The eyes are innervated by both the SNS and PSNS, which yield opposing functional results. The systems control two functions related to the eye and sight. First, the pupillary constriction and dilation, which alters the gathering of light. Second, altering the shape of the lens allowing for focal plane adjustments. The pupillary opening is controlled by both the PSNS and SNS in different ways. The PSNS is responsible for putting into effect the constriction of the pupil in response to light hitting the retina. The SNS causes dilation of the pupil to let more light in during times of increased stimulation. Lens shape and focusing is almost exclusively a PSNS function. Stimulation of the PSNS causes excitation and constriction of the ciliary muscle, making the lens convex and suitable for near field vision. SNS stimulation, on the other hand, relaxes the ciliary muscle thinking the lens for distance vision. The aforementioned facts that both SNS and PSNS demonstrate both an excitation and relaxation effect in different areas proves that no generalized statement can be made regarding the final effects of either subsystem of the ANS.

The heart is innervated by both the SNS and PSNS, each acting in opposition to modulate function in three ways. The SNS and PSNS affect cardiac pump function in three ways. First, by changing the rate (chronotropism); SNS increasing the rate and PSNS decreasing it. Second, by changing the strength of contraction (inotropism); SNS increasing the strength and PSNS decreasing it. Finally, both systems modulate coronary blood flow. The PSNS, via the vagus nerve, predominantly innervates the sinoatrial and atrioventricular nodes, affecting choronotropy more than inotropy. Overall the role of PSNS in cardiac contractility is poorly understood. Sympathetic stimulation increases overall activity of the heart, increasing rate and contractility. While the effects of the ANS on coronary artery blood flow are not well understood, it is known that the SNS, via α(alpha) receptors, can cause constriction of the large coronary vessels, which normally have no role in the coronary resistance. The SNS can also cause dilation via β(beta)2 receptor stimulation, providing balance to the effects of SNS stimulation.

The lungs receive innervation from both the PSNS and SNS. The effect of SNS stimulation leads to bronchial dilation and pulmonary vasoconstriction. The increased pulmonary vascular resistance may be important in maintaining the balance between right and left ventricular output during stress and exercise. PSNS stimulation leads to bronchial constriction with little to no vascular dilation.

SNS nerves are the most important regulators of the peripheral circulation and overall systemic vascular tone. Stimulation by the SNS generally causes vasoconstriction in all organs except the heart, brain, and muscle where there are less SNS fibers. PSNS has almost no effects on the blood vessels as far as direct stimulation of relaxation. SNS stimulation results in increased blood pressure via increased cardiac activity and increased flow resistance in the circulation. As stated before, the PSNS has little effect on the overall systemic resistance, but can render a rapid decrease in blood pressure via vagal stimulation of the nodal cardiac conduction for a brief period of time.