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Response of single nephron glomerular filtration rate to distal nephron microperfusion. The observation that single nephron glomerular filtration rate (SNGFR) measured with proximal tubular collections is higher than SNGFR based on distal tubular collections has been attributed to the blockade of distal delivery during proximal collections, thus leading to an altered status in a distal nephron feedback mechanism thought to participate in the control of SNGFR. This hypothesis was tested further by evaluating SNGFR (measured from complete early proximal tubule collections) in the presence or absence of distal nephron perfusion via a late proximal nephron site. SNGFR measurements were also obtained from other nonperfused tubules selected at random. Artificial tubular fluid (ATF), Ringer's solution with or without calcium, or 0.9% sodium chloride solution was perfused at 25 nl/min; at least two solutions were used in nine of the 19 dogs. When distal delivery was maintained with ATF (19 tubules, seven dogs), SNGFR averaged 45 ± 6 nl/min and rose to 72 ± 9 nl/min following cessation of perfusion. SNGFR in other nonperfused tubules was 72 ± 6 nl/min. During distal perfusion with Ringer's solution (21 tubules, eight dogs), SNGFR was 52 ± 7 nl/min and was also significantly lower than SNGFR in nonperfused tubules (76 ± 9 nl/min). Thus, SNGFR was lower when distal perfusion was maintained with ATF or Ringer's solution. In contrast, when 0.9% NaCl was used as the perfusion solution (19 tubules, seven dogs), SNGFR averaged 71 ± 9 nl/min and did not differ significantly from SNGFR in nonperfused tubules (75 ± 6 nl/min). During perfusion with calcium-free Ringer's solution (15 tubules, six dogs), SNGFR was 16 ±12 nl/min and it, also, did not differ significantly from SNGFR in nonperfused tubules (82 ± 11 nl/min). The results support the concept that one or more functions of distal delivery participate in the control of SNGFR and they suggest that at least one of these functions may be reflected by changes in distal calcium delivery. Reponse du debit de filtration glomerulaire du nephron a la microperfusion de son segment distal. Le fait que le debit de filtration glomerulaire individuel d'un nephron (SNGFR) mesure par une collection tubularie proximale est plus eleve que le SNGFR mesure par une collection tubulaire distale a ete attribue a l'arret de l'ecoulement dans le distal pendant une collection proximale, ce qui entrainerait une alteration des mecanismes de feedback du nephron distal que l'on pense participer au controle de SNGFR. Cette hypothese a ete examinee plus avant par la mesure de SNGFR (a partir d'une collection proximale complete) en presence ou en l'absence d'une perfusion du nephron distal assuree a partir d'un site proximal tardif. Des mesures de SNGFR ont aussi ete obtenues a partir d'autres tubules, non perfuses et selectionnes au hasard. Du liquide tubulaire artificiel (ATF), du Ringer avec ou sans calcium ou du NaCl a 0,9% ont ete perfuses a 25 nl/min; au moins deux solutions ont ete utilisees chez 9 des 19 chiens. Quand le debit distal est maintenu avec de l'AFT (19 tubules, 7 chiens), le SNGFR est en moyenne de 45 ± 6 nl/min et augmente a 72 ± 9 nl/min quand on cesse la perfusion. SNGFR dans les autres tubules non perfuses est de 72 ±6 nl/min. Au cours de la perfusion distale avec du Ringer (21 tubules, 8 chiens), le SNGFR est de 52 ± 7 nl/min, significativement inferieur a la valeur obtenue dans les tubules non perfuses (76 ±9 nl/min). Ainsi le SNGFR est-il inferieur quand une perfusion distale est maintenue avec de l'AFT ou du Ringer. Au contraire; quand de NaCl 0,9% est perfuse (19 tubules, 7 chiens) SNGFR est en moyenne de 71 ± 9 nl/min et n'est pas significativement different de des valeurs obtenues dans les tubules non perfuses (75 ± 6 nl/min). Au cours de la perfusion par un Ringer sans calcium (15 tubules, six chiens), SNGFR est de 76 ± 12 nl/min, et, la encore, n'est pas significativement different de SNGFR des tubules non perfuses (82 ±11 nl/min). Ces resultats sont en faveur de l'idee qu'une ou des fonctions de la charge delivree au distal participeraient au controle de SNGFR et ils suggerent qu'au moins l'une de ces fonctions pourrait etre traduite par des modifications de la charge de calcium delivree au distal.

Angriffspunkt und Wirkungsmechanismus von Furosemid wurden am Menschen unter den Bedingungen der forcierten Wasserdiurese und der osmotischen Diurese untersucht. Wahrend einer Wasserdiurese stieg das Harnzeitvolumen nach Furosemid intravenos kurzfristig bis auf 40% des Glomerulusfiltrates an, so das zunachst ein proximaltubularer Angriffspunkt vorliegt. Gleichzeitig nahm CH2O unmittelbar nach Furosemid intravenos trotz Zunahme von Cosm erheblich ab, d.h. es kam zu einer weitgehenden Hemmung des Natriumtransportes auch im distalen Nephron zwischen aufsteigendem Schenkel der Henleschen Schleife und Sammelrohren. Unter osmotischer Diurese (10% Mannitol) wurde TmcH2O durch Furosemid bis auf Null reduziert und die effektive Nierengesamtdurchblutung um durchschnittlich 27% erhoht. Diese Befunde bei gleichzeitiger Zunahme der Kaliurese sprechen fur eine Hemmung des Natriumtransportes im aufsteigenden eines hypotonen Diuresezuwachses zeigt — nicht komplett sein kann. Daneben ist eine partielle „Auswaschung“ des medullaren Natriumpool im Rahmen der gesteigerten Nierengesamtdurchblutung moglich.

SummaryThe present experiments demonstrate that raising renal perfusion pressure in the isolated kidney caused a significant increase in sodium excretion in the absence of detectable changes in proximal tubule sodium transport suggesting that the natriuresis resulted primarily from a decrease in sodium transport along more distal nephron segments. The constancy of SNGFR/Cin argues against a role for redistribution of glomerular filtrate in the natriuresis.

Potassium transport in the distal nephron has been investigated, using stop flow and slow flow techniques. Results indicate that potassium is secreted in the collecting duct and far distal tubule, and that sodium must be present for this secretion to occur. The usual stop flow distal potassium dip would appear to be a true site of active potassium reabsorption. This reabsorptive area includes the collecting duct and distal tubule and is completely coextensive with the sodium reabsorptive area. Potassium reabsorption and secretion can occur simultaneously in the collecting duct and far distal tubule. This phenomenon explains the observation (confirmed in this study) that the stop flow potassium peak diminishes as duration of occlusion is increased.

In 1961, at the Symposium on shock in Stockholm, we presented evidence of persistent renal vasoconstriction in and following hemorrhagic shock which was suggested to take place on the preglomerular level (1). However, total renal blood flow was not so much reduced that hypoxia resulted. This was concluded from measurements of oxygen saturations of cortical blood in the low pressure phase of shock (2).

In 17 male Wistar rats in antidiuresis 10 different nephron segments and arteries are identified with the aid of Lowry's technique, dissected and total-and (Mg++)-adenosintriphosphatase (=ATPase) determined. (Na+K+)-activated ATPase in the distal tubule is four to five times (max. eight times) more active than in the proximal segment. This difference of activity may speak for a high pump mechanism mediated by the way of a (Na+K+)-activated enzyme system in the distal nephron and for a partially passive reabsorption of sodium from the proximal convolution.

SummaryDuring water diuresis stop flow-analysis the nephron volume is less than during osmotic diuresis stop flow analysis, there is a demonstrable increase in osmolal U/P in the distal nephron samples, and sodium U/P minimum occurs near the PAH peak. During water diuresis stop flow analysis active proximal reabsorption of sodium is demonstrable or para-aminohippurate is not a valid marker of proximal nephron samples.

Stop-flow analysis performed in the dog using Mg-28 demonstrated active reabsorption of magnesium in the proximal portion of the distal nephron. ‘Interrupted’ stop-flow analysis failed to document the existence of a renal tubular secretory mechanism for magnesium. During magnesium-loading reabsorption of potassium occurs in the distal nephron despite the presence of hyperkalemia.