3 Homeostasis of the cardiovascular system

Regulation of the circulatory function ensures that sufficient blood is provided to all parts of the body, whether the individual is resting or working and whatever the ambient conditions.

It must:

Silbernagl & Despopoulos (1985) emphasize that maximal and simultaneous perfusion of all the organs would overtax the heart.

To maintain vital circulatory homeostasis for optimal organ function, the cardiovascular system must continually adapt itself to variations in hemodynamic parameters. These adjustments depend upon cardiac output and vascular resistance.

Changes in vascular diameter regulate perfusion to a particular body part or organ. The smooth muscle tone of the vessels depends on local factors, as well as neural and hormonal signals.

Circulatory function regulation includes three levels of control: local vascular control mechanisms, the autonomic nervous system, and the endocrine system.

Each system has a particular time limit and duration.

3.1 Cardiovascular adaptation factors

3.1.1 Local circulatory regulation

Within each tissue, vasomotion depends first of all on local activities, continuously adapting blood flow to tissue requirements, within the limits imposed by systemic neural and hormonal control. Arterioles are the main site of circulatory adjustment.

Arterioles respond to:

• metabolic changes

• local chemical messages

• temperature

• myogenic stretch.

Vascular self-regulation

If the vascular system were passive, there would be a linear relationship between debit and pressure: an increase in the pressure gradient would cause a proportional rise in blood flow through an organ.

In fact many organs, including the brain and the kidney, are equipped with vessels that respond to a rise in blood pressure through vasoconstriction. Such vasoconstriction opposes the increase in blood flow that would otherwise cause pressure to go up in a totally passive vascular system.

Thus, across a gamut of pressures, perfusion in such organs remains stable. Autoregulation is achieved mainly by the arterioles in their significant vasomotor capacity. Their action protects the capillary network from pressure variations that would otherwise be harmful to the equilibrium of its tiny exchange vessels.

Vascular self-regulation has two functions:

• One is to ensure constant blood flow to an organ in the face of changing arterial pressure. For example, in the kidneys, the arterial resistance of the nephrons adapts automatically to prevailing blood pressure. When systemic arterial pressure rises, renal vasoconstriction occurs in order to maintain constant renal blood flux.

• The other adjusts blood flow to the demand and need of organ activity. For example, in the case of cardiac or active skeletal muscles, the rate of perfusion can be several times greater than the value of resting blood flow.

Mechanisms of autoregulation

Myogenic effects

Myogenic stretch response means that, when a vascular smooth muscle is stretched, it contracts. If arterial pressure rises, the arteriole muscle responds with increased myogenic activity. This passive stretch depends upon the volume of blood reaching the arterioles. The lessening of the stretch prompts the reduction of myogenic tone.

Temperature

In most tissues, a rise in temperature causes vasoconstriction. This is because cutaneous circulation is rich in α₂ receptors, whose affinity for norepinephrine (noradrenaline) increases with a reduction in temperature. However, higher temperature at the skin produces vasorelaxation, via the central nervous system command and vascular characteristics.

Calories are conveyed towards the skin and evacuated to the external environment by the process of cutaneous vasodilation occurring when the individual must compensate for heat.

Conversely, cutaneous vasoconstriction occurs with exposure to cold, reducing thermal exchange with the environment and limiting caloric loss.

Oxygen deficiency

Generally, local hypoxia provokes vasodilation, which means that perfusion varies as a function of tissue oxygen consumption.

Metabolites

Most products of local tissue exchange, whose levels increase as a function of metabolism, have a vasorelaxing effect. In a general way, carbon dioxide (CO₂), nitrogen monoxide, acidic ions (H⁺), adenosine diphosphate (ADP), and adenosine monophosphate (AMP), as well as all the substances with an osmotic effect, such as potassium (K⁺), increase perfusion, in effect regulating the evacuation of these very products.

Autacoids

Autacoids are ‘local hormones’ in immediate proximity to their site of production. Numerous substances belong to this group. The main ones are:

• Histamine produces either vasoconstriction, with an accompanying increase in the permeability of the vascular wall, or vasodilation. In inflammatory processes, histamines produce arteriole vasorelaxation, venular vasoconstriction, and increased capillary permeability. Allergy symptoms such as hay fever illustrate the resulting effect.

• Bradykinin is produced by salivary glands and sweat glands.

• 5-Hydroxytryptophan (5-HTP) is produced by blood platelets, the central nervous system, and some cells of the digestive tube wall.

• Prostaglandins are made by macrophages, fibroblasts, leukocytes, and vascular endothelium. These compounds have an array of significant effects. Prostaglandin F (PGF) is a vasoconstrictors, whereas, for example, prostaglandin E (PGE) and prostacyclin are vasorelaxants, very much involved in inflammatory phenomena.

• Leukotrienes are released by leukocytes during the inflammatory response. They are vasoconstricting and also increase the permeability of the capillary wall.

• Platelet activating factor (PAF) is produced by macrophages as part of the inflammatory response. It causes vasodilation and increased capillary permeability.

Vascular endothelium

The endothelium lining the lumina of the vascular wall plays an important role in vasomotion.

• It constitutes a mechanical barrier, guaranteeing relative vessel water tightness and controlling permeability, especially at the capillary level.

• It is a true interface between the blood and the vascular wall, ensuring the transmission and translation of chemical messages.

• It is involved in variation of the vascular diameter.

• By way of its surface characteristics and secretions, it is able to limit platelet aggregation.

These various endothelial functions are carried out only when the structural integrity of the endothelium is protected. Consequently any factor altering endothelial cell morphology or physiology (e.g. nicotine, cholesterol, or mechanical overload accompanying arterial hypertension) changes the permeability of the endothelium, diminishing its antithrombogenic capacity as well as its secretion of vasorelaxing factors.

This is how endothelial changes are implicated in numerous pathological processes, and even lie at the heart of the physiology of atherothrombosis.

Results

• In functional or metabolic hyperemia, blood flow to an organ is proportional to its metabolic activity. Changes in arteriole diameter achieve this result. Every tissue adapts its blood flow to its own metabolic requirements.

• By the mechanism of flux-dependent vasodilation, involving nitrous oxide and prostaglandins, there is an adjustment in arterial diameter and in the distribution of the blood flow that they transport. Every vessel adapts its diameter to its flow.

Local factors are depicted in Table 3.1.

Table 3.1 Local factors

Local vasodilators	Local vasoconstrictors
Produced by blood-deficient tissues	Produced as a reaction to a rise in systemic arterial pressure
Vasodilation of smooth muscles of the pre-capillary sphincters	Vasoconstriction of pre-capillary sphincters. At high concentration, a narrowing of arterioles and reduced blood flow to the tissue
Hypoxia ↑ CO2 (carbon dioxide) ↑ K+ (potassium) ADP, AMP Histamine Acidity (lactic acid) Nitrous oxide (N2O) Warmth	Endothelin Prostaglandins Thromboxanes Leukotrienes

3.1.2 The nervous system

The autonomic nervous system regulates blood flow on the basis of interactions and reflexes coming from the receptors and passing to autonomic centers where it is integrated and acted upon.

The autonomic nervous system plays a role in the short-term control of systemic arterial pressure.

Receptors

Arterial pressure is under the constant surveillance of arterial baroreceptors. These receptors stimulate a short-term response in a matter of seconds.

Baroreceptors modify heart rate and total systemic resistance via autonomic nervous system activity at the heart and the smooth arteriole muscles.

Long-term adaptations are made by adjustments in blood volume, in response to thirst and urine volume.

Arterial receptors

Baroreceptors and chemoreceptors are essential to homeostasis.

Baroreceptors

Baroreceptors are pressure-sensitive free nerve endings found in the adventitia of the carotid sinus and the aortic arch.

Carotid baroreceptors are optimally located to monitor the pressure in arteries supplying the brain, whereas the aortic baroreceptors relay information about the major arteries that furnish the rest of the body.

Information from the carotid sinus baroreceptors is carried to the brainstem on the carotid sinus nerve, which joins the glossopharyngeal nerve.

Fibers issuing from the baroreceptors of the aortic arch form the aortic nerve, which merges with the vagus nerve. These two nerves ascend to the nucleus of the tractus solarius at the brainstem.

Baroreceptors are mechanoreceptors that are sensitive to pressure or stretch of the vascular wall. Thus, changes in arterial pressure cause more or less stretch on the baroreceptors. Some receptors respond to increased stretch whereas others are designed to detect decreased stretch.

Chemoreceptors

Chemoreceptors are sensitive to chemical changes and are located in the corpuscles of the carotid glomus and the aortic arch.

Fibers issuing from the carotid glomus travel the length of the IXth pair of cranial nerves. Fibers from the aortic corpuscle accompany the Xth cranial nerves along their pathway. They join together at the brainstem.

Chemoreceptors are sensitive to hypoxia and hypercapnic acidosis. In response to these stimuli, chemoreceptors signal an increase in sympathetic activity, resulting in peripheral arterial vasoconstriction and splanchnic venoconstriction. They signal an increase or decrease in respiration during extreme conditions such as asphyxia or severe hemorrhage.

Chemoreceptors help keep arterial pressure constant in cases of grave hypertension, when the limits of baroreceptor reflexes are overcome.

Other receptors

Beyond aortic and carotid receptors are receptors that contribute to cardiovascular regulation.

Venous baroreceptors situated in the wall of the right atrium detect variations in central venous pressure. In addition, stretch receptors are located in the pulmonary vessel walls.

These mechanisms relay information to the brainstem, signaling the autonomic nervous system to adapt to variations in intrathoracic venous pressure due to respiration.

Venoatrial receptors are involved in the hormonal response of atrial natriuretic peptide, which aids in regulating mean arterial pressure.

Striated skeletal muscles have muscular or ergo receptors, sensitive to metabolic perturbation and mechanical actions. They inform the central nervous system about muscle activity.

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