Influence of nutritional factors on the renotrophic action of ACTH in the uninephrectomized rat.
In the rat, renal compensatory hypertrophy (RCH) was apparent 48 h after uninephrectomy; it was significantly enhanced by long-acting beta1-24-corticotrophin (ACTH) when the animals had free access to food and a NaCl solution (9 g/l). In rats starved after uninephrectomy but drinking the NaCl solution freely, RCH was suppressed: the weights of the body, heart, liver, and solitary kidney were reduced. In similarly starved rats treated with ACTH, the weights of the heart and the solitary kidney were normal. RCH was also impaired in rats fed only a glucose solution (30 g/dl) after uninephrectomy, but it is restored by ACTH, which significantly increases the weight of the remaining kidney. This renotrophic action of ACTH may be related to hyperglycemia and, perhaps, elevated urinary K excretion, which occur in hyper-adrenocorticism and increase the work load of the nephron.
D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000596:Amino Acids / Q000097:blood; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight / Q000187:drug effects; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D005947:Glucose / Q000494:pharmacology; D006984:Hypertrophy / Q000139:chemically induced; D007328:Insulin / Q000097:blood; D007668:Kidney / Q000187:drug effects* / Q000473:pathology; D009392:Nephrectomy; D009929:Organ Size / Q000187:drug effects; D011188:Potassium / Q000378:metabolism; D051381:Rats; D012964:Sodium / Q000378:metabolism; D012965:Sodium Chloride / Q000494:pharmacology; D013217:Starvation; D014508:Urea / Q000097:blood
D000596:Amino Acids; D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D012965:Sodium Chloride; D014508:Urea; D000324:Adrenocorticotropic Hormone; D012964:Sodium; D005947:Glucose; D011188:Potassium