Reflex control of the circulation (Physiology)

Arterial baroreceptors are blood pressure sensors located in the walls of the carotid arteries and aorta.

They inform the brain of pressure changes in these key feeder vessels by detecting arterial wall stretch

Arterial baroreceptors are vital for maintaining blood flow to the brain and myocardium.

They play a crucial role in regulating blood pressure by detecting changes in arterial pressure and signaling the brain to make necessary adjustments

Arterial baroreceptors monitor blood pressure changes, reflecting alterations in either cardiac output (CO) or total peripheral resistance (TPR).

A decrease in arterial pressure (Pa) indicates a decrease in either cardiac output or total peripheral resistance, compromising blood flow to the brain and heart.

Blood flow (CO) is determined by dividing arterial pressure (Pa) by total peripheral resistance (TPR).

The formula for blood flow is CO = Pa / TPR, where CO represents cardiac output.

Baroreceptors respond to changes in pressure by adjusting their firing rate.

An increase in pressure initially results in minimal firing at rest, followed by fast firing which eventually slows down and becomes constant, albeit at a higher level than before, reflecting adaptation to a new normal.

A decrease in pressure leads to a proportionate slowing down of firing in baroreceptors

In the face of continued high or low pressure, the threshold for baroreceptor activation can change.

For example, in long-term hypertension, baroreceptors may become normalized to the new pressure level and consequently less activated

An increase in BP, termed loading (e.g., due to stress or exercise), leads to several responses:

-Pulse pressure (compliance) falls due to decreased stroke volume

-Vasodilation decreases total peripheral resistance (TPR) and BP

-There is a decrease in sympathetic nerve activity.

-Vagus nerve activity increases (parasympathetic activity)

A decrease in BP, termed unloading (e.g., due to hemorrhage), results in the following responses:

-Increased sympathetic activity and decreased vagus nerve activity.

-Increased heart rate (HR) and force of contraction, leading to increased cardiac output.

-Arteriolar constriction increases total peripheral resistance (TPR).

-Venous constriction increases central venous pressure, leading to increased stroke volume and cardiac output by Starling's law.

These responses collectively maintain blood pressure and blood flow to vital organs

In response to decreased BP, adrenaline secretion, vasopressin (ADH) secretion, and stimulation of the renin-angiotensin-aldosterone system (RAAS) occur.

Angiotensin II increases Na+/H2O absorption in the kidneys, raising blood volume

Arterial Vasoconstriction decreases capillary pressure, which increases absorption of interstitial fluid, thereby increasing blood volume

-Veno-atrial mechanoreceptors

-Ventricular mechanoreceptors

-Nociceptive sympathetic afferents

-Nucleus tractus solitarius (NTS)

-Stimulated by an increase in cardiac filling or central venous pressure (CVP)

-Reduces sympathetic activity to renal arteries, increasing glomerular filtration

-Secretes atrial natriuretic peptide, increasing sodium excretion, which lowers blood volume and reduces ADH (antidiuretic hormone) and RAAS (renin-angiotensin-aldosterone system) activity

-Stimulated by over-distension of ventricles, leading to the depressor response (A response to lower blood pressure)

-Results in mild vasodilatation, lower blood pressure, and preload reduction, serving as a protective mechanism

-Stimulated by substances such as potassium (K+), hydrogen ions (H+), lactate, and bradykinin during ischemia

-Converge onto the same neurons in the spinal cord as somatic afferents, leading to referred pain

-Mediate the pain of angina and myocardial infarction, and reflexively increase sympathetic activity, manifesting as symptoms like pallor, sweating, and tachycardia

An integrative centre in the brainstem involved in cardiovascular regulation, respiratory, gustatory (taste), and visceral sensations from various organs.

-It is stimulated by Baroreceptors, Chemoreceptors, Visceral sensations and Taste sensation

When afferent fibers from baroreceptors are removed:

-Arterial pressure varies enormously

-Means of regulation aren't significantly different

When afferent fibers from cardiac receptors are also removed:

-Arterial pressure still varies significantly

-The means of regulation become notably different

-Normally, arterial pressure remains relatively stable around 100 mmHg

-A decrease to 50 mmHg could cause insufficient perfusion to end organs

-An increase to 150 mmHg could potentially damage the cardiovascular system

-Located in carotid and aortic bodies

-Stimulated by low O2 (hypoxia), high CO2 (hypercapnia), H+, and K+

-Well supplied with blood flow around 20 ml/g/min

Regulate ventilation and drive cardiac reflexes during:

-Asphyxia (low O2/high CO2)

-Shock (systemic hypotension)

-Haemorrhage

Pressor Response (Raising Blood Pressure):

-They activate sympathetic activity, leading to increased heart rate (tachycardia) and selective constriction of arteries and veins.

-This response enhances cardiac output and blood pressure, particularly to maintain adequate blood flow to the brain.

-Even when blood pressure falls below the range of the baroreflex (the body's automatic blood pressure regulation system), chemoreceptors remain active and may compensate to stabilize blood pressure.

Sensory fibers in Group IV motor fibers located in skeletal muscle.

Activated via metabolites: K+, lactate, adenosine.

Increase sympathetic activity.

Tachycardia.

Increase arterial/venous constriction.

Increase cardiac output/blood pressure.

Important during isometric exercise.

Occurs when muscles are continually contracted without changes in joint angle or muscle length (e.g., weight lifting/handgrip).

Higher blood pressure drives blood into the contracted muscle to maintain perfusion.

These muscles undergo metabolic hyperaemia, allowing blood flow to the contracted tissue.

1. Signal from stretched baroreceptor sent via afferent fibres enter Nucleus Tractus Solitarius (NTS)

2. This then sends information out to the Caudal Ventrolateral Medulla (CVLM)

3. The CVLM sends information to the rostral ventrolateral medulla (RVLM)

4. This results in INHIBITION of sympathetic efferent nerves to heart and vessels

5. Less sympathetic efferent signals result in reduction in HR, less vasoconstriction, lower BP etc

-Loading of the baroreceptors (stretching or deformation due to changes in blood pressure) stimulates the vagus nerve, activating the Nucleus Tractus Solitarius (NTS)

-The signal from the NTS stimulates the nucleus ambiguous (vagal nuclei)

-Vagal parasympathetic impulses are sent to the heart, exerting a depressor effect (a sustained and long-lasting increase in blood pressure resulting from an increase in peripheral vascular resistance)

-Vagal parasympathetic outflow exerts inhibitory control over heart rate by releasing acetylcholine onto muscarinic receptors in the sinoatrial node.

-Decreased vagal tone or withdrawal of vagal input allows sympathetic influence to predominate, leading to an increase in heart rate.

-Sinus tachycardia often occurs in response to stress, exercise, or other factors that increase sympathetic activity or reduce parasympathetic tone.

-Respiratory sinus arrhythmia may modulate heart rate during the respiratory cycle, with slight increases in heart rate during inspiration due to reduced vagal activity.

The limbic system, known as the emotional center, stimulates the Nucleus Tractus Solitarius (NTS)

The NTS then activates the nucleus ambiguus, leading to increased activity of the vagal nerve

This results in a depressor effect on the atrioventricular (AV) and sinoatrial (SA) nodes

Activation of the limbic system can trigger a vasovagal attack

Syncope, or fainting, can occur due to a sudden drop in arterial cardiac output and blood pressure

This leads to decreased cerebral blood flow, resulting in syncope