Systemic Arterial Pressure - Autonomic Control

Overview

Second-to-minute regulation of the systemic arterial pressure is ultimately modulated by the autonomic nervous system under the control of the vasomotor center. Thus, the autonomic nervous system forms the output arm of the feedback control circuit which is the primary controller of short-term systemic arterial pressure regulation. Both the sympathetic and parasympathetic components of the autonomic nervous system are involved in arterial pressure control although the Sympathetic is far more influential. We describe the cardiovascular effects of each arm separately and then describe how they are coordinated as a unit to modulate systemic arterial pressure.

Sympathetic Nervous System Regulation

The Sympathetic Nervous System (SNS) innervates the heart as well as the arterioles and veins of a wide variety of tissues. Activation of the SNS by the vasomotor center results in a nearly body-wide modulation of all three of these components, together serving to boost the systemic arterial pressure as described below. Importantly, it appears that base-line SNS tone is critical for maintenance of the resting systemic arterial pressure. Thus, merely inhibiting the SNS can result in a reduction in blood pressure whereas activation beyond the baseline tone can result in near doubling of the systemic arterial pressure.

SNS fibers release norepinephrine on the arteriolar vascular smooth muscle, resulting in arteriolar vasoconstriction. This reduces the arteriolar diameter and as a result increases the arteriolar resistance to blood flow
Because this is coordinated on a body-wide scale by the SNS, this results in increased systemic vascular resistance.

SNS fibers also release norepinephrine on the venous vascular smooth muscle, resulting in venoconstriction. Recall from venous physiology that the veins normally possess a large reservoir of the body's blood volume. Venoconstriction results in a reduction in the vascular compliance of the veins and thus reduces the volume of blood they can accommodate at low pressures. Consequently, SNS activity results in the veins pushing reservoir blood volume into the heart, increasing its preload and in consequence boosting the cardiac output courtesy of the Frank-Starling Relationship.

As described more fully in autonomic cardiac regulation SNS innervation to the heart serves to increase cardiac heart rate and contractility. These two effects together serve to increase cardiac output.

Parasympathetic Nervous System Regulation

In terms of cardiovascular impact, the parasympathetic nervous system appears to functionally innervate the heart with little control over the circulation. As described more fully in Autonomic Cardiac Regulation, parasympathetic fibers release acetylcholine on muscarinic receptors in the heart which serve to reduce the heart rate and slightly reduce contractility. Together, these effects reduce the cardiac output.

Coordination

The Vasomotor Center ultimately controls the above-mentioned effects of the SNS and PNS in a coordinated fashion to increase or decrease the systemic arterial pressure. Thus, decrements in PNS activity are matched with increments of SNS activity, and vice-versa, so that a unified, body-wide response is achieved. Again, it is important to point out that in a resting individual, there is a base-line SNS tone which is responsible for some of the resting systemic arterial pressure. Thus, reductions in systemic arterial pressure are first achieved by inhibition of the SNS and then further reduced by activation of the PNS. Increased arterial pressure above the resting pressure is achieved solely by enhancing SNS tone.

Effects on Systemic Arterial Pressure

The Systemic Arterial Pressure is ultimately dependent on the cardiac output and the systemic vascular resistance. Formally, Systemic Arterial Pressure = Cardiac Output x Systemic Vascular Resistance. This is merely the rearrangement of the more general equation described in hemodynamic integration applied on a body-wide scale. Here, the cardiac output is simply the total-body blood flow volume, the systemic vascular resistance is the total-body resistance, and the systemic arterial pressure is roughly equivalent to the total-body, systemic blood pressure gradient since venous pressure is very close to zero.

As described above, SNS tone boosts both the systemic vascular resistance and the cardiac output. In this way, SNS tone results in increased arterial pressure.

As describe above, PNS tone reduces cardiac output. In this way, PNS tone, together with reduced SNS tone, can potently reduce arterial pressure.

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