The arterioles are the extension and terminal vessels of the arterial system. The major arteries possess larger quantities of smooth muscle and elastic components than the arterioles. The arterioles are composed mostly of smooth muscle and the contraction or relaxation of the smooth muscle in the arteriole walls controls the microvascular flow and its distribution. In fact, the state of contraction or relaxation of the smooth muscles in the arterial system are responsible for arterial compliance and the change in SBP and DBP.

Regulation of local blood flow

Resistance to blood flow by the arterioles is the greatest in the terminal arterioles; however, this resistance to flow is diminished as blood flow becomes laminar in nature due to the reduced diameter of the arteriole. The steepest drop in blood pressure occurs in the arterioles and the arterial pulse pressure is greatly reduced. Pulse pressure is completely damped out by the time it reaches the capillaries.

Autoregulation

Autoregulation is the intrinsic ability of an organ to maintain a constant blood flow to match the metabolic demands of the organ. Autoregulation is a function that maintains blood flow to an organ despite changes in pressure (perfusion pressure). Autoregulation is also a characteristic that is independent of extrinsic control. Autoregulation of blood flow is limited to arterial pressure ranges, beyond which flow changes with perfusion pressures.

• The autoregulatory response may be myogenic. If the smooth muscles of the arterioles are rapidly stretched due to a rapid increase in pressure then there could be a reflex response of the smooth muscles to contract, reduce vessel diameter, and thus reduce or "autoregulate" blood flow. The myogenic response theory is questionable because is it is pressure, not flow, that is the sensed regulatory mechanism and flow is the regulated mechanism. It would be a more sensitive mechanism if it was the flow that was sensed and then pressure was autoregulated to adjust for flow.
• The endothelium of the arterioles may also assist in autoregulation of blood flow. As the pressure increases in an arteriole (due to increased resistance) there is additional shear force exerted on the endothelium (see picture above). This shear force causes the release of nitric oxide (a.k.a. EDRF : endothelium-derived relaxing factor ) which, in turn, causes a relaxation of the arteriole smooth muscle (vasodilation).
• It is known that an increase in local metabolic agents will cause a reflex vasodilation of the arteriolar vessels. Thus, blood flow is linked to the tissue metabolism and metabolite production. Because an increase in oxygen supply is directly linked to blood flow, the metabolite concentration is a direct result of matching the blood supply with oxygen demand. If blood flow is mismatched with metabolism, there is an increase metabolite production and a mismatch of oxygen supply to metabolite production . If the two are mismatched, and supply does not meet the demand, then there is a buildup of metabolites. This buildup of metabolites will then cause a reflex vasodilation to adjust or "Autoregulation" blood flow. The increased metabolite production produces a functional hyperemia. The functional hyperemia is an increase in local flow that accompanies an increase in local metabolism. The arteriolar dilation from metabolites will also be propagated back up arterial vasculature and cause a vasodilation of the larger arterioles. This will result in an increased flow into the smaller arterioles. The increased flow into the smaller arterioles will also increase the shear stress of the endothelium of the smaller arterioles. This increased shear stress may, in turn, further increase blood flow.

  Extrinsic Control

Outflow or sympathetic stimulation of the arterial smooth muscle causes vasoconstriction. Thus arterial vasoconstriction is a result of increased sympathetic stimulation from the central nervous system. Inhibition of the sympathetic signal occurs in the brain and spinal cord. Thus, arterial dilation is a passive event when considering the extrinsic control of the central nervous system.

Sympathetic tone of the arterial system is increased with the activation of the sympathetic nervous system (Branch of the Autonomic Nervous System). Sympathetic nerve activation causes vasoconstriction in all vascular beds. Norepinephrine (NE) is released from the sympathetic nerve endings acting on the smooth muscle receptors in the arterial system (especially arterioles and the capacitance vessels). The release of NE also produces fluid shifts that occur in the capacitance vessels and resultant fluid shift of extracellular fluid into the capillary network that assist in increasing venous return.

Note that muscular movement causes an increase in sympathetic discharge from the CNS. This increase in sympathetic discharge will concurrently move the blood stored in the capacitance vessels towards the heart as venous return. The increase in venous return will enhance an increase in cardiac output by stretching the ventricular chambers. Heart rate will also increase as will contractility from the increase sympathetic activity of the CNS. Thus, there are many coordinated events that occur in different regions of the vasculature to promote an increase in blood flow / oxygen delivery once physical movement begins.

Baroreceptor Functions

Baroreceptors function to maintain arterial pressure. Shifts in arterial pressure may occur with postural changes and exercise. The baroreceptors are sensitive to the changes in arterial pressure due to changes in blood flow. Regulation of arterial pressure is accomplished through changes in cardiac output and arterial diameter changes (peripheral vascular resistance). Thus, the control and monitoring of blood pressure is a function the arterial baroreceptors. The arterial baroreceptors are integrated with the Autonomic Nervous System and stimuli sent from the baroreceptors will either increase sympathetic tone or diminish sympathetic tone of the arterial system.

The components of the baroreceptor reflex include the baroreceptors, both aortic and carotid bodies, sensory nerve fibers, cells in the central nervous system, efferent autonomic nerves and cardiac and smooth muscle acted upon by the ANS to alter cardiac contractility (change CO), and peripheral vascular resistance (change arterial resistance).

The carotid and aortic baroreceptors has afferent neural inputs to the central nervous system, specifically, the nucleus tractus solitarius (NTS) in the medulla oblongata. Impulses arriving here from the baroreceptors will alter the discharge in the efferent nerve fibers that travel to the SA node of the heart and to the ventricular myocardium. There will also be an efferent discharge to the arteriolar system. An increase in efferent discharge will increase the heart rate, contractility (subsequently CO), and increase PVR. A decrease in efferent discharge will produce the opposite response. An increase in baroreceptor stimulation of the NTS will decrease the efferent discharge (decrease sympathetic tone) and may enhance vagal stimulation of the heart. A decrease in baroreceptor stimulation produces the opposite response.

Discharge rates from the baroreceptors are dependent upon the changes in length (stretch) of the tissues in which they lie. When arterial pressure increases, there is an increased stretch in the tissue, and increased firing rate of the baroreceptors. If the pressure falls, the receptors decrease firing rate.

An increased efferent discharge of the sympathetic nervous system will cause an increase in NE release to increase heart rate and contractility while promoting vasoconstriction of the arterioles and of the conductance vessels. Increased sympathetic activity will also cause the release of Epinephrine from the adrenal gland which supports the same response of NE.

Summary of Reflexes

Changes in the arterial pressure effect the carotid and aortic baroreceptors. Impulses from the receptors are sent (afferent) to the medulla (specifically NTS), and the activity in the baroreceptors is roughly proportional to the arterial pressure. The output of the medulla is to the vagal and sympathetic efferent fibers. If baroreceptor activity increases, there is an increase in vagal activity and a decrease in efferent sympathetic discharge. Vagal activity effects heart rate, whereas sympathetic activity has important effects on heart rate, contractility (stroke volume), and consequently CO. Sympathetic activity also has a large effect on peripheral vascular resistance. The product of an increased CO and peripheral vascular resistance is an increase in arterial pressure.

 

 

Cardiopulmonary Receptors

The cardiopulmonary receptors are located in the walls of the atrial chambers and in the pulmonary artery and can alter peripheral vascular resistance with changes in intracardiac, venous, or pulmonary pressures. The response of the cardiopulmonary receptors has an effect on fluid balance and may have a delayed effect on blood pressure maintenance whereas the aortic and carotid receptors have a large influence on short term blood pressure maintenance. Increased intercardiac pressure will stimulate the cardiopulmonary receptors and inhibit vasoconstriction while increasing kidney filtration and renal blood flow which will regulate blood volume. Renal vasoconstriction occurs with a decreased firing rate from the cardiopulmonary receptors. The decreased renal blood flow volume causes the release of renin, that is converted to angiotensin I - II (vasoconstrictor) and aldosterone (ADH) to increase plasma (blood volume).

Hormonal regulation

The excretion of renin from the kidney is changed if arterial pressure changes. If there is an increase in renal sympathetic activity, renin is converted to angiotensin I in the plasma which is converted to angiotensin II at the lung. Angio tensin II has powerful effects on the secretion of aldosterone and is a vasoconstrictor.

 

 

 

 

Chemoreceptors

The chemoreceptors are located in the carotid and aortic sinus, and in the medullary region of the brain. These receptors are sensitive to the concentration of both carbon dioxide and oxygen in the bloodstream. The receptors of the carotid sinus and aortic sinus are most sensitive to changes in arterial oxygen concentration (PaO₂), whereas the receptors in the medulla are most sensitive to changes in carbon dioxide and hydrogen ion concentration. The regulation of cardiovascular functions are less pronounced than ventilatory functions when considering the efferent sympathetic drive prompted by the chemoreceptors. An decrease in PaO₂ will increase the afferent stimulus of the carotid and aortic chemoreceptors to the medullary (vasomotor) centers. This increase in afferent stimulus will cause an increase in sympathetic discharge from the vasomotor centers to the resistance and capacitance vessels resulting in vasoconstriction. Likewise, and increase in PaCO₂ will have the same effect. The culmination of both an increase in PaCO₂ and a decrease in PaO₂ will cause a greater sympathetic efferent discharge than with only one. An increase in one gas concentration is most likely reciprocated as a decrease in the other. Baroreceptor function will superimpose the function of the chemoreceptors if both are responding to local changes.

Other Central Control Mechanisms

Hypothalamus and Cerebrum

Increased neural activity in the hypothalamus will either stimulate or inhibit the vasomotor region of the medulla. Cerebral activity can also effect the activity of the vasomotor center. Thus, vascular resistance and blood pressure may be altered by neural input from the hypothalamus and cerebrum. Stimuli initiated from these regions are generated by the mental, emotional, and stimuli from the external environment (pain, cold, etc., ). Events that effect the function of the hypothalamus and cerebrum can, in turn, change blood pressure.

Integration of the system

Arterial pressure and resultant blood flow is a result of integration of the various control mechanisms. The organs the require a standard blood flow rate (autoregulated) are under secondary control by extrinsic control mechanisms. Other organs, such as skeletal muscle have variable control mechanisms. For example, skeletal muscle blood flow at rest is extrinsic control, but under exercise conditions, flow is regulated by local metabolites which override the global sympathetic discharge of the ANS.