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Am J Physiol Heart Circ Physiol 275: H1411-H1418, 1998;
0363-6135/98 $5.00
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Vol. 275, Issue 4, H1411-H1418, October 1998

Effects of coronary artery disease on expression and microvascular response to VEGF

Caroline Métais1, Jianyi Li1, Jian Li2, Michael Simons2, and Frank W. Sellke1

1 Division of Cardiothoracic Surgery, Department of Surgery, and 2 Cardiovascular Division, Department of Medicine of Beth Israel-Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215

The effects of coronary artery disease (CAD) on human coronary microvascular responses to vascular endothelial growth factor (VEGF) and the alterations of the myocardial expressions of VEGF and its flk-1 and flt-1 receptors were examined in 48 patients. Microvascular studies were performed in vitro with video microscopy. The expressions of VEGF and its receptors were examined using Northern analysis of total mRNA, and the expressions of constitutive nitric oxide synthase (cNOS) and inducible nitric oxide synthase (iNOS) were examined by RT-PCR. VEGF and hepatocyte growth factor (HGF) caused potent relaxations of microvessels. These responses were reduced in the presence of NG-nitro-L-arginine and the tyrosine kinase inhibitor genistein or in microvessels from patients with CAD. Relaxations to substance P and sodium nitroprusside were similar in both groups. The substance P response was abolished in the presence of NG-nitro-L-arginine. The expression of VEGF and its receptors and the expression of cNOS and iNOS were not altered in patients with CAD. In conclusion, VEGF and HGF elicit the release of nitric oxide through activation of tyrosine kinase receptors. CAD is associated with reduced vascular responses to both VEGF and HGF; this is not likely due to a reduced expression of VEGF or flt-1 or flk-1 receptors and not due to a generalized endothelium dysfunction despite the presence of mild hypercholesterolemia in these patients with CAD. These findings may have important implications regarding the efficacy of endogenous and exogenous VEGF in patients with risk factor for CAD.

growth factor; coronary microcirculation; human heart; endothelium; inducible nitric oxide synthase; vascular endothelial growth factor


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