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Cardiovascular Reflexes


The cardiovascular system is centrally regulated by automic reflexes. These work with local mechanisms to minimize fluctuations in the mean arterial blood pressure (MABP) and to maintain adequate perfusion of each organ. Intrinsic reflexes respond to stimuli originating from within the cardiovascular system. These include the baroreceptor, cardiopulmonary and chemoreceptor reflexes, and their properties are summarized below in Table 1. The extrinsic reflexes mediate the cardiovascular response to stimuli originating from for example pain and temperature changes.

Reflexes involve three components:

  1. afferent nerves sense a change in the state of the system, and communicate this to the brain
  2. the brain process this information and implements an appropiate response
  3. which results in altering the activity of efferent nerves controlling cardiac and pulmonary function, thereby causing homeostatic response that reverse the change in state

Table 1. Intrinsic Cardiovascular Reflexes

Receptors Reflex Location

Stimulated By

Response Activated

Arterial baroreceptors; carotid sinus and aortic arch

Change in arterial blood pressure, affects degree of stretch of arterial wall

If pressure decreases: vagal and sympathetic tachycardia; sympathetic vasoconstriction; renin release. If pressure increases opposite effects.

Cardiopulmonary receptors:

  • atrial mechanoreceptors / Bainbridge reflex
  • atrial nonmyelinated vagal efferents
  • ventricular and coronary nonmyelinated vagal efferents

Change in blood volume and pressure in central thoracic compartment; affects degree of stretch of atria, ventricles, coronary arteries

Net effect:

Decrease in pressure and volume:

Sympathetic and/or vagal tachycardia; vasoconstriction; venoconstriction; reduced production of urine

Opposite with volume and pressure increase

  • venticular chemoreceptors / Bezold-Jarisch effect

Cardiac ischeamia, drugs

Bradycardia; vasodilation

  • J-receptors / Lung

Marked lung inflation, pulmonary congestion

Tachycardia; vasodilation

Arterial chemoreceptors: carotid sinus and aortic arch

Severe hypotension, hypoxia, asphyxia causing decreased pO2, increased pCO2 and H+ in blood

Sympathetic vasoconstriction; indirect tachycardia; stimulation of respiration

CNS ischeamic response / Cushing reflex

Brainstem ischeamia

Sympathetic peripheral vasoconstriction

Intrinsic Cardiovascular Reflexes

The Baroreceptor Reflex

It shows rapid action to minimize momental fluctuations in the MABP. They are afferent (sensory) nerve endings in the walls of the carotid sinuses (thin walled dilatations at the origins of the internal carotid arteries) and the aortic arch. a_Atrial_Barorecept_ECC These mechanoreceptors sense alterations in wall stretch resulting from pressure changes, and repsond by modifying the frequency at which they fire action potentials. Pressure elevations increase impulse frequency; pressure decreases have the opposite effect.

When MABP decreases, the fall in baroreceptor impulse frequency causes the brain to reduce the firing of vagal efferents supplying the sinoatrial node, causing tachycardia. Simultaneously, the activity of the sympathetic nerves innervating most blood vessels is increased, leading to vasoconstriction. Stimulation of renal sympathetic nerves increases renin release, consequently angiotension II production and aldosterone secretion. The resulting tachycardia, vasoconstriction and fluid retention act together to raise MABP. Opposite effects occur when arterial blood pressure rises. The baroreceptors quickly show partial adaptation to new pressure levels. Therefore alterations in frequency are greatest while pressure is changing, and tend to moderate when a new steady-state pressure level is established. If unable to prevent MABP from changing to a new level, the reflex will within a several hours become reset to maintain pressure around this level.

There are two types of baroreceptors. A fibres have a large, myelinated axons, and are activated over lower levels of pressure. C fibres have small, unmyelinated axons and respond over higher levels of pressure. Together, these provide an input to the brain, that is most sensitive to pressure changes between 80 - 150 mmHg. Increases in pulse pressure render the baroreceptors more sensitive to changes in MABP.

The brain is able to reset the baroreflex to alow increases in mABP to occur. Ageing, hypertension and athersclerosis decrease arterial wall compliance and thus baroreceptor reflex sensitivity.

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Cardiopulmonary Reflexes

Diverse intrinsic cardiovascular reflexes originate in the heart and lungs. Cutting vagal afferent fibres that mediate these cardiopulmonary reflexes causes an increased heart rate and vasoconstriction, especially in skeletal muscle, renal and mesenteric vascular beds. The net effect of cardiopulmonary reflexes is therfore thought to be a tonic depression of heart rate and vascular tone. The receptors for these reflexes are located mainly in low pressure regions of the cardiovascular system, and are well placed to sense the blood volume in the central thoracic compartment. These rflexes are thought to be particularly important in controlling blood volume and vascular tone, and act together with baroreceptors to stabalize blood pressure. The best defined cardiopulmonary reflex is initiated by mechanoreceptors with myelinated vagal afferents, that are located mainly at the juncture of the atria and great veins. These respond to increased atrial volume and pressure by causing a sympathetically mediated tachycardia (the Brainbridge reflex). This reflex also helps to control blood volume; its activation decreases the secretion of antidiuretic hormone (vasopressin), cortisol and renin, causing diuresis.

Other Cardiopulmonary Reflexes is:

  1. Atrial mechanoreceptors with nonmyelinated vagal afferents respond to increased atrial volume and pressure by causing bradycardia and vasodilation.
  2. Mechanoreceptors in the left ventricle and coronary arteries mainly nonmyelinated vagal afferents respond to increased ventricular diastolic pressure and afterload by causing vasodilation.
  3. Ventricular chemoreceptors are stimulated by substances such as bradykinin and prostaglandins released during cardiac ischeamia. These recepptors activate the coronary chemoreflx. This response is called the Bezold-Jarisch effect, occurs after the IV injection of several types of drugs, and involve marked bradycardia and widespread vasodilation.
  4. Marked lung inflation, especially if oedema is present, activates juxtapulmonary receptors (J receptors), causing tachycardia and vasodilation.

Chemoreceptors Reflexes

Chemoreceptors activated by hypoxia, hypocapnia and acidosis are located in the aortic arch and carotid sinusis. These receptors are stimulated suring asphyxia and severe hypotension. The resulting chemoreceptor reflex is mainly involved in stimulating breathing, but also has cardiovascular affects. These include sympathetic constriction of (mainly skeletal muscle) arterioles, splanchnic venoconstriction, and tachycardia resulting indirectly from the increased lung inflation. This reflex is important because its effects help maintain the bloodflow to the brain at arterial pressure too low to activate the baroreceptors.

The CNS Ischeamic Response

A powerful generalized peripheral vasoconstriction is stimulated by brainstem hypoxia. This response develops during severe hypotension, helping to maintain the flow of blood to the brain during shock. It also causes the Cushing reflex, in which vasoconstriction and hypertension develop when increased cerebrospinal fluid pressure, e.g. due to brain tumour, produces brainstem hypoxia.

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Extrinsic Reflexes

Stimuli that are external to the cardiovascular system also exert effects on the heart and vasculature via extrinsic reflexes. Moderate pain causes tachycardia and increases in MABP. Severe pain has the opposite effect. Cold causes cutaneous and coronary vasoconstriction, possibly precipitating angina in susceptible indicviduals.

Central Regulation of Cardiovascular Reflexes

The view that the brainstem contains a specific vasomotor centre responsible for controlling cardiovascular aspects of autonomic control arises as a result of interaction between areas of the brainstem, the hypothalamus, the cerebral cortex, and the cerrebellum.

The afferent nerves carrying impulses from cardiovascular receptors terminate in the nucleus tractus solitarius (NTS) of the medulla. Neurons from the nTS project to areas of the brainstem which control both parasympathetic and sympathetic outflow, influencing theoir level of activation. The nucleus ambiguus and dorsal motor nucleus contain the cell bodies of the preganglionic vagal parasympathetic neurons, which slow the heart when the cardiovascular receptors report an increased blood pressure to the NTS columns of the spinal cord. These neral circuits are capable of mediating the basi cardiovascular reflexes. The NTS, the other brainstem centres and the IML neurons receive descending inputs from the hypothalamus, whihc in turn is influenced by impulses from the limbic system of the cerebral cortex. Input from these higher centres, allowing the generation of integrated responses in which the functions of the cardiovascular system and other organs are coordinated in such a way that the appropiate respnses to changing conditions can be orchestrated.

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