The final common pathway of platelet aggregation is mediated through
Glycoprotein (GP) IIb/IIIa receptor. ADP, collagen, and thrombin bind independently, leading to platelet activation and, ultimately, to expression of the GP IIb/IIIa receptor. GP IIb/IIIa receptor expression leads to platelet clumping by binding to surrounding activated platelets. The αvβ3 receptor does not lead to platelet aggregation.
Inducers of smooth muscle cell proliferation include the following except:
Transforming growth factor-β (TGF-β). Platelet-derived growth factor-β, bFGF, and thrombin are all smooth muscle mitogens. Oxidized LDL causes smooth muscle cell proliferation through the autocrine release of bFGF. TGF-β alters the smooth muscle cell phenotype from a proliferative to a synthetic state and, thus, is antiproliferative.
Inhibitors of cardiac myocyte apoptosis include:
Insulin-like growth factor-1β. Insulin-like growth factor-1β overexpression has been shown to be cardioprotective because of decreased apoptosis in the setting of myocardial ischemia. Dobutamine has been shown to induce cardiomyocyte apoptosis. Caspase 3 and Bid cleavage are cytoplasmic markers of apoptosis, but do not directly influence apoptosis itself.
The following are endothelium-independent vasodilators except:
Acetylcholine (ACh). ACh, acting through muscarinic receptors, exerts its effect on the endothelium by promoting the conversion of L-arginine to NO. This in turn produces smooth muscle cell relaxation and consequent vasodilation. ACh is therefore an endothelium-dependent vasodilator. In patients with endothelial dysfunction, this effect is lost, and the direct action of ACh on smooth muscle cells producing vasoconstriction is more pronounced. The other agents listed are all endothelium-independent vasodilators.
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