Literature DB >> 9128206

Adrenocorticotropin-induced hypertension in rats: role of ouabain-like compound.

K Yamada1, A Goto, M Omata.   

Abstract

We examined the role of ouabain-like compound (OLC) in hypertension associated with corticotropin (ACTH) excess in rats. Physiological saline solution (1 mL/kg) or synthetic ACTH-Z (0.5 mg/kg) was injected intramuscularly for 15 days to 14 control and 13 male Wistar rats. Significant increases in blood pressure and plasma sodium/potassium ratio, and decreases in plasma potassium concentration and urinary sodium/potassium ratio were observed in ACTH-treated rats. The plasma OLC level was higher in ACTH-treated group (control; 76 +/- 13, ACTH; 202 +/- 48 pmol/L, P < .05). Plasma OLC level correlated with systolic blood pressure (SPB; r = 0.53, P < .01). Urinary OLC excretion was also higher in ACTH-treated group (control; 0.95 +/- 0.01, ACTH; 3.32 +/- 0.67 pmol/day, P < .01). A significant relation was also found between urinary OLC excretion and SBP (r = 0.66, P < .01). Plasma potassium concentration negatively correlated with SBP (r = -0.48, P < .01) and urinary sodium/potassium ratio also correlated inversely with urinary OLC excretion (r = -0.55, P < .01). Measurement of OLC levels after the fractionation of urine by reverse-phase high performance liquid chromatography showed that the major OLC peak in urine from both groups coincided with that of authentic ouabain. These results suggest the contribution of OLC to ACTH-induced hypertension in rats.

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Year:  1997        PMID: 9128206

Source DB:  PubMed          Journal:  Am J Hypertens        ISSN: 0895-7061            Impact factor:   2.689


  5 in total

1.  Renovascular hypertension using a modified two-kidney, one-clip approach in mice is not dependent on the α1 or α2 Na-K-ATPase ouabain-binding site.

Authors:  John N Lorenz; Valerie M Lasko; Michelle L Nieman; Thomas Damhoff; Vikram Prasad; William H Beierwaltes; Jerry B Lingrel
Journal:  Am J Physiol Renal Physiol       Date:  2011-06-01

2.  ACTH-induced hypertension is dependent on the ouabain-binding site of the alpha2-Na+-K+-ATPase subunit.

Authors:  John N Lorenz; Elizabeth L Loreaux; Iva Dostanic-Larson; Valerie Lasko; J Renee Schnetzer; Richard J Paul; Jerry B Lingrel
Journal:  Am J Physiol Heart Circ Physiol       Date:  2008-05-16       Impact factor: 4.733

Review 3.  Signaling mechanisms that link salt retention to hypertension: endogenous ouabain, the Na(+) pump, the Na(+)/Ca(2+) exchanger and TRPC proteins.

Authors:  Mordecai P Blaustein; John M Hamlyn
Journal:  Biochim Biophys Acta       Date:  2010-03-06

4.  The highly conserved cardiac glycoside binding site of Na,K-ATPase plays a role in blood pressure regulation.

Authors:  Iva Dostanic-Larson; James W Van Huysse; John N Lorenz; Jerry B Lingrel
Journal:  Proc Natl Acad Sci U S A       Date:  2005-10-21       Impact factor: 11.205

Review 5.  Natriuretic hormones in brain function.

Authors:  Anastasia Hodes; David Lichtstein
Journal:  Front Endocrinol (Lausanne)       Date:  2014-11-28       Impact factor: 5.555

  5 in total

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