21.6 nGU arteriole−1 min−1. In the last 30 min the renin release was 96.5 nGU arteriole−1 min−1. In the second series of experiments (n=8) the renin release was 26.5 nGU arteriole−1 min−1 throughout the course of the experiment. These results indicate that under these conditions there is no relation between renin release and intraluminal pressure in afferent arterioles.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 391 (1981), S. 129-134 
    ISSN: 1432-2013
    Keywords: Kidney physiology ; Amphibian ; Glomerular function
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A single nephron tubulo-glomerular feedback control of the glomerular filtration rate, which is known in mammlian animals, could be one way by which amphibians regulate the glomerular filtration rate (GFR). To investigate whether theAmphiuma means shows any sign of a tubuloglomerular feedback control, micropuncture experiments were carried out. Six different series of experiments were performed. In the first series, tubular stop-flow pressure (SFP) was measured during distal tubular perfusion with amphibian Ringer solution at a rate of 10, 25 and 50 nl/min. A significant decrease of SFP was found at the three perfusion rates compared to the controls. In the second group, single nephron glomerular filtration rate (SNGFR) was measured, while the distal tubule was perfused at 10, 25 and 50 nl/min. At a perfusion rate of 10 nl/min the SNGFR did not decrease, whereas at 25 and 50 nl/min it decreased significantly. In the third group the perfusion pipette was located in the proximal tubule and the nephron was perfused at 10, 25 and 50 nl/min, while at the same time the proximal tubular stop-flow pressure was measured. No reduction of SFP was found at a perfusion rate of 10 nl/min, while significant reductions were noted at rates of 25 and 50 nl/min. In the fourth group the SNGFR was measured in the distal tubule beyond the macula densa and in Bowman's space of the same nephron. No significant difference was found. In the fifth group, the glomerular capillary pressure (GCP) was measured before and after blockade of the tubular fluid flow. No significant difference was found between these two measurements. The sixth series deals with the changes occuring at the single nephron level by the tubulo-glomerular feedback control. The single nephron filtration fraction (FF) was determined from efferent arteriolar protein concentration with and without a feedback-induced reduction of the SNGFR. The FF values were not significantly different from one another. From these results and data from the other series, the afferent (R aff) and efferent (R eff) arteriolar resistances were calculated.R eff did not change, whileR aff increased significantly when a feedback stimulus was applied. These experiments indicate the existence of a tubuloglomerular feedback control which depresses the SNGFR and SFP by contracting the afferent arteriole.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-2013
    Keywords: Rat ; Micropuncture ; Microperfusion ; Loop of Henle ; Stop-flow pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The behavior of the feedback mechanism, that causes glomerular capillary pressure and filtration rate to decrease when tubule fluid flow rate through the loop of Henle of the same nephron is increased, was examined in rats before and during isotonic extracellular fluid volume expansion. The loop of Henle was perfused from the late proximal tubule at either 10 or 40 nl/min while proximal fluid was collected to measure single nephron filtration rate (SNGFR), while proximal stop-flow pressure (PSF) was measured, or while fluid was collected from the early distal tubule to assess reabsorption of fluid and electrolytes by the loop of Henle. During control periods increasing loop perfusion caused SNGFR to decrease 37%, PSF to decrease 19%, and absorption of fluid, sodium and chloride by the loop of Henle to increase. After 1 h of infusion of isotonic NaCl solution the same change in loop flow causes a 19% decrease in SNGFR and an 8% decrease in PSF. Fluid absorption by the loop of Henle did not increase with increased loop perfusion. Increases in Na and Cl absorption were similar to the increases in control periods. The smaller decreases in SNGFR and PSF indicate that acute volume expansion decreases the sensitivity of the feedback response. The mechanism of this decrease in gain could involve interference with local generation or action of angiotensin, or a change in the composition or pressure of interstitial fluid tending to dilate the pre-glomerular resistance vessels.
    Type of Medium: Electronic Resource
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