Calcium antagonists decrease calcium entry through L-type cellular calcium channels, acting on vascular smooth muscle, the heart and pancreas. They can cause coronary and peripheral vasodilation, reduced cardiac contractility, slowed atrioventricular nodal conduction, and depressed sinus node activity. Lowering of blood pressure through a fall in peripheral vascular resistance may be moderated by reflex tachycardia, although this reflex response is often blunted by depressant effects on AV and sinus node activity. In addition, these agents are metabolic poisons causing increased dependence of the heart on carbohydrate metabolism rather than the usual free fatty acids. This toxic effect is compounded by the inhibition of pancreatic insulin release, making it difficult for the heart to use carbohydrates during shock.