Indomethacin blunts the orthostatic increase in plasma aldosterone in glomerulonephritis.
To determine factors mediating the aldosterone secretory response to orthostasis, we examined the effect of angiotensin-converting enzyme inhibition (CEI) on orthostasis in eight normal subjects and 10 normotensive patients with primary glomerulonephritis ingesting a normal sodium intake. On standing with CEI, the mean plasma aldosterone concentration (PAC) did not change [68.6 +/- 3.9 (+/- SE) and 63.4 +/- 6.9 pg/ml] in normal subjects, while PAC rose significantly from 72.3 +/- 7.5 to 129.5 +/- 13.2 pg/ml (P less than 0.001) in the glomerulonephritis patients without a concurrent rise in plasma angiotensin II, serum potassium, plasma ACTH, or mean blood pressure. There was a good correlation (r = -0.7064; P less than 0.03) between the changes in PAC and the changes in fractional sodium excretion in the patients. Pretreatment with indomethacin blunted the rise in PAC from 159.0 +/- 21.5 to 63.3 +/- 10.2 pg/ml upon standing with CEI, without a concurrent change in circulating 6-keto prostaglandin F1 alpha (from 57.7 +/- 9.5 to 56.0 +/- 11.1 pg/ml) in 4 patients. These results suggest that the aldosterone secretory response to orthostasis in patients with glomerulonephritis is dependent on factors blunted by pretreatment with indomethacin in addition to angiotensin II.
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D000450:Aldosterone / Q000097:blood*; D000804:Angiotensin II / Q000097:blood; D005921:Glomerulonephritis / Q000097:blood* / Q000503:physiopathology; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology*; D008297:Male; D011187:Posture; D011188:Potassium / Q000097:blood; D012083:Renin / Q000097:blood
D000804:Angiotensin II; D000450:Aldosterone; D015121:6-Ketoprostaglandin F1 alpha; D000324:Adrenocorticotropic Hormone; D012083:Renin; D011188:Potassium; D007213:Indomethacin