Characterization of alterations of hemodynamics and neuroendocrine hormones in dexamethasone induced hypertension in dogs

Clin Exp Hypertens A. 1991;13(4):587-606. doi: 10.3109/10641969109045071.


The serial changes in systemic and renal hemodynamics, water and electrolyte balances and various vasoactive hormones were examined in 12 conscious dogs before, during (10 days) the administration of dexamethasone (DEX: 0.5 mg/kg/day) and after the cessation of DEX. In addition, during the administration of DEX, pressor responses to angiotensin II, norepinephrine, an angiotensin II analogue, saralasin, and an alpha-1-blocker, prazosin, were studied. Abrupt elevation of blood pressure to 106 +/- 5 mmHg on Day 1 (vs. 91 +/- 6 mmHg control: P less than 0.05) associated with marked increases in total peripheral resistance (P less than 0.01) was shown in DEX treated animals. Accompanied with these changes, renal blood flow increased to 146 +/- 12 ml/min (vs. 103 +/- 8 ml/min control: P less than 0.05) on Day 1 and maintained. In contrast, the results of serial alterations in hormones could not show any significant changes except significant elevations in atrial natriuretic peptide and reductions of cortisol and arginine vasopressin. Also, marked natriuresis and diuresis were observed in DEX administration dogs. Pressor response to norepinephrine was significantly increased and administration of either saralasin and prazosin significantly reduced the blood pressure of DEX treated animals. These results in DEX-treated conscious dogs confirmed our previous findings in human and rats. Glucocorticoid-induced hypertension mainly depends on the increases in total peripheral resistance but not volume factors.

MeSH terms

  • Animals
  • Blood Pressure / drug effects
  • Body Weight
  • Cardiac Output
  • Dexamethasone*
  • Dogs
  • Heart Rate
  • Hemodynamics*
  • Hormones / metabolism*
  • Hypertension / chemically induced
  • Hypertension / metabolism
  • Hypertension / physiopathology*
  • Male
  • Neurosecretory Systems / metabolism*
  • Norepinephrine / pharmacology
  • Prazosin / pharmacology
  • Renal Circulation
  • Saralasin / pharmacology
  • Vascular Resistance


  • Hormones
  • Dexamethasone
  • Saralasin
  • Norepinephrine
  • Prazosin