Reversal of atrial natriuretic peptide resistance by increasing distal tubular sodium delivery in patients with decompensated cirrhosis
✍ Scribed by William T. Abraham; Marije E. Lauwaars; Jin K. Kim; Ricardo L. Peñna; Robert W. Schrier
- Publisher
- John Wiley and Sons
- Year
- 1995
- Tongue
- English
- Weight
- 783 KB
- Volume
- 22
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
✦ Synopsis
To test the hypothesis that diminished sodium delivery to the distal tubular site of atrial natriuretic peptide (A") action accounts for renal ANP resistance in cirrhosis, 12 cirrhotic patients with ascites were studied at baseline and during the infusion of ANP alone (0.15 pg/ kg/min), mannitol alone (4 g/hr), and ANP plus mannitol for 3 hours each. Distal tubular sodium delivery, as assessed by lithium clearance, was increased during the infusion of mannitol (13.8 2 3.4 to 23.7 2 5.7 d m i q P < .05) and during the A " plus mannitol infusion (13.8 5 3.4 to 28.5 5 6.3 mllmin; P < .001) in 6 patients, subsequently termed "responders." Both responders and nonresponders were resistant to the natriuretic effect of ANP infused alone, and mannitol alone did not produce an increase in urinary sodium excretion. However, in responders, the mannitol-induced increase in distal tubular sodium delivery resulted in a fivefold increase in urinary sodium excretion during ANP infusion (29 2 6 to 154 t 40 pmoVmin, P < .01). Urinary cyclic guanosine monophosphate (cGMP) excretion increased significantly and to a similar extent during ANP and ANP plus mannitol in all 12 patients, supporting the active biological responsiveness of renal ANP receptors. Unlike re-