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  • 1
    ISSN: 1432-2013
    Keywords: Glomerular filtration rate ; Juxta-glomerular apparatus ; Macula densa ; Tubulo-glomerular feedback ; Chloride
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It has been concluded that tubulo-glomerular feedback mechanism is triggered by changes in NaCl concentration ([NaCl]) at the macula densa. This conclusion is based on the demonstration that changes in filtration rate produced during retrograde perfusion of the loop of Henle depend upon the perfusate [NaCl]. Experiments were performed to evaluate whether the effect on glomerular function of orthograde perfusion of the loop of Henle is consistent with this conclusion. Early proximal flow rate ( $$\dot V_{EP} $$ ), stop-flow pressure (P SF), early distal chloride concentration ([Cl]), and flow rate were measured during perfusion of the loop of Henle with mannitol solution (300 mosm kg−1), 30 mM NaCl+mannitol (300 mosm kg−1), 140 mM Na isethionate and artificial tubular fluid. When distal flow exceeded 10 nl min−1, the magnitude of the glomerular response was predictable from the [Cl]. The linear regression line, $$\Delta \dot V_{EP} = - 0.027{\text{ }}[Cl]{\text{ + 4}}{\text{.3}}$$ , did not differ from that obtained previously with the retrograde technique. Retrograde perfusion with 140 mM Na isethionate was without effect on $$\dot V_{EP} $$ . We conclude that the effect on glomerular function of perfusion of the loop of Henle in either an orthograde or a retrograde direction with these solutions depends upon the chloride concentration at the macula densa.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2013
    Keywords: Kidney ; Glomerular filtration rate ; Atrium ; NaCl excretion ; Volume regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Micropuncture studies of the renal effects of atrial natriuretic substance. Injection of atrial extract produced by homogenization, boiling and centrifugation of atrial tissue from one heart caused a 10 fold increase in urine flow rate and a 30-fold increase in Na excretion. Similarly prepared extracts of ventricle were without effect. To identify the site of action of atrial natriuretic substance, extract was infused intravenously at rates corresponding to 3 or 6 atria per hour. During infusion at a rate of 3 atria per hour mean urine flow increased from 9.5±2.8 to 17.2±1.2 μl/min and Na excretion from 0.14±0.06 to 1.78±0.14 μmol/min. Glomerular filtration rate (GFR), single nephron filtration rate (SNGFR) and proximal and loop of Henle fluid absorption did not change significantly. During infusion of 6 atria per hour, paralleling a greater rise in urine flow rate (from 6.4±2.09 to 40.3±7.5 μl/min) and in sodium excretion (from 0.18±0.0008 to 5.97±0.93 μmol/min), filtration rate, measured for either the single nephron or the whole kidney, rose. As a consequence of the rise in GFR, delivery of fluid and chloride into the distal tubule increased significantly. These data suggest that to a major extent the natriuresis is caused by transport inhibition along collecting tubules and collecting ducts. In addition, at high doses a rise in filtration rate contributes to the natriuretic effect of atrial extracts.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 406 (1986), S. 237-239 
    ISSN: 1432-2013
    Keywords: Atrial natriuretic factor ; atriopeptin II ; glomerular pressure ; natriuresis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present experiments were undertaken to assess the effect of an atrial extract (ANF) and of the synthetic atriopeptin II (APII) on filtration pressure of rat kidneys. Continuous recordings of stop flow pressure (SFP) were made to obtain an index of the change of glomerular capillary pressure produced by atrial peptides and its time course. Short-term infusion of ANF or APII increased SFP from 40.6±0.99 to 50.7±1.42 mm Hg (p〈0.001) and from 44.0±1.28 to 52.7±1.75 mm Hg (p〈0.001) respectively. The maximum response was achieved promptly. Return of SFP to control was slow: 20 minutes after termination of the infusion SFP was still elevated by 4.9±1.27 mm Hg (p〈0.01). Tubule and stellate vessel pressures increased less than 2mm Hg, changes that were not significant. Arterial pressure fell 6 mm Hg (p〈0.05). When arterial pressure was reduced by an aortic clamp to 85–90 mmHg prior to administration of APII the response of SFP was markedly blunted (from a mean increase of 9.0±1.07 mm Hg to 4.5±0.53 mm Hg). The increase of SFP probably reflects an increase of glomerular capillary pressure. The finding suggests that atrial peptides increase glomerular filtration rate at least in part by increasing filtration pressure.
    Type of Medium: Electronic Resource
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