Micropuncture study of distal tubular potassium and sodium transport in rat nephron

Malnic, Gerhard; Klose, RM; Giebisch, Gerhard

doi:10.1152/ajplegacy.1966.211.3.529

Cited by 296 publications

(150 citation statements)

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“…7, early distal TF/P-inulin ratios declined with increasing arterial blood pressure. At a blood pressure of 100 mm Hg an early distal TF/P-inulin ratio of 5.1 is obtained from the regression line, a value which is in good agreement with the results of other authors (21,22 urinary excretion observed in the chronically hypertensive rats must be due to a diminished reabsorption somewhere in the more distal parts of the nephron. According to our experiments, the site of this change is the loop of Henle.…”

Section: Methodssupporting

confidence: 90%

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Fluid reabsorption in Henle's loop and urinary excretion of sodium and water in normal rats and rats with chronic hypertension

Stumpe¹,

Lowitz²,

Ochwadt³

1970

J. Clin. Invest.

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A B S T R A C T The function of the short loops of Henle was investigated by micropuncture technique in normal rats, in rats with spontaneous hypertension, and in the untouched kidney of rats with experimental renal hypertension. All animals received a standard infusion of 1.2 ml of isotonic saline per hr.With increasing arterial blood pressure (range from 90 to 220 mm Hg), a continuous decrease in transit time of Lissamine green through Henle's loop from 32 to 10 sec was observed. Fractional water reabsorption along the loop declined progressively from 26 to 10%, and fractional sodium reabsorption decreased from 40 to 36% of the filtered load. The fluid volume in Henle's loop calculated from transit time and mean flow rate also decreased with increasing blood pressure. There was no change in superficial single nephron filtration rate but there was a slight increase in total glomerular filtration rate (GFR). Sodium and water reabsorption in the proximal tubule remained unchanged.Urine flow rate, sodium excretion, osmolar clearance, and negative free water clearance increased with increasing blood pressure. The osmolal urine to plasma (U/P) ratio declined but did not fall below a value of 1.5. It is concluded that the increase in sodium and water excretion with chronic elevation of arterial blood pressure is caused by a decrease of sodium and water reabsorption along the loop of Henle, presumably as a consequence of increased medullary blood pressure. The following three groups of animals were used: (a) normal rats, (b) rats with a moderate spontaneous hypertension, and (c) rats with experimental hypertension 4-5 wk after clamping one renal artery with a Goldblatt clamp. In the last group, only the untouched kidney, which is exposed to the high blood pressure, was investigated. All animals received an isotonic saline infusion of 1.2 ml/hr. Micropuncture experiments were done on superficial nephrons. Accordingly, only the function of short loops of Henle was studied. METHODSThe experiments were performed on Albino rats of about the same weight (190-210 g). The animals were divided into three groups differing from each other by the level of arterial blood pressure. For the first group male rats-of the FW4, strain (Paderborn) were chosen, having a mean arterial blood pressure between 90 and 110 mm Hg. The second group consisted of female rats of the Wistar strain with a blood pressure from 110 to 160 mm Hg. In the third group female Wistar rats with experimental renal hypertension of 4-5 wk duration (for the method see reference 12, 13) were used, their blood pressure ranging from 160 to 220 mm Hg. In this last group only the untouched kidney exposed to the high arterial blood pressure was investigated. All animals were kept on the same standard rat diet (Altromin, sodium content: 1200 mg/kg) and had free access to water. The animals were anaesthetized by intraperitoneal injection of Inactin Hamburg,(70)(71)(72)(73)(74)(75)(76)(77)(78)(79)(80) mg/kg body weight) and prepared for micropuncture as previously describe...

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Section: Methodssupporting

confidence: 90%

Section: Methodssupporting

confidence: 90%

Fluid reabsorption in Henle's loop and urinary excretion of sodium and water in normal rats and rats with chronic hypertension

Stumpe¹,

Lowitz²,

Ochwadt³

1970

J. Clin. Invest.

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“…Borenstein et al (1983) reported that injection of atrial extract into anesthetized rats increased total and medullary blood flow in the kidney. In the present study, the prolonged kaliuresis was accompanied by the diuresis, which suggests that urine flow into the distal tubule may have increased after the injection of a-hANP, since it has been shown that potassium secretion is increased when flow into the distal tubule is increased (Malnic et al 1966;Morgan and Berliner 1969;Kunau et al 1974; Khuri et al 1975;Reineck et al 1975;Diezi et al 1976). This increase in urine flow into the distal tubule could have been elicited by the dissipation of corticomedullary osmotic gradient by medullary washout.…”

Section: Resultssupporting

confidence: 60%

The effects of intravenous injection of .ALPHA.-human atrial natriuretic polypeptide on blood pressure, renal hemodynamics and urinary kinin excretion in anesthetized rabbits.

Nushiro

Abe

Seino

et al. 1987

Tohoku J. Exp. Med.

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Studies were performed in anesthetized rabbits to examine the effects of a-human atrial natriuretic polypeptide (a-hANP) on blood pressure, renal hemodynamics and urinary kinin excretion. Intravenous bolus injection of a-hANP at a dose of 5pg resulted in a transient increase in renal blood flow from 26.6+2.2 to 33.7+2.2 ml/min (p <0.05) and a decrease in mean arterial pressure from 113+1.8 to 107±2.2mmHg (p< 0.01). The calculated renal vascular resistance decreased from 4.50+0.34 to 3.28+0.20 mmHg/ml/min (p <0.05). This vasodilatory effect of a-hANP was immediate and lasted for 30 min. These hemodynamic alterations were not associated with the changes in glomerular filtration rate estimated by creatinine clearance. Intravenous injection of a-hANP also produced marked increases in urine volume from 1.99+0.43 to 5.7+1.20 ml 10 min (p <0.01), urinary sodium from 42.2± 7.6 to 243±54 ,u Eq/ 10 min (p <0.01), urinary potassium from 37.5± 5.5 to 74.8± 10.3 ,u Eq/ 10 min (p <0.01), and urinary kinin excretion from 3.44± 0.49 to 5.26±0.82 ng/ 10 min (p <0.05). The observed natriuretic effect of ahANP lasted only for 30 min, whereas diuretic and kaliuretic effects were sustained for 120 min. Hematocrit levels did not change significantly throughout the experiment. These results indicate that a-hANP is a potent vasodilator substance and that the natriuretic effect induced by the bolus injection of a-hANP is mediated mainly through its renal vasodilatory action. It is also suggested that the renal kinin, at least in part, contributes to the natriuretic effect of a-hANP. a-human atrial natriuretic polypeptide (a-hANP) ; renal hemodynamics ; fluid and electrolyte excretion ; urinary kinin excretion It is well informed that mammalian atrial extract when administered to rats produces a marked natriuresis and diuresis (de Bold et al. 1981;

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“…In conditions of Na ϩ restriction, although the Na ϩ concentration in the distal tubule is little affected, it falls progressively in the CD and may be as low as 3 mM in the final urine. 47 Under the latter condition, it would be expected that stimulation of apical P2X 4 and/or 4/6 receptors should increase apical ENaC activity and facilitate Na ϩ reabsorption in the CD (see Figure 9).…”

Section: Mechanism Of P2r-mediated Regulation Of Enacmentioning

confidence: 99%

Sodium-Dependent Regulation of Renal Amiloride-Sensitive Currents by Apical P2 Receptors

Wildman

Marks

Turner

et al. 2008

Journal of the American Society of Nephrology

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The epithelial sodium channel (ENaC) plays a major role in the regulation of sodium balance and BP by controlling Na ϩ reabsorption along the renal distal tubule and collecting duct (CD). ENaC activity is affected by extracellular nucleotides acting on P2 receptors (P2R); however, there remain uncertainties over the P2R subtype(s) involved, the molecular mechanism(s) responsible, and their physiologic role. This study investigated the relationship between apical P2R and ENaC activity by assessing the effects of P2R agonists on amiloride-sensitive current in the rat CD. Using whole-cell patch clamp of principal cells of split-open CD from Na ϩ -restricted rats, in combination with immunohistochemistry and real-time PCR, we found that activation of metabotropic P2R (most likely the P2Y 2 and/or 4 subtype), via phospholipase C, inhibited ENaC activity. In addition, activation of ionotropic P2R (most likely the P2X 4 and/or 4/6 subtype), via phosphatidylinositol-3 kinase, either inhibited or potentiated ENaC activity, depending on the extracellular Na ϩ concentration; therefore, it is proposed that P2X 4 and/or 4/6 receptors might function as apical Na ϩ sensors responsible for local regulation of ENaC activity in the CD and could thereby help to regulate Na ϩ balance and systemic BP.

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Micropuncture study of distal tubular potassium and sodium transport in rat nephron

Abstract: study of distal tubular potassium and sodium transport in rat nephron. Am. J. Physiol.

Cited by 296 publications

References 1 publication

Fluid reabsorption in Henle's loop and urinary excretion of sodium and water in normal rats and rats with chronic hypertension

Fluid reabsorption in Henle's loop and urinary excretion of sodium and water in normal rats and rats with chronic hypertension

The effects of intravenous injection of .ALPHA.-human atrial natriuretic polypeptide on blood pressure, renal hemodynamics and urinary kinin excretion in anesthetized rabbits.

Sodium-Dependent Regulation of Renal Amiloride-Sensitive Currents by Apical P2 Receptors

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