negative feedback control system: Negative Feedback mechanisms operate to promote stability and equilibrium, maintaining a system at a set point. All physiological homeostatic mechanisms operate by negative feedback. Negative feedback operates when input level is inversely related to output level. An example is the baroceptor reflex for arterial pressure control. (Physiology Coloring Book, 109)
This negates a change in the variable and brings it back to normal. It reduces the error and brings it back to set point. It is called negative because it reduces the error – not because it goes negative on the scale. An example would be in the arterial pressure system – a high pressure causes a series of reactions that promote a lowered pressure, or a low pressure causes a series of reactions that promote an elevated pressure. In both instances, these effects are negative with respect to the initiating stimulus.
arterial baroreceptors: Stretch receptors located in the walls of several of the large systemic arteries. A rise in pressure stretches the baroreceptors and causes them to transmit signals into the central nervous system, and "feedback" signals are then sent back through the ANS to the circulation to reduce arterial pressure downward toward the normal level. (Guyton,213)
carotid sinus: The wall of each internal carotid artery slightly above the carotid bifurcation (baroreceptors are extremely abundant here). Signals are transmitted from each carotid sinus through the very small Hering's nerve to the glossopharyngeal nerve and then to the tractus solitarius in the medullary area of the brain stem. (Guyton, 213)
aortic sinus: Wall of the aortic arch where baroreceptors are extremely abundant. Signals from the arch of the aorta are transmitted through the vagus nerves also into the same area of the medulla. (Guyton, 213)
cardiac stretch receptors: These are the baroreceptors located in the superior and inferior vena cava and in the right and left atria.
peripheral chemoreceptors: Chemosensitive cells which are sensitive to lack of oxygen, excess of carbon dioxide or excess of hydrogen ions. These receptors are located adjacent to the aortic arch and in the bifurcation of each common carotid artery, known as aortic and carotid bodies. The chemoreceptors excite nerve fibers that, along with the baroreceptor fibers, pass through Hering's nerves and the vagus nerves into the vasomotor center. (Guyton, 216)
medullary cardiovascular center: After the baroreceptor signals have entered the tractus solitarius of the medulla, secondary signals eventually inhibit the vasoconstrictor center of the medulla and excite the vagal center. The net effects are vasodilation of the veins and the arterioles throughout the peripheral circulatory system and decreased heart rate and strength of heart contraction. Therefore, excitation of the baroreceptors by pressure in the arteries causes the arterial pressure to decrease because of both a decrease in peripheral resistance and a decrease in cardiac output. Conversely, low pressure has opposite effects, causing the pressure to rise back toward normal.
The adrenal medulla is stimulated by sympathetic nerve impulses to secrete epi and norepi into the circulating blood. These hormones vasoconstrict the peripheral circulation and the epi will affect the beta 2 receptors on the heart to increase heart rate and contractility and in the lungs to brochodilate.
vasomotor area (vasopressor area): Located bilaterally mainly in the reticular substance of the medulla and lower third of the pons, transmitting parasympathetic impulses through the vagus nerves to the heart and sympathetic impulses through the cord and peripheral sympathetic nerves to almost all of the blood vessels in the body. Three areas within the "vasomotor center" have been identified; a vasoconstrictor area, a vasodilator area and a sensory area.
The lateral portions of the vasomotor center transmit excitatory impulses through the sympathetic nerve fibers to the heart to increase heart rate and contractility, whereas the medial portion of the vasomotor center, which lies in the immediate apposition to the dorsal motor nucleus of the vagus nerves, transmits impulses through the vagus nerves to the heart to decrease heart rate.
cardioaccelerator area: The lateral portions of the vasomotor center transmit excitatory impulses through the sympathetic nerve fibers to the heart to increase heart rate and contractility. (Guyton,212)
cardioinhibitory area: The medial portion of the vasomotor center, which lies in immediate apposition to the dorsal motor nucleus of the vagus nerves, transmits impulses through the vagus nerves to the heart to decrease heart rate. (Guyton, 212)
short-term control: Is handled by the baroreceptors and chemoreceptors. The cerebral ischemic reflex is another method of short-term control.
intermediate-term control: These include the renin-angiotensin-aldosterone reflex, the stress-relaxation mechanism and the capillary fluid shift mechanism.
long-term control: The stretch of the atria causes reflex dilatation of the afferent arterioles in the kidneys. Signals are also transmitted to the hypothalamus to decrease the secretion of ADH to diminish the reabsorption of water in the tubules. Atrial stretch also releases atrial natriuretic peptide which also leads to more sodium excretion and an increase in urine output and thus a decrease in ECF volume. Long term control ultimately falls to the kidneys to perform with fluid balance maintenance.
baroreceptor reflex: Nervous system mechanism for arterial BP control. This reflex is initiated by stretch receptors called baroreceptors, which are located in the walls of the major arteries, especially the carotid arteries and the aorta. A few baroreceptors are located in the wall of almost every large artery of the thoracic and neck regions, but are extremely abundant in the wall of each internal carotid artery slightly above the carotid bifurcation (carotid sinus) and the wall of the aortic arch. When these become stretched by high pressure, signals are transmitted to the brainstem, where they inhibit the sympathetic impulses to the heart and blood vessels; this allows the arterial pressure to fall back toward normal. (Guyton, 213)
A rise in pressure stretches the baroreceptors and causes them to transmit signals into the central nervous system, and "feedback" signals are then sent back through the autonomic nervous system to the circulation to reduce arterial pressure downward toward the normal level.
chemoreceptor reflex: Chemoreceptors become stimulated whenever the arterial pressure falls below a critical level. This is because of diminished blood flow to the bodies, and therefore diminished availability of oxygen as well as excess buildup of carbon dioxide and hydrogen ions (that are not removed by the slow flow of blood). The signals transmitted from the chemoreceptors into the vasomotor center excite the vasomotor center, and this elevates the arterial pressure. This reflex helps to return the arterial pressure back toward the normal level whenever it falls too low. (Guyton, 216)
They excite nerve fibers that, along with the baroreceptor fibers, pass through Hering’s nerves and the vagus nerve into the vasomotor center. Whenever arterial pressure falls below a critical level, the chemoreceptors become stimulated because of diminished blood flow to the bodies and therefore diminished availability of oxygen as well as excess buildup of carbon dioxide and hydrogen ions that are not removed by the slow flow of blood. The signals transmitted from the chemoreceptors into the vasomotor center excite the vasomotor center, and this elevates the arterial pressure. It is not, however, a powerful reflex and is not stimulated strongly until arterial pressure falls below 80mmHg
central nervous system ischemic reflex: This is an emergency arterial pressure control system that acts rapidly and powerfully to prevent further decrease in arterial pressure whenever blood flow to the brain decreases dangerously close to the lethal level which begins around 60mmHg and continues and increases its responses at 15-20mmHg. It is called also the "last ditch" effort but is one of the most powerful of all the activators of the sympathetic vasoconstrictor system.
renin-angiotensin-aldosterone system: Renin is released by the juxtoglomerular cells in afferent arterioles of the kidney in response to SNS stimulation. The receptors that mediate this are beta receptors on cells. Renin will then increase the production of angiotensin I which will lead to Angiotensin II which is a potent vasoconstrictor which then increases total peripheral resistance. Angiotensin II will also stimulate the release of aldosterone from the medulla which will increase sodium reabsorption so less Na leaves the body and more stays in which increase ECF volume. ADH or vasopressin is also stimulated when there is a low MSAP to hold on to water in the renal tubules and thus increase ECF volume.
stress relaxation mechanism: When the pressure in the blood vessels becomes too high, they become stretched and keep on stretching more and more for minutes or hours; as a result, the pressure in the vessels falls toward normal. This continuing stretch of the vessels, called stress-relaxation, can serve as an intermediate-term pressure "buffer."
capillary fluid shift: This means that any time the capillary pressure falls too low, fluid is absorbed by osmosis from the tissue into the circulation, thus building up the blood volume and increasing the pressure in the circulation. Conversely, when the capillary pressure rises too high, fluid is lost out of the circulation into the tissues, thus reducing the blood volume as well as all the pressures throughout the circulation.
renal-body fluid mechanism: These involve the renal output of water and sodium. To increase the water output there will be an increase in the pressure, which will increase the GFR, which will drive more water through the filter and thus decrease total body water. This is called pressure diuresis. The same thing can be said of sodium, which is called pressure natriuresis. The third factor has two sections – one is the release of ANP, which increases sodium excretion, and the second is Endogenous-digitalis-like substance (EDLS) which decreases the Na/K/ATPase pump activity so when the pump is inhibited, more sodium will be excreted in the urine.
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