The pathophysiology of hyperuricemia in essential hypertension: a pilot study.
We have examined whether hyperuricemia in essential hypertension may be related to an increased insulin secretion thereby enhancing the tubular reabsorption of sodium and thus uric acid. Insulin hypersecretion, as elicited by the oral glucose tolerance test (OGTT), increased a mean of 5-fold in 12 essential hypertensive patients. Urinary uric acid to creatinine ratio significantly diminished by a mean of 62% after the OGTT. Simultaneously, urinary sodium to creatinine ratio decreased by a mean of 54%. These results suggest that insulin may mediate uric acid underexcretion due to its tubular sodium retaining effect in essential hypertensive patients.
Puig
Juan G
JG
Division of Internal Medicine, Hospital La Paz, Madrid, Spain.
Torres
Rosa J
RJ
Ruilope
Luis M
LM
Campo
C
C
Grande
Cristina
C
Sancho
Teresa
T
Bernardino
José I
JI
D000328:Adult; D000368:Aged; D003404:Creatinine / Q000652:urine; D005951:Glucose Tolerance Test; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000503:physiopathology*; D033461:Hyperuricemia / Q000150:complications / Q000503:physiopathology*; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D008875:Middle Aged; D010865:Pilot Projects; D012964:Sodium / Q000378:metabolism; D014527:Uric Acid / Q000378:metabolism / Q000652:urine
D007328:Insulin; D014527:Uric Acid; D012964:Sodium; D003404:Creatinine