Vasomotor center

Where is the vasomotor center located and how is it organized?

The localization of the center is the reticular formation of the medulla oblongata. Electrical stimulation of these reticular structures elicits vascular responses.

Functionally, the vasomotor center includes two interacting areas:

• Depressor zone (D) — inhibits the activity of the pressor zone.
• Pressor zone (P).

Blood pressure regulation under normal conditions

In a state of physiological rest, the vasomotor center maintains a normal level of blood pressure (about 120/80 mm Hg).

• Afferentation: Baroreceptors of vascular reflexogenic zones (aortic arch and carotid sinus) constantly generate impulses at a moderate frequency. This tonic activity continuously informs the CNS about the current pressure.
• Central processing: The vasomotor center maintains a balance between sympathetic and parasympathetic influence.
• Efferentation: Moderate tonic activity of the sympathetic nervous system is ensured. This maintains basal vascular tone and a normal heart rate (HR).

When exposed to emotional stimuli, moderate activation of the sympathoadrenal system occurs. However, homeostasis is preserved because baroreceptors generate depressor impulses that feed back into the vasomotor center and counterbalance the excitation.

Mechanism of the depressor (baroreceptor) reflex

This is a self-regulation mechanism aimed at lowering high blood pressure.

• Stimulus: Increase in blood pressure.
• Reception: Baroreceptors of the aortic arch and carotid sinus are stimulated, and the impulse frequency increases.
• Afferent pathway: Signals are transmitted via the depressor nerve (N. depressor, a branch of the vagus nerve) to the medulla oblongata.
• Central link: The depressor zone is activated in the vasomotor center, which inhibits the activity of the pressor zone.
• Efferent pathway: Activation of the vagus nerve nuclei (N. vagus, parasympathetic system) and inhibition of sympathetic centers occur.
• Effect: The rate and force of heart contractions decrease, the tone of vascular smooth muscle drops, and vasodilation occurs. The outcome is a systemic decrease in pressure.

Clinical significance and drug effects

• General anesthesia: Various CNS structures have different sensitivities to general anesthetics. Synaptic transmission in the cerebral cortex and reticular formation is depressed first, whereas the vasomotor and respiratory centers of the medulla oblongata are depressed last. This accounts for the distinct stages of anesthesia. Overdose of anesthetic agents, most commonly halothane, can lead to depression of the vasomotor center and the development of arterial hypotension.
• Infections (tetanus): The tetanospasmin exotoxin enters the CNS via retrograde vesicular axonal transport. Further progression to the reticular formation occurs through synapses. Blockade of reticular formation neurons can affect the vasomotor center and pose a risk of cardiac arrest.
• Radiation injuries: In the I and II periods of acute radiation sickness, analeptics stimulating the respiratory and vasomotor centers should be used with caution due to a narrowed therapeutic index. In the III period of acute radiation sickness, a paradoxical reaction to analeptics is possible; all medications except antibiotics are recommended to be used in reduced doses.
• N-cholinomimetics: Cytisine exerts a stronger stimulating effect on the respiratory center and causes only a pressor effect — a sustained increase in blood pressure without a depressor phase.

Class and exam questions

What else to study on this topic

• Respiratory center
• Baroreceptor (depressor) reflex
• Reticular formation
• Sympathetic and parasympathetic nervous system

Other topics in "Physiology concepts"

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