1966
DOI: 10.1007/bf00362490
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A micropuncture study of the relationship between flow-rate through the loop of Henle and sodium concentration in the early distal tubule

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Cited by 45 publications
(10 citation statements)
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“…The mechanism responsible for this is ngt clear. It is possible that this reflects a limitation of sodium transport in the ascending limb at high rates of flow through the loop of Henle (24,25) or is the result of an impairment of active sodium transport in the ascending limb due to altered interstitial factors which affect peritubular capillary absorption, evidence for which has been presented in the proximal tubule (26).…”
Section: Discussionmentioning
confidence: 99%
“…The mechanism responsible for this is ngt clear. It is possible that this reflects a limitation of sodium transport in the ascending limb at high rates of flow through the loop of Henle (24,25) or is the result of an impairment of active sodium transport in the ascending limb due to altered interstitial factors which affect peritubular capillary absorption, evidence for which has been presented in the proximal tubule (26).…”
Section: Discussionmentioning
confidence: 99%
“…It is widely accepted that the MD presumably represents a sensor capable of detecting the changes in concentrations of some critical substance. The function sensed could be Na concentration [18], glucose [19], osmolality [20], or adenosine [21]. It is not far fetched to postulate that specific substances, including peptides, could reach the sensor through filtration and/or tubular reabsorption and secretion.…”
Section: Discussionmentioning
confidence: 99%
“…They proposed the following sequence: increased renin release, local angiotensin II formation, afferent arteriolar constriction, and a de creased glomerular filtration rate with resultant proximal tubule collapse. Other data that support this hypothesis include: the presence of myofibrils in the juxtaglomerular cells [47], the presence of renin substrate and coverting enzyme for angiotensin in the juxtaglomerular apparatus [44] and the presence of denovo angiotensin II in renal lymph [4], Schnerm a n n [87], however, could not confirm the original observations of C ortney et al [29], and found that the sodium concentration in the early distal tubule was not necessarily de pendent upon delivery rate. In fact, both Schnerm a n n et al [88] and M o r g a n and Berliner [69] noted that sodium concentration was high at very low delivery rates, then fell, but rose once again at perfusion rates greater than 20 nl/min in late proximal tubules.…”
Section: Autoregulationmentioning
confidence: 40%
“…This hypothe sis received its first experimental support in 1964 when Vander and M iller [114] found that the increased renin release induced by aortic constriction could be obviated with chlorothiazide, acetazolamide, or mannitol. Subse quent studies demonstrated that the increased renin release seen with elevated ureteral pressure [114], infusion of catecholamines at a constant renal per fusion pressure [29], and renal nerve stimulation [115] could be blocked with mannitol, sodium sulfate, chlorothiazide or acetazolamide. It was suggested that an inverse relationship existed between sodium delivery to the macula densa and renin release.…”
Section: Macula Densa Theorymentioning
confidence: 99%