Effect of vitamin A deficiency on cardiovascular function in the rat

Can J Physiol Pharmacol. 2002 Jan;80(1):1-7. doi: 10.1139/y01-093.

Abstract

Selected parameters of cardiovascular function were evaluated in vitamin A-deficient rats at 70 days of age. Resting heart rate was increased by an average of 100 bpm (21.4+/-2.7%), whereas resting systolic blood pressure was normal in vitamin A-deficient animals. The maximal contractile force developed per milligram weight of tissue by aortic rings excised from vitamin A-deficient animals was reduced in response to high potassium (-25.0+/-8.7%) and phorbol 12,13-dibutyrate (-36.8+/-8.4%) but was only slightly reduced in response to norepinephrine (-17.8+/-11.1%). Intimal rubbing to remove the endothelium had no effect on the loss in contractile responsiveness, and the relaxant response to acetylcholine was similar between control and vitamin A-deficient tissue groups. This suggests that the decrease in contractility of vascular smooth muscle from the vitamin A-deficient rats did not involve altered release of endothelium-derived vasoactive factors. Western blot analysis suggested a reduction in the protein levels of several differentiation markers including alpha-actin (-22%), calponin (-37%), desmin (-37%), and vinculin (-40%), whereas the level of PKCalpha was unchanged from control values. Our findings indicate a significant decrease in contractile responsiveness of aortic smooth muscle of the vitamin A-deficient rat that may be associated with a down regulation in the expression of contractile-related proteins.

MeSH terms

  • Animals
  • Aorta, Thoracic / drug effects
  • Blood Pressure / physiology
  • Blotting, Western
  • Body Weight / physiology
  • Female
  • Hemodynamics / physiology*
  • In Vitro Techniques
  • Muscle Contraction / drug effects
  • Muscle Contraction / physiology
  • Muscle Relaxation / drug effects
  • Muscle, Smooth, Vascular / drug effects
  • Organ Size / physiology
  • Proteins / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Vitamin A Deficiency / physiopathology*

Substances

  • Proteins