What is the role of vasomotor centre role in heart rate and bp

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The Vasomotor Centre (VMC): Role in Heart Rate and Blood Pressure

Location and Basic Anatomy

The vasomotor centre (VMC) is located bilaterally in the reticular substance of the medulla oblongata and the lower one-third of the pons. It is the primary cardiovascular control centre of the central nervous system and integrates signals from throughout the body to regulate both heart rate (HR) and blood pressure (BP).

Anatomy of sympathetic nervous control of the circulation, showing the vasomotor center, sympathetic chain, and vagus nerve pathways to blood vessels and heart

Guyton & Hall: Anatomy of sympathetic nervous control of the circulation. The dashed red line shows the vagus nerve carrying parasympathetic signals to the heart.

Three Functional Subdivisions

The VMC has three distinct functional areas:

Subdivision	Location	Action
Vasoconstrictor area (C1)	Upper medulla / lower pons (lateral)	Transmits sympathetic excitatory impulses - increases HR, contractility, and vascular tone
Vasodilator area	Lower medulla (lateral)	Inhibits the vasoconstrictor area, causing vasodilation
Sensory/integrating area	Medulla and lower pons	Receives input via CN IX & X; relays to vasoconstrictor and vasodilator areas

Guyton and Hall Textbook of Medical Physiology
Costanzo Physiology 7th Edition

Role in Heart Rate

The VMC controls heart rate through dual autonomic outflow:

1. Sympathetic (Accelerator) Pathway - Increases HR

The lateral portions of the VMC transmit excitatory impulses through sympathetic nerve fibers.
These fibers reach the SA node and increase its firing rate, thereby increasing heart rate.
They also increase AV node conduction velocity and myocardial contractility (positive chronotropic and inotropic effects).

2. Parasympathetic (Decelerator) Pathway - Decreases HR

The medial portion of the VMC sends signals to the dorsal motor nuclei of the vagus nerve (CN X).
These parasympathetic impulses travel to the SA node and decrease heart rate.

"The lateral portions of the vasomotor center transmit excitatory impulses through the sympathetic nerve fibers to increase heart rate and contractility. Conversely, the medial portion of the vasomotor center sends signals to the adjacent dorsal motor nuclei of the vagus nerves, which then transmit parasympathetic impulses through the vagus nerves to the heart to decrease heart rate and heart contractility."

Guyton and Hall Textbook of Medical Physiology

Key principle: Heart rate and strength of contractions ordinarily increase when vasoconstriction occurs and ordinarily decrease when vasoconstriction is inhibited, meaning the VMC coordinates both vascular and cardiac responses together.

Role in Blood Pressure

The VMC regulates BP through multiple mechanisms:

1. Vasomotor Tone (Basal Vascular Tone)

The vasoconstrictor area of the VMC continuously fires at 0.5-2 impulses/second through sympathetic vasoconstrictor fibers throughout the body. This constant low-level firing creates vasomotor tone - maintaining blood vessels in a state of partial constriction. This tone:

Sets resting BP (~100 mmHg mean arterial pressure)
Allows BP to be increased or decreased by modulating tone up or down
If suddenly abolished (e.g., total spinal anesthesia), BP can plummet from ~100 to ~50 mmHg

2. Control of Peripheral Vascular Resistance (TPR)

Sympathetic outflow from the vasoconstrictor area acts on arterioles to alter resistance. Arterioles in skin, kidneys, spleen, and mesentery have heavy sympathetic innervation. Constriction raises total peripheral resistance and therefore raises BP; dilation lowers it.

3. Venous Return and Preload

Sympathetic venoconstriction reduces venous capacitance, mobilizing the ~80% of total blood volume stored in veins. This increases venous return, raises cardiac preload, and increases cardiac output and BP via the Frank-Starling mechanism.

The Baroreceptor Reflex - The Main Feedback Loop

The VMC is the central processing hub of the baroreceptor reflex, the most important short-term BP regulatory system:

Baroreceptor reflex pathway showing nucleus tractus solitarius, cardiac decelerator/accelerator centers, vasoconstrictor center, and effects on heart and blood vessels

Costanzo Physiology: The baroreceptor reflex arc and its medullary cardiovascular centers.

When BP rises:

Baroreceptors in the carotid sinus (CN IX) and aortic arch (CN X) increase their firing rate
Afferent signals travel to the nucleus tractus solitarius (NTS) in the medulla
The NTS inhibits the vasoconstrictor/cardiac accelerator centers and activates the cardiac decelerator center
Result: decreased sympathetic outflow + increased vagal (parasympathetic) tone → HR decreases, contractility decreases, arterioles dilate → BP falls back to normal

When BP falls (e.g., hemorrhage):

Baroreceptors reduce firing
NTS reduces its inhibitory effect on the VMC
VMC becomes more active - increased sympathetic outflow
HR and contractility increase, arterioles constrict → BP is restored

Higher Centre Modulation

The VMC does not act in isolation. It receives modulatory inputs from:

Hypothalamus: Posterolateral areas cause excitation (raise BP/HR); anterior areas may inhibit
Cerebral cortex: Emotional states (fear, anger) raise BP via cortical-hypothalamic-VMC pathways
Reticular formation of pons and mesencephalon: Lateral/superior regions excite; medial/inferior regions inhibit
Chemoreceptors: Hypoxia activates the VMC, raising BP (Cushing reflex at extreme levels)

Summary Table

VMC Action	Mechanism	Net Effect
Lateral VMC activation	SNS → SA node, myocardium	HR increases, contractility increases
Medial VMC activation	PNS (vagus) → SA node	HR decreases
Vasoconstrictor area tone	SNS → arterioles, venules	TPR increases, BP rises
Vasodilator area activation	Inhibits vasoconstrictor area	TPR decreases, BP falls
Baroreceptor reflex (high BP)	NTS inhibits VMC	HR, contractility, TPR all decrease
Baroreceptor reflex (low BP)	NTS activates VMC	HR, contractility, TPR all increase

The VMC is thus the integrating hub that continuously balances sympathetic and parasympathetic outflow to keep BP and HR within normal limits, responding within seconds to any perturbation.

Guyton and Hall Textbook of Medical Physiology
Costanzo Physiology 7th Edition
Barash, Cullen & Stoelting's Clinical Anesthesia, 9e

What is RVLM and CVLM

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RVLM and CVLM: The Core of Medullary Cardiovascular Control

Overview

The vasomotor centre is not a single homogeneous area - it is organized into functionally distinct subregions. The two most important are:

Region	Full Name	Functional Role
RVLM	Rostral Ventrolateral Medulla	Pressor area - drives sympathetic outflow, raises BP and HR
CVLM	Caudal Ventrolateral Medulla	Depressor area - inhibits RVLM via GABA, lowers BP

RVLM - Rostral Ventrolateral Medulla

Location

Neurons are located near the pial surface of the medulla, in the rostral (upper) portion of the ventrolateral medulla.

What It Does

The RVLM is the primary tonic driver of sympathetic outflow to the cardiovascular system. Its neurons:

Send axons that course dorsally and medially, then descend in the lateral column of the spinal cord to the thoracolumbar intermediolateral cell column (IML)
Activate preganglionic sympathetic neurons in the IML using glutamate as their excitatory neurotransmitter
Contain the enzyme phenylethanolamine-N-methyltransferase (PNMT) (marker of adrenergic neurons)

Effects of RVLM Activation

Increased heart rate (via sympathetic fibers to SA node)
Increased myocardial contractility (positive inotropy)
Arteriolar vasoconstriction - raises total peripheral resistance (TPR)
Venoconstriction - increases venous return and preload
Net effect: raised blood pressure

"One of the major sources of excitatory input to sympathetic nerves controlling the vasculature is a group of neurons located near the pial surface of the medulla in the rostral ventrolateral medulla (RVLM). The axons of RVLM neurons course dorsally and medially and then descend in the lateral column of the spinal cord to the thoracolumbar intermediolateral cell column (IML)... glutamate is the excitatory transmitter they secrete to activate preganglionic sympathetic neurons."

Ganong's Review of Medical Physiology, 26th Edition

Inputs to RVLM

The RVLM receives signals from multiple sources:

Input Source	Effect on RVLM
Limbic cortex → Hypothalamus	Excitation (emotions: fear, anger, stress raise BP)
Baroreceptors (via CVLM/GABA)	Inhibition (high BP suppresses RVLM)
Carotid/aortic chemoreceptors	Excitation (hypoxia activates RVLM)
Pain afferents	Usually excitation (acute pain raises BP)
Lung inflation (vagal afferents)	Inhibition (causes vasodilation)
Exercise muscle afferents	Excitation (somatosympathetic reflex)

CVLM - Caudal Ventrolateral Medulla

Location

Located in the caudal (lower) portion of the ventrolateral medulla, below the RVLM.

What It Does

The CVLM is an inhibitory relay station interposed between the NTS and the RVLM. Its neurons:

Receive excitatory (glutamatergic) input from the nucleus tractus solitarius (NTS)
Release GABA (gamma-aminobutyric acid) onto RVLM neurons - inhibiting them
Act as the critical "off switch" for sympathetic drive

Effects of CVLM Activation

Inhibits RVLM → reduces sympathetic outflow
Decreases HR and contractility
Produces vasodilation and venodilation
Net effect: lowered blood pressure

"These NTS neurons then excite neurons in the caudal ventrolateral medulla (CVLM). These CVLM neurons release the inhibitory neurotransmitter γ-aminobutyric acid (GABA) into the RVLM to reduce the firing rate of these [RVLM neurons]."

Ganong's Review of Medical Physiology, 26th Edition

How They Work Together: The Full Baroreceptor Reflex Circuit

This is the complete neural pathway, with RVLM and CVLM at the core:

Neural pathways in blood pressure control showing NTS, CVLM, RVLM, IML (spinal cord), heart, and blood vessels - Comprehensive Clinical Nephrology

Ganong's: Detailed NTS-CVLM-RVLM-IML circuit with neurotransmitters (Glu, GABA, ACh, NE) at each synapse

When BP Rises (e.g., exercise, stress):

Baroreceptors ↑ firing
     ↓ (CN IX / X, Glutamate)
    NTS activated
     ↓ (Glutamate - excitatory)
    CVLM activated
     ↓ (GABA - inhibitory)
    RVLM inhibited
     ↓
  Sympathetic outflow ↓ + Vagal outflow ↑
     ↓
  HR ↓, Contractility ↓, TPR ↓
     ↓
  BP returns toward normal

When BP Falls (e.g., haemorrhage, standing up):

Baroreceptors ↓ firing
     ↓
    NTS less active
     ↓
    CVLM less active (less GABA onto RVLM)
     ↓
    RVLM disinhibited (becomes more active)
     ↓
  Sympathetic outflow ↑ + Vagal outflow ↓
     ↓
  HR ↑, Contractility ↑, TPR ↑
     ↓
  BP restored

"The activation of RVLM presympathetic neurons in response to hypotension is thus predominantly due to disinhibition."

Harrison's Principles of Internal Medicine, 22nd Edition

This is a key exam point: when BP drops, RVLM is not directly activated - it is disinhibited (the CVLM brake is released).

Summary Comparison

Feature	RVLM	CVLM
Location	Rostral (upper) VLM	Caudal (lower) VLM
Also known as	C1 area / Vasoconstrictor area (pressor area)	Depressor area
Neurotransmitter released	Glutamate (to IML)	GABA (to RVLM)
Effect on sympathetic outflow	Increases it	Decreases it (by inhibiting RVLM)
Effect on BP	Raises BP	Lowers BP
Receives input from	NTS, hypothalamus, cortex, chemoreceptors	NTS (glutamatergic)
Projects to	IML of thoracic spinal cord	RVLM
Tonic activity	Yes - maintains resting sympathetic tone	Yes - tonically inhibits RVLM
Clinical relevance	Overactive in neurogenic hypertension; target for renal denervation	Dysfunction may contribute to orthostatic hypotension

Ganong's Review of Medical Physiology, 26th Edition
Comprehensive Clinical Nephrology, 7th Edition
Harrison's Principles of Internal Medicine, 22nd Edition

So VMC present RVLM?

Yes, essentially. Here is the precise relationship:

VMC vs RVLM - Same Region, Different Level of Detail

The Vasomotor Centre (VMC) is the older, broader, classical term used in physiology textbooks (especially Guyton). It refers to the entire medullary cardiovascular control region.

The RVLM is the modern, more precise anatomical term that identifies the specific subregion within the VMC that generates sympathetic pressor drive.

How They Map to Each Other

Classical VMC Subdivision	Modern Anatomical Term	Function
Vasoconstrictor area (lateral VMC)	RVLM	Pressor - raises BP, increases HR
Vasodilator area (lower VMC)	CVLM	Depressor - inhibits RVLM, lowers BP
Sensory/integrating area	NTS (Nucleus Tractus Solitarius)	Receives baroreceptor input, relays to CVLM/RVLM

So when Guyton says:

"The lateral portions of the vasomotor center transmit excitatory impulses through sympathetic nerve fibers to increase heart rate and contractility"

...he is describing what Ganong calls the RVLM.

Think of It This Way

VMC (broad classical term)
 ├── Vasoconstrictor area  =  RVLM  (pressor, sympathetic driver)
 ├── Vasodilator area      =  CVLM  (depressor, GABAergic brake)
 └── Sensory area          =  NTS   (baroreceptor integrator)

Older textbooks (Guyton, Sembulingam) use VMC and its subdivisions
Newer/research-oriented texts (Ganong, Harrison's) use RVLM/CVLM as specific anatomical labels

Both are correct - the RVLM is the vasoconstrictor area of the VMC, described with greater anatomical precision.

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