Effect of vitamin A deficiency on cardiovascular function in the rat

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.

Moderate maternal vitamin A deficiency alters myogenic regulatory protein expression and perinatal organ growth in the rat

“…This is the first study to show an increase in relative heart weight in the offspring at birth from mothers with moderate vitamin A deficiency. This result would agree with the finding of increased relative heart weight with marginal vitamin A deficiency in rats at day 18 of life by Wright et al (34). However, a previous moderate vitamin A deficiency study (3) did not detect this increase; however, this latter study measured relative organ weights at 20 days gestation and not at birth.…”

The Membrane Receptor for Plasma Retinol-Binding Protein, A New Type of Cell-Surface Receptor

“…Retinoids may be useful in the management of hypertrophic/hyperproliferative disorders of the heart and vascular wall (Gardner, D. G., and Chen, S., 1999). In addition, vitamin A deficiency causes a significant decrease in contractile responsiveness of aortic smooth muscle as a result of a down-regulation in the expression of contractile-related proteins (Wright, G. L. et al ., 2002). Retinoids have also been shown to regulate cardiac mitochondrial membrane potential (Korichneva, I. et al ., 2003).…”

Vitamin A: a drug for prevention of restenosis/reocclusion after percutaneous coronary intervention?

“…Wright and co-workers [68] showed that the contractility of aortic SMCs could be restored in aortic rings when incubated with atRA [68]. A more recent report from the same group [67] showed a reduced contraction of aortic rings from vitamin-A-deficient rats. A study [69] from the group that identified KLF5 as a potential target for retinoid-induced inhibition of SMC proliferation showed that Am80, a synthetic RARα agonist, inhibits serum-induced down-regulation of smooth muscle α-actin and MHC both in vitro as well as in vivo.…”

“…Endogenous RA signalling has been shown to co-localize with the expression of the adult smooth muscle MHC during development of the ductus arteriosus [66]. Furthermore, the level of α-actin has been shown to be reduced in SMCs from vitamin-A-deficient rats compared with controls [67]. One definition of fully differentiated SMCs is the ability of these cells to respond to contractile agonists.…”