title: Adrenocorticotropic hormone, blood pressure, and serum erythropoietin concentrations in the rat.
abstract: BACKGROUND
  This study was designed to investigate the effects of adrenocorticotropic hormone (ACTH) on systolic blood pressure (BP) and serum erythropoietin (EPO) concentrations in two strains of rats. We hypothesized that ACTH-induced hypertension in the rat is characterized by increased EPO production.
  
  
  METHODS
  Male Sprague-Dawley (SD) and Wistar out-bred (Wistar) rats were treated with saline or ACTH (0.2 mg/kg/d). Systolic BP was measured using the tail-cuff method. Serum EPO concentrations were assayed using an ELISA kit for human EPO, which cross-reacts with but underestimates rat EPO. Thymus weight was used as a marker of glucocorticoid activity.
  
  
  RESULTS
  In SD rats, ACTH increased systolic BP (from 109 +/- 4 to 142 +/- 5 mm Hg, P <.0005), significantly greater than in saline-treated rats (P <.01). Systolic BP in ACTH-treated Wistar increased from 120 +/- 3 to 133 +/- 4 mm Hg (P <.05), but was not significantly different from saline-treated Wistar rats. The ACTH-induced increase in systolic BP was greater in SD than in Wistar rats (P <.05). Serum EPO levels were 5.6 +/- 0.4 in SD and 5.9 +/- 0.3 IU/L in Wistar rats, and decreased to undetectable levels with ACTH treatment in 10 of 10 SD and 7 of 10 Wistar rats. The ACTH treatment increased hemoglobin and hematocrit, and decreased thymus weight in both strains.
  
  
  CONCLUSIONS
  1) ACTH decreased serum EPO concentrations in both strains; 2) EPO is inversely related to ACTH-induced hypertension in the rat; and 3) Wistar rats are relatively resistant to the BP raising effects of ACTH treatment but not to the ACTH-induced decrease in thymus weight. These data suggest that EPO is not causal in ACTH-induced hypertension.
authors.affiliation: High Blood Pressure Research Unit, John Curtin School of Medical Research, Australian National University, GPO Box 334, Canberra, ACT 2601, Australia.
authors.forename: Yi
authors.initials: Y
authors.lastname: Zhang
authors.forename: Miles C
authors.initials: MC
authors.lastname: Andrews
authors.forename: Christopher G
authors.initials: CG
authors.lastname: Schyvens
authors.forename: Katja U S
authors.initials: KU
authors.lastname: McKenzie
authors.forename: Judith A
authors.initials: JA
authors.lastname: Whitworth
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000818:Animals; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects*; D001835:Body Weight / Q000187:drug effects; D004921:Erythropoietin / Q000097:blood*; D006400:Hematocrit; D006454:Hemoglobins / Q000187:drug effects / Q000378:metabolism; D007275:Injections, Intravenous; D008297:Male; D023421:Models, Animal; D008955:Models, Cardiovascular; D010919:Placebos / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017208:Rats, Wistar; D012965:Sodium Chloride / Q000494:pharmacology; D013599:Systole / Q000187:drug effects; D013950:Thymus Gland / Q000187:drug effects / Q000378:metabolism
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D006454:Hemoglobins; D010919:Placebos; D004921:Erythropoietin; D012965:Sodium Chloride; D000324:Adrenocorticotropic Hormone