Casopis lekaru ceskych · 1994
[Renal resistance to atrial natriuretic factor as a cause of the escape failure phenomenon in patients with non-ascitic liver cirrhosis].
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Tesar V, Spicák J, Horký K, Zabka J, Widimský J, Jedlicka J, Marecek Z
Аннотация
BACKGROUND: Chronic administration of synthetic mineralocorticoids leads in healthy subjects only to temporary fluid retention with subsequent restoration of sodium balance, i.e. the so-called mineralocorticoid escape phenomenon. There is a failure of mineralocorticoid escape in patients with ascitic liver cirrhosis with progressive fluid retention. The aim of this study was to contribute to the elucidation of the mechanisms of the escape phenomenon in patients with preascitic liver cirrhosis.
METHODS AND RESULTS: Synthetic mineralocorticoid, fludrocortisone, was administered for 7 days to 8 patients with non-ascitic liver cirrhosis (LC) and 6 controls (CO) on a high sodium diet. CI seemed to have some central volume expansion before fludrocortisone administration, as assessed from a higher left atrial diameter and lower plasma aldosterone. Fludrocortisone administration in CI led to a comparable increase of ANF and suppression of plasma aldosterone as in CO with a higher diameter of the left atrium and lower PRA than in controls. Despite a comparable increase of ANF after fludrocortisone administration cGMP excretion was significantly higher in CO than in CI (434.5 + 247.1 vs. 824.6 + 317.3 pmol/min, p < 0.05). Natriuresis of CI seemed to depend on urinary cGMP excretion before fludrocortisone administration. The natriuretic response of these CI to a high sodium diet was exaggerated (290.0 + 53.9 vs. 160.0 + 18.3, p < 0.05), but they were unable to escape completely from the retaining effect of fludrocortisone.
CONCLUSIONS: Failure of mineralocorticoid escape in patients with preascitic liver cirrhosis may be due to the renal resistance to ANF with insufficient increase of urinary cGMP excretion.
METHODS AND RESULTS: Synthetic mineralocorticoid, fludrocortisone, was administered for 7 days to 8 patients with non-ascitic liver cirrhosis (LC) and 6 controls (CO) on a high sodium diet. CI seemed to have some central volume expansion before fludrocortisone administration, as assessed from a higher left atrial diameter and lower plasma aldosterone. Fludrocortisone administration in CI led to a comparable increase of ANF and suppression of plasma aldosterone as in CO with a higher diameter of the left atrium and lower PRA than in controls. Despite a comparable increase of ANF after fludrocortisone administration cGMP excretion was significantly higher in CO than in CI (434.5 + 247.1 vs. 824.6 + 317.3 pmol/min, p < 0.05). Natriuresis of CI seemed to depend on urinary cGMP excretion before fludrocortisone administration. The natriuretic response of these CI to a high sodium diet was exaggerated (290.0 + 53.9 vs. 160.0 + 18.3, p < 0.05), but they were unable to escape completely from the retaining effect of fludrocortisone.
CONCLUSIONS: Failure of mineralocorticoid escape in patients with preascitic liver cirrhosis may be due to the renal resistance to ANF with insufficient increase of urinary cGMP excretion.