The sympathetic presynaptic fibers that supply the heart originate in the lateral horns at the level of the T1 to T6 segments of the spinal cord. They conduct electrical signals to the cell bodies of postsynaptic neurons located in the cervical and thoracic paravertebral ganglia of sympathetic trunks (see Fig. 12.25, page 380). The postsynaptic fibers terminate at the SA and AV nodes, extend into the myocardium, and also pass through the epicardium to reach the coronary arteries. The autonomic fibers secrete norepinephrine that regulates the rate of impulses emanating from the SA node. The sympathetic component causes the rate of contraction to increase (an effect known as tachycardia) and increases the force of muscle contraction. Sympathetic stimulation produces dilation of the coronary arteries by inhibiting their constriction.
The heart rate and the force of contraction can be regulated by circulating hormones and other substances.
Changes in the force and rate of cardiac muscle contractions are regulated by hormones secreted from the adrenal medulla. These hormones include epinephrine and norepinephrine that reach the heart muscle cells via the coronary circulation.
Activation of adrenergic receptors (mainly 1 type) by epinephrine and less efficiently by norepinephrine increases the force of contraction (a positive inotropic effect) and the heart rate (a positive chronotropic effect). Other substances that have positive inotropic and chronotropic effects on the heart include Ca2, thyroid hormones, caffeine, theophylline, and the cardiac glycoside digoxin. These substances all increase intracellular Ca2 levels in cardiac myocytes. Substances that have negative inotropic and chronotropic actions on the heart muscle include adrenergic-receptor antagonists such as propranolol or Ca2 channel blockers. These substances decrease the heart rate and the force of cardiac muscle contraction.
The central nervous system monitors arterial pressure and heart function through specialized receptors located within the cardiovascular system.
The activity of the cardiovascular system is monitored by specialized centers in the central nervous system (CNS). Specialized sensory nerve receptors that supply afferent information about blood pressure are located in the walls of large blood vessels near the heart and within the heart itself. The information received from all types of cardiovascular receptors initiates the appropriate physiologic reflexes. The receptors function as follow.
blood pressure. These receptors are located in the carotid sinus and aortic arch.  Volume receptors (low-pressure receptors) located within the walls of the atria and ventricles sense central ve nous pressure and provide the CNS with information about cardiac distention.  Chemoreceptors detect alterations in oxygen, carbon dioxide tension, and pH. These receptors are the carotid and aortic bodies located at the bifurcation of the com mon carotid arteries and in the aortic arch, respectively.
The carotid bodies consist of cords and irregular groups of epithelioid cells. A rich supply of nerve fibers is associated with these cells. The neural elements are both afferent and efferent. The structure of the aortic bodies is essentially similar to that of the carotid bodies. Both receptors function in neural reflexes that adjust cardiac output and respiratory rate.
Layers of Vascular Wall
The walls of arteries and veins are composed of three layers called tunics.
The three layers of the vascular wall, from the lumen outward (Fig. 13.11 and Plate 33, page 434), are the following.