Chronic Glucose Infusion Increases Tubular Sodium Reabsorption and Renal Blood Flow in Dogs

This study tested the hypothesis that inducing hyperinsulinemia and hyperglycemia in dogs, by infusing glucose chronically intravenously, would increase tubular sodium reabsorption and cause hypertension. Glucose was infused for 6 days (14 mg·kg−1·min−1 iv) in five uninephrectomized (UNX) dogs. Mean arterial pressure (MAP) and renal blood flow (RBF) were measured 18 h/day using DSI pressure units and Transonic flow probes, respectively. Urinary sodium excretion (UNaV) decreased significantly on day 1 and remained decreased over the 6 days, coupled with a significant, sustained increase in RBF, averaging ∼20% above control on day 6. Glomerular filtration rate and plasma renin activity (PRA) also increased. However, although MAP tended to increase, this was not statistically significant. Therefore, the glucose infusion was repeated in six dogs with 70% surgical reduction in kidney mass (RKM) and high salt intake. Blood glucose and plasma insulin increased similar to the UNX dogs, and there was significant sodium retention, but MAP still did not increase. Interestingly, the increases in PRA and RBF were prevented in the RKM dogs. The decrease in UNaV, increased RBF, and slightly elevated MAP show that glucose infusion in dogs caused a sustained increase in tubular sodium reabsorption by a mechanism independent of pressure natriuresis. The accompanying increase in PRA, together with the failure of either RBF or PRA to increase in the RKM dogs, suggests the site of tubular reabsorption was before the macula densa. However, the volume retention and peripheral edema suggest that systemic vasodilation offsets any potential renal actions to increase MAP in this experimental model in dogs.

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Renal blood flow, early distal sodium, and plasma renin concentrations during osmotic diuresis

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.2000.279.4.r1268 ◽

2000 ◽

Vol 279 (4) ◽

pp. R1268-R1276 ◽

Cited By ~ 20

Author(s):

Paul P. Leyssac ◽

Niels-Henrik Holstein-Rathlou ◽

Ole Skøtt

Keyword(s):

Blood Flow ◽

Renal Blood Flow ◽

Sodium Excretion ◽

Plasma Renin ◽

Urine Flow ◽

Sodium Reabsorption ◽

Osmotic Diuresis ◽

Nacl Concentration ◽

Proximal Tubular ◽

Distal Tubules

Inconsistencies in previous reports regarding changes in early distal NaCl concentration (EDNaCl) and renin secretion during osmotic diuresis motivated our reinvestigation. After intravenous infusion of 10% mannitol, EDNaCl fell from 42.6 to 34.2 mM. Proximal tubular pressure increased by 12.6 mmHg. Urine flow increased 10-fold, and sodium excretion increased by 177%. Plasma renin concentration (PRC) increased by 58%. Renal blood flow and glomerular filtration rate decreased, however end-proximal flow remained unchanged. After a similar volume of hypotonic glucose (152 mM), EDNaClincreased by 3.6 mM, ( P < 0.01) without changes in renal hemodynamics, urine flow, sodium excretion rate, or PRC. Infusion of 300 μmol NaCl in a smaller volume caused EDNaCl to increase by 6.4 mM without significant changes in PRC. Urine flow and sodium excretion increased significantly. There was a significant inverse relationship between superficial nephron EDNaCl and PRC. We conclude that EDNa decreases during osmotic diuresis, suggesting that the increase in PRC was mediated by the macula densa. The results suggest that the natriuresis during osmotic diuresis is a result of impaired sodium reabsorption in distal tubules and collecting ducts.

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Influence of the renal medullary circulation on the control of sodium excretion

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1993.265.5.r963 ◽

1993 ◽

Vol 265 (5) ◽

pp. R963-R973 ◽

Cited By ~ 16

Author(s):

R. J. Roman ◽

A. P. Zou

Keyword(s):

Blood Flow ◽

Renal Perfusion ◽

Sodium Reabsorption ◽

Doppler Flowmetry ◽

Medullary Blood Flow ◽

Tubular Sodium Reabsorption ◽

Vasa Recta ◽

Urinary Concentrating Ability ◽

Reliable Methods

Although the role of the renal medullary circulation in the control of urinary concentrating ability is well established, its potential influence on tubular sodium reabsorption is not generally recognized. Nearly 30 years ago, changes in the intrarenal distribution of blood flow were first proposed to contribute to the natriuretic response to volume expansion. However, the lack of reliable methods for studying medullary blood flow limited progress in this area. The recent development of laser-Doppler flowmetry and videomicroscopic techniques for the study of the vasa recta circulation has renewed interest in the role of medullary hemodynamics in the control of sodium reabsorption. Results of these studies indicate that changes in renal medullary hemodynamics alter renal interstitial pressure and the medullary solute gradient and play an important role in the natriuretic response to elevations in renal perfusion pressure, intravenous infusion of saline, and changes in tubular sodium reabsorption produced by vasoactive compounds. What is emerging from these studies is the view that changes in renal medullary hemodynamics represent an important but misunderstood and long-ignored factor in the control of tubular sodium reabsorption.

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Chronic glucose infusion significantly decreases 24 hr/day renal blood flow and increases arterial pressure in dogs with reduced renal mass

The FASEB Journal ◽

10.1096/fasebj.20.5.a1170-b ◽

2006 ◽

Vol 20 (5) ◽

Author(s):

Michael W Brands ◽

Tracy D Bell ◽

Vanessa Springfield ◽

Cassandra Fleming ◽

Rajiv Janardhanan

Keyword(s):

Blood Flow ◽

Arterial Pressure ◽

Renal Blood Flow ◽

Renal Mass ◽

Glucose Infusion

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Neurogenic regulation of renal tubular sodium reabsorption

AJP Renal Physiology ◽

10.1152/ajprenal.1977.233.2.f73 ◽

1977 ◽

Vol 233 (2) ◽

pp. F73-F81 ◽

Cited By ~ 11

Author(s):

G. F. DiBona

Keyword(s):

Blood Flow ◽

Rat Kidney ◽

Basement Membranes ◽

Adrenergic Nerve ◽

Sodium Reabsorption ◽

Electron Microscopic ◽

Renal Nerve ◽

Tubular Sodium Reabsorption ◽

Renal Tubular ◽

Sites Of Action

The evidence supporting a role for direct neurogenic control of renal tubular sodium reabsorption is reviewed. Electron microscopic and fluorescence histochemical studies have demonstrated adrenergic nerve terminals in direct contact with basement membranes of mammalian (rat, dog, and monkey) renal tubular epithelial cells. Low-level direct or baroreceptor reflex stimulation of renal sympathetic nerves produces an increase in renal tubular sodium reabsorption without alterations in glomerular filtration rate, renal blood flow, or intrarenal distribution of blood flow. Antinatriuresis was prevented by prior treatment of the kidney with guanethidine or phenoxybenzamine. Rat kidney micropuncture studies have localized a site of enhanced tubular sodium reabsorption to the proximal tubule. Possible indirect mediation of the antinatriuresis by other humoral agents known to be released from the kidney on renal nerve stimulation (angiotensin II, prostaglandin) was excluded by experiments with appropriate blocking agents. The possible effects of anesthesia and uncertainties about the completeness of surgical renal denervation and other tubular segmental sites of action are critically analyzed. The clinical implications of this mechanism in pathologic conditions of sodium and water retention are discussed and and a prospectus for future work is presented.

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