Bartters Syndrome: Effect of Indomethacin on Prostaglandins, Urinary Kallikrein, Renin-Angiotensin-Aldosterone System, and the Response to Angiotensin II Antagonist

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• In two patients with Bartters syndrome, significant increases in serum immunoreactive prostaglandin E like-material (iPGE) and urinary kallikrein excretion were observed during the control period. Urinary PGE excretion was not always increased as serum iPGE. After an administration of indomethacin, an inhibitor of prostaglandins (PGs) synthetase, their clinical symptoms, hyperactivity of renin-angiotensinaldosterone (R-A-A) system and resistence to the pressor effects of angiotensin II and norepinephrine were apparently eliminated, but hypokalemia was not corrected completely. Indomethacin caused a remarkable decline in urinary kallikrein excretion and in serum and urinary PGs values. Spironolactone also produced a significant fall in urinary kallikrein excretion in spite of an extreme increase in the R-A-A system activity. However, spironolactone did not suppress the urinary PGE excretion. After an administration of aminoglutethimide, the urinary kallikrein excretion decreased gradually, followed by a decline in aldosterone production.Short-term administration of aspirin, ibuprofen, aminoglutethimide and dexamethasone did not improve hypokalemia despite the normalization of aldosterone production.<BR>An angiotensin II antagonist, [Sar<SUP>1</SUP>, Ile<SUP>8</SUP>] angiotensin II, lowered the blood pressure of hyperreninemic patients. After indomethacin, a significant improvement in blood pressure response to this antagonist was observed. These results indicate that angiotenin II receptors of arteriolar smooth muscle in patients with Bartters syndrome are still responsive to endogenous angiotensin II, andthat the R-A-A system plays a considerable role in the regulation of blood pressure. Moreover, our observations suggest that a more “proximal” cause of Bartters syndrome is renal potassium wasting i. e., hypokalemia which causes an inappropriate production of PGs in the kidney and vascular walls, resulting in vasocontrictor insensitivity and hyperactivity of the R-A-A system. Likewise, it appears that hyperactivity of the renal kallikrein-kinin system does not stimulate the production of PGs in this syndrome, but rather is secondary to increased PGs synthesis

• 社団法人 日本内分泌学会の論文

著者

• Sasaki Haruka

  Division Of Endocrine And Metabolic Medicine Chikushi Hospital Fukuoka University

• ABE KEISHI

  Department of Internal Medicine, Tohoku University School of Medicine

• Abe Keishi

  Department Of Internal Medicine Tohoku University School Of Medicine

• Sasaki Haruka

  Department Of Internal Medicine Chikushi Hospital Fukuoka University

• Asano Takashi

  Department Of Electronic Science And Engineering Kyoto University

• KAWASAKI TERUKAZU

  Department of Internal Medicine, Faculty of Medicine, Kyushu University

• OKUMURA MAKOTO

  Department of Internal Medicine, Fukuoka University School of Medicine

• ARAKAWA KIKUKO

  Department of Internal Medicine, Fukuoka University School of Medicine

• Abe Keishi

  Department Of Cardiovascular Medicine Graduate School Of Medical Sciences Kumamoto University

• Asano Takashi

  Department Of Child Neurology Okayama University Medical School

• SASAKI HARUKA

  Department of Internal Medicine, Fukuoka University School of Medicine

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