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  • 2000-2004
  • 1985-1989  (2)
  • Glomerular ultrafiltration  (1)
  • Munich-Wistar rat  (1)
Material
Years
  • 2000-2004
  • 1985-1989  (2)
Year
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 407 (1986), S. 221-227 
    ISSN: 1432-2013
    Keywords: Tubulo-glomerular feedback ; Micropuncture ; Munich-Wistar rat ; Proximal reabsorption
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract An analysis of glomerulo-tubular balance in the rat proximal tubule. Flow dependence of absolute proximal reabsorption (APR) or glomerulo-tubular balance (GTB) has been observed with spontaneous alterations in flow and attributed to both intraluminal and extraluminal factors. Flow dependent alterations in APR were demonstrated when 1. nephron filtration rate (SNGFR) was decreased by tubulo-glomerular feedback mechanisms by increasing late proximal tubular microperfusion rates, and 2. when SNGFR was increased by addition of [Sar1, Ala8] angiotensin II to the adjacent peritubular capillary flow. Selective reduction in early proximal tubular flow rate by pump aspiration also resulted in flow dependent reductions in APR. However, selective additions of perfusion fluids of various native and artificial constituency to the early proximal tubule did not result in flow dependent increase in APR. Conclusions. 1. GTB with both increases and decreases in SNGFR can be demonstrated at the level of the single nephron, 2. selective reductions in luminal flow rate produces parallel reductions in APR; however, 3. increases in flow rate with either artificial or native fluids of different ionic concentrations did not result in increases in APR. This lack GTB may be due to lack of parallel changes in peritubular physical factors or that APR in the S2 segment is less sensitive to increase in flow rate.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Pediatric nephrology 1 (1987), S. 348-358 
    ISSN: 1432-198X
    Keywords: Acute renal failure ; Glomerular ultrafiltration ; Tubular injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Acute renal failure (ARF) is a common clinical entity which results from multiple causes. Experimental models in animals have duplicated many of the clinical syndromes which can be classified into (1) ARF due to increased filtered load of endogenous and exogenous materials, (2) ARF associated with exogenous nephrotoxins and (3) ischemic forms of renal failure secondary to hypoperfusion and hypotension. The mechanisms leading to the reduction in GFR are multiple and the alterations in determinants of nephron filtration rate and degree of tubular backleak and obstruction are described for each of these subtypes of experimental ARF. The specific mechanisms whereby tubular damage translates into a reduction in GFR in ARF are discussed for each sub-type of ARF. Tubular damage can often be dissociated from the reduction in GFR, possibly by inhibiting tubuloglomerular feedback responses, but such increases in GFR and nephron filtration rate are not necessarily beneficial to the organism because of potential volume depletion and the risk of magnifying further tubular damage. Information on the physiologic role of tubuloglomerular feedback activity in ARF is provided and supports the concept that feedback induced reductions in GFR after tubular injury may preserve extracellular volume and minimize further tubular damage. Reductions in tubular metabolic work appears to prevent and ameliorate further tubular injury after the initial insult. The mechanisms which associate changes in GFR and tubular damage can now be described, and therapies which improve GFR without correcting the tubular damage may compound the clinical problem and increase renal damage.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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