Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Allen, W.R. et al.

Sodium reabsorption during intrarenal diazoxide infusion in the dog.

Infusion of diazoxide, a potent benzothiazide antihypertensive, into the renal artery results in diuresis and natriuresis. The site within the nephron of decreased reabsorption has been controversial. Thus free flow recollection micropuncture studies of the superficial proximal tubule of the dog were undertaken to determine if diazoxide decreased sodium reabsorption from this part of the nephron. Renal blood flow, monitored by an electromagnetic flow meter, was increased by about 15% with the diazoxide infusion. Systemic blood pressure and hematocrit remained unchanged. Glomerular filtration rate increased significantly from 26 +/- 2 to 34 +/- 3 ml/min, urine flow and sodium excretion also increased (0.13 +/- 0.01 to 0.33 +/- 0.06 ml/min and 5.5 +/- 0.90 to 35.5 +/- 11.0 microEq/min, respectively). Decreased sodium reabsorption from the proximal tubule was demonstrated by a decrease in the tubular fluid to plasma inulin ratio (1.62 +/- 0.1 1.47 +/- 0.1) thus giving a reduction in fractional sodium reabsorption to the site of micropuncture (36.1 +/- 4.3 to 29.5 +/- 5.1%, p less than 0.05). To examine peritubular effects of diazoxide infusion, capillary protein concentration and pressure were measured; the former increasing significantly (9.17 +/- 0.32 to 9.80 +/- 0.35, p less than 0.05) and the latter did not change (13.1 +/- 1.0 vs. 15.2 +/- 1.4 mm Hg). Thus intrarenal diazoxide causes whole kidney vasodilatation with diuresis, natriuresis and decreased sodium reabsorption from the superficial proximal tubule. Additional studies provided no data to indicate that changes in peritubular physical factors account for the changes in sodium handling.(ABSTRACT TRUNCATED AT 250 WORDS)[1]

References

Sodium reabsorption during intrarenal diazoxide infusion in the dog. Allen, W.R., Brouhard, B.H., Lynch, R.E. Pharmacology (1983) [Pubmed]

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