Abstract |
The renal kallikrein-kinin system is involved in the regulation of intrarenal blood flow and natriuresis. To study whether deranged sodium and water excretion in terminal cirrhosis is associated with an altered renal kallikrein-kinin system, urinary kallikrein excretion (UkalV) was measured. Low UkalV excretion was found in cirrhosis. In particular, nine cirrhotics with ascites showed a significantly lowered ratio of UkalV to urinary aldosterone excretion when compared with eight cirrhotics without ascites. Continuous infusion in cirrhosis and ascites of prostaglandin E1 (0.1 ng/kg/min) for 3 days resulted in marked increases in both daily urine volume and urinary sodium excretion; this was associated with a significant elevation of UkalV. These results suggest that in cirrhosis the impairment in renal sodium and water excretion may be attributed, at least in part, to deficient activation of the renal kallikrein-kinin system.
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Authors | K Hattori, Y Hasumura, J Takeuchi |
Journal | Scandinavian journal of gastroenterology
(Scand J Gastroenterol)
Vol. 19
Issue 6
Pg. 844-8
(Sep 1984)
ISSN: 0036-5521 [Print] England |
PMID | 6393317
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Kinins
- Prostaglandins E
- Angiotensin II
- Aldosterone
- Sodium
- Kallikreins
- Renin
- Alprostadil
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Topics |
- Adult
- Aged
- Aldosterone
(metabolism)
- Alprostadil
- Angiotensin II
(blood)
- Body Water
(metabolism)
- Female
- Humans
- Infusions, Parenteral
- Kallikreins
(metabolism)
- Kidney
(metabolism)
- Kidney Function Tests
- Kinins
(metabolism)
- Liver Cirrhosis
(metabolism)
- Male
- Middle Aged
- Prostaglandins E
(administration & dosage)
- Renin
(blood)
- Sodium
(metabolism)
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