In humans and other mammals, multiple cardiovascular regulatory mechanisms have evolved. These mechanisms increase or decrease the blood supply to active tissues and increase or decrease heat loss from the body by redistributing the blood.
In the face of challenges such as hemorrhage, they maintain the blood flow to the heart and brain. When the challenge faced is severe, flow to these vital organs is maintained at the expense of the circulation to the rest of the body.
Generally, body redistributes the circulation through systemic and local mechanisms. With the sympathetic nerve system’s systemic effects via signals from CNS, the diameter of vascular system (arteriolar vasoconstriction) decreases and the stroke volume (SV) and heart rate (HR), which in together contribute a rise/maintain in blood pressure.
For vein system, venoconstriction and a decrease in the stores of blood in the venous reservoirs usually accompany increases in arteriolar constriction, although changes in the capacitance vessels do not always parallel changes in the resistance vessels.
The systemic regulation for vascular system (we doesn’t discuss the affects on heart in this thread) consists of the centre nerve system (1), the baroreceptors (2), cardiopulmonary receptors (3), carotid and aortic chemoreceptors (4), central chemoreceptors (5), the afferent nerve system (glossopharyngeal nerve, vagus nerve) (6), the autonomic nerve system (7), and the endocrine system (primary the adrenal medulla). The CNS play its role as the vascular control centre – the vasomotor. Information or “sense” perceived by baroreceptors, cardiopulmonary receptors, and chemoreceptors is transferred into vascular center via the afferent nerve system. Thereafter, vascular center analyses the inputs and form regulatory signals which then are transferred to the effector tissues or organs via the autonomic nerve system. However, several fibres from other parts of the nervous system can alter the activity of RVLM.
The baroreceptors are stretch receptors in the walls of the heart and blood vessels. However, in this thread the term “baroreceptor” is used to describe the baroreceptors in the arterial circulation, in order to distinguish them from cardiopulmonary receptors which are located in the low-pressure part of the circulation. The carotid sinus and aortic arch receptors monitor the arterial circulation, whereas cardiopulmonary receptors are located in the walls of the right and left atria at the entrance of the superior and inferior venue cave and the pulmonary veins, as well as in the pulmonary circulation. Inputs (intensity of stretch, more intensive, more frequent the rate of discharge of the receptors) are transferred through the afferent fibers to the CNS. These afferent fibers belong to glossopharyngeal nerve (carotid sinus nerve) and the vagus nerve (aortic depressor nerve).
The cardiopulmonary receptors are stretch receptors located in the walls of the right and left atria at the entrance of the superior and inferior venue cave and the pulmonary circulation, where the pressure of the circulation is low. Among cardiopulmonary receptors, the atria receptors are of two types, which also response to stretch: 1.those that discharge primarily during atrial systole (type A), and those that discharge primarily late in diastole, at the time of peak atrial filling (type B). The discharge of type B cardiopulmonary receptors is increased when venous return is increased and decreased by positive-pressure breathing, including that these receptors respond primarily to distention of the atrial walls.
The peripheral chemoreceptors locate in the carotid and aortic bodies where the rates of blood flow is very high. These receptors are activated by reduction of PaO2/pH and/or increase of PaCO2/[H+]. More accurately, the rates of discharge of peripheral chemoreceptors get more intensively with low PaO2/pH and/or high PaCO2/[H+], which then are transferred into the CNS and increase the excitement of vasomotor. Therefore the final result is vasoconstriction. Note that when blood flow is compromised due to settings such as hemorrhage etc., the PaO2/pH and PaCO2/[H+] in peripheral chemoreceptors is significant affected due to the lack of blood supply.
Chemoreceptor discharge may also contribute to the production of Mayer waves. These should not be confused with Traube-Hering waves, which are flections in blood pressure synchronised with respiration. The Mayer waves are slow, regular oscillations in arterial pressure that occur at the rate of about one per 20-40 second during hypotension. Under these conditions, hypoxia stimulates the chemoreceptors. The stimulation raises the blood pressure, which improves the blood flow in the receptor organs and eliminates the stimulus to the chemoreceptors, so that the pressure falls and a new cycle is initiated.
The central chemoreceptors. Central chemoreceptors locate on the ventrolateral surface of the medulla. These receptors are activated by reduction of PaO2/pH and/or increase of PaCO2/[H+]. In cases such as when intracranial pressure is increased, the blood supply to RVLM neurons is compromised, and the local hypoxia and hypercapnia increase their discharge. However, a change in plasma pH alone will not stimulate central chemoreceptors as H+ are not able to diffuse across the blood–brain barrier into the CSF. Only CO2 levels affect this as it can diffuse across, reacting with H2O to form carbonic acid and thus decrease pH. Central chemoreception remains, in this way, distinct from peripheral chemoreceptors.
Most of the vasculature is an example of an autonomic effector organ that receives innervation from the sympathetic but not the parasympathetic division of the autonomic nervous system. However, few walls of arterioles, for instance the arterioles in skeletal muscles, are innervated by cholinergic fibres [still sympathetic nerves], which dilate the vessels after stimuli. However, in humans, evidence for a sympathetic cholinergic vasodilator system is lacking. It seems that activation of β2-adrenoceptors on skeletal muscle blood vessels promotes vasodilation. It is more likely that vasodilation of skeletal muscle vasculature in response to activation of the sympathetic nervous system is due to the action of epinephrine released from the adrenal medulla. And more is that a few exceptions exists that the arteries in the erectile tissue of the reproductive organs, uterine and some facial blood vessels, and blood vessels in salivary glands, may also be controlled by parasympathetic nerves. For the detail of autonomic nerves system please refer to thread of “The Pain – The Basic Concepts” at http://www.tomhsiung.com/wordpress/2014/11/the-pain-the-basic-concepts/.
Sympathetic noradrenergic fibers terminate on vascular smooth muscle in all parts of the body to mediate vasoconstriction. For the arterial and capillary system (aorta, artery, small artery, arteriole, metarteriole, and capillary), the walls of the aorta and other arteries of large diameter contain a relatively large amount of elastic tissue, primarily located in the inner and external elastic laminas. The walls of the arterioles contain less elastic tissue but much more smooth muscle. The innervation of metarterioles is unsettled. The openings of capillaries are sounded on the upstream side by minute smooth muscle called pre capillary sphincters, which are not innervated.
The cardiovascular system is under neural influences coming from several parts of the brain stem, forebrain, and insular cortex. One of the major sources of excitatory input to sympathetic nerves controlling the vasculature is a group of neurons located near the pill surface of the medulla in the rostral ventrolateral medulla (RVLM). This region is sometimes called a vasomotor area. The axons of RVLM neurons course dorsally and medially and then descend in the lateral column of the spinal cord to the thoracolumbar intermediolateral gray column (IML). They contain phenylethanolamine-N-methyltransferase (PNMT), but it appears that the excitatory transmitter they secrete is glutamate rather than epinephrine.
The activity of RVLM neurons (the more intensive the RVLM discharge, the more intensive the activity of autonomic nerve system [primary the sympathetic nerve system]) is determined by many factors. They include not only the very important fibres from material baroreceptors, cardiopulmonary receptors, and chemoreceptors, but also fibres from other parts of the nervous system. In addition, some stimuli act directly on the vasomotor area. They include,
1.Descending tracts to the vasomotor area from the cerebral cortex (particularly the limbic cortex) that relay in the hypothalamus. These fibres are responsible for the blood pressure rise and tachycardia (the heart) produced by emotions such as stress, sexual excitement, and anger. The connections between the hypothalamus and the vasomotor area are reciprocal, with afferents from the brain stem closing the loop.
2.Inflation of the lungs, which causes inhibition of vasomotor discharge via afferent fibers of vagal nerve.
3.Pain usually causes a rise in blood pressure via afferent impulses in the reticular formation converging in the RVLM. However, prolonged severe pain may cause vasodilation and fainting.
4.The activity in afferents from exercising muscles probably exerts a similar pressor effect via a pathway to the RVLM. The pressor response to stimulation of somatic afferent nerves is called the somatosympathetic reflex.
Parasympathetic Motor Center
The medulla is also a major site of origin of excitatory input to cardiac vagal motor neurons in the nucleus ambiguus. The significance of parasympathetic motor neurons is that, release of acetylcholine from vagal nerve terminals inhibits the release of norepinephrine from sympathetic nerve terminals, which can enhance the effects of vagal nerve activation on the effector (the heart). This effect is induced by cholinergic receptors (adrenergic receptors for sympathetic system vice versa) that modulate transmitter release from nerve endings (see Clinical Pharmacology).