Intrarenal regulatory factors of salt excretion during renal venous pressure elevation

Wathen, RL; Ee, Selkurt

doi:10.1152/ajplegacy.1969.216.6.1517

Cited by 28 publications

(16 citation statements)

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“…The finding that extracellular volume expansion alters the renal response to changes in intrarenal pressures has also been reported by Wathen and Selkurt (20).…”

Section: Discussionsupporting

confidence: 73%

Effect of increased peritubule protein concentration on proximal tubule reabsorption in the presence and absence of extracellular volume expansion.

Ott¹,

Haas²,

Cuche³

et al. 1975

J. Clin. Invest.

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“…The finding that extracellular volume expansion alters the renal response to changes in intrarenal pressures has also been reported by Wathen and Selkurt (20).…”

Section: Discussionsupporting

confidence: 73%

Effect of increased peritubule protein concentration on proximal tubule reabsorption in the presence and absence of extracellular volume expansion.

Ott¹,

Haas²,

Cuche³

et al. 1975

J. Clin. Invest.

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“…Since changes in both renal arterial (10) and venous pressure (11) are known to affect tubular fluid reabsorption, it seemed important to examine whether acute TIVC constriction affects water excretion independent of these intrarenal hemodynamic alterations. In each Group I experiment performed in dogs undergoing a water diuresis, acute TIVC constriction diminished CO and caused an antidiuresis.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of Effect of Thoracic Inferior Vena Cava Constriction on Renal Water Excretion

Anderson¹,

Cadnapaphornchai²,

Harbottle³

et al. 1974

J. Clin. Invest.

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A B S T R A C T Persistent secretion of vasopressin and/ or diminished distal fluid delivery have been proposed to explain the impaired water excretion associated with low-output cardiac failure. In the present investigation cardiac output (CO) was diminished in anesthetized dogs undergoing a water diuresis by constriction of the thoracic inferior vena cava (TIVC). In intact animals (group I) acute TIVC constriction decreased CO from 3.5 to 2.2 liters/min (P < 0.005) as urinary osmolality (U05m) increased from 103 to 543 mosmols/ kg (P < 0.001) and free water clearance (CH20) decreased from 2.1 to -0.6 ml/min (P < 0.001). This antidiuretic effect was disassociated from changes in renal arterial and venous pressures, glomerular filtration rate, solute excretion, and renal innervation. To examine the role of vasopressin in this antidiuresis, studies.,(group II) were performed in acutely hypophysectomized, steroid-replaced animals. In these animals TIVC constriction decreased CO to a similar degree from 3.4 to 2.1 liters/min (P <0.001). However, the effects on U03m; (87-104 mosmols/kg) and CH20 (2.1-1.6 ml/min) were significantly less than in intact dogs. In another group of hypophysectomized animals, (group III) renal arterial and venous pressures were not controlled, and the effect of TIVC constriction on Uosm was not significant (65-79 mosmols/kg) although CH20 decreased from 3.3 to 1.9 ml/min (P < 0.001). In both the group II and III studies, there were linear correlations between the changes in CH2o and the urine flow.Studies were also performed in baroreceptor-denervated animals with intact hypothalamo-neurohypophyseal tracts, and acute TIVC constriction altered neither Uosm nor CH2o when renal arterial pressure was controlled. These (TIVC) ' has been used by numerous investigators (1-4) as an experimental model of cardiac failure and is known to be associated with a diminished cardiac output (CO) (4) and increased tubular reabsorption of sodium (1-4). The effect of acute TIVC constriction on renal diluting capacity has not been previously investigated. An impairment in renal water excretion is, however, a frequent accompaniment of low-output cardiac failure (5). Although the mechanism of this defect in water excretion is unknown, it has been suggested to be mediated by either increased release of vasopressin (6) or diminished delivery of fluid to the distal diluting segment of the nephron (5). The present studies were therefore undertaken to examine the effect of acute TIVC constriction on renal water excretion and to define the mechanism of any such effect.METHODS 40 experiments were performed on 24 mongrel dogs of either sex weighing 20-30 kg. Food was withheld 18 h before the experiment and all animals had free access to water. The animals were anesthetized with i.v. pentobarbital (30 mg/kg) and intubated and ventilated with a Harvard respirator (Harvard Apparatus Co. Inc., Millis, Mass.). Nine animals underwent transbuccal hypophysectomy through the hard palate on the morning of the experiment (7). ...

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“…This seemed to be, to a certain extent, a reversible phenomenon as lowering of renal vein pressure immediately improved urine output and GFR 18 24. Other studies have also indicated that temporary renal vein compression results in reduced sodium excretion, increased renal interstitial pressure and reduced GFR 25 26…”

Section: Pathophysiologymentioning

confidence: 96%

Cardiorenal syndrome in decompensated heart failure

Tang

Mullens

2009

Heart

119

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Worsening renal function during treatment of acute decompensated heart failure (ADHF) often complicates the treatment course of heart failure. Furthermore, the development of worsening renal function is a strong independent predictor of long-term adverse outcomes. Sometimes referred to as 'cardiorenal syndrome,' the definition varies widely, and the overall understanding of pathogenesis is limited. This is probably owing to the lack of precision and characterisation of renal compromise during treatment of heart failure. Traditionally, the predominant cause has been attributed to impairment of cardiac output and relative underfilling of arterial perfusion. Emerging data have led to a resurgence of interest in the importance of venous congestion and elevated intra-abdominal pressure rather than confining it to impaired forward cardiac output as the primary driver of renal impairment. These revived concepts may support the role of novel renal-sparing approaches to salt and water removal and renal preservation, but better ways to distinguish haemodynamic versus other nephrotoxic aetiologies are needed.

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Intrarenal regulatory factors of salt excretion during renal venous pressure elevation

Cited by 28 publications

References 0 publications

Effect of increased peritubule protein concentration on proximal tubule reabsorption in the presence and absence of extracellular volume expansion.

Effect of increased peritubule protein concentration on proximal tubule reabsorption in the presence and absence of extracellular volume expansion.

Mechanism of Effect of Thoracic Inferior Vena Cava Constriction on Renal Water Excretion

Cardiorenal syndrome in decompensated heart failure

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