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Physiology II
Cardiovascular Physiology
Short-Term Control Of MSAP
Objectives

Learning Objectives

describe in words what is meant by a "NEGATIVE FEEDBACK CONTROL SYSTEM" and list or diagram the basic components of physiological control systems of this type:  Feedback control. The operation of any system, be it physical or biological, involves an input and an output. If the system is intended to work by self-regulation, the output must exert some control over the input. This is referred to as feedback control. When the relationship between the input and the output is inverse, so that an increase in output leads to a decrease in input, the regulation is by negative feedback. In general, negative feedback mechanisms operate to promote stability and equilibrium, maintaining a system at a setpoint. Most physiologic homeostatic mechanisms operate by negative feedback. The regulation of numerous endocrine glands and their hormones falls into this category.

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.

for the BARORECEPTOR REFLEX, describe in words and charts or diagrams the anatomical location and nature of the RECEPTOR(s), the nature of the EFFECTIVE STIMULUS, and the AFFERENT PATHWAY carrying information back to the medullary cardiovascular center:  

Baroreceptors are stretch receptors in the walls of blood vessels. They are nerve endings or mechanoreceptors. To stretch them will get an increase in the frequency of depolorizations or an increase in the frequency of action potentials. The nerves leaving the baroreceptors will have an increase in impulses going to the integrating centers. If the stimulus is that the MSAP has increased then there will be an increase in firing of the APs to the vasomotor center. This has an inhibitory effect on the SNS so that the SNS decreases its stimulation so that HR and contractility can decrease and MSAP can fall back to normal.

A baroreceptor is a sensory nerve terminal that is stimulated by changes in pressure, as those in blood vessels.

A reflex is a reflected action or movement; the sum total of any particular automatic response mediated by the nervous system.

Stretching increasing something in one of its dimensions; extending

Baroreceptors are abundantly located in the walls of the aortic arch and in the internal corotid artery wall slightly above the corotid bifurcation (in the area known as the corotid sinus which is a small dilation just above the bifurcation) as well as in the walls of almost every large artery of the thoracic and neck regions. Primary control over sudden changes in blood pressure involves reflexes that originate in these baroreceptors, which happen to be sensitive to stretch.

At normal pressure the walls are stretched and the receptors are active, sending impulses via sensory nerves to centers in the brain that are responsible for coordinating information and regulating the cardiovascular system. These cardiovascular centers control the ANS nerves to the heart and blood vessels.

Baroreceptors respond to

  1. The actual pressure in the corotid sinus and aortic arch and
  2. To the rate of change of that pressure. The pattern of nerve impulses sent to the CV centers contain information info @:
    1. The mean pressure
    2. The steepness of rise of the pulse curve
    3. the pulse pressure
    4. The HR

Corotid sinus signals are transmitted through the very small Herings nerve to the glossopharyngeal (9th cranial nerve) nerve and then to the tractus solitarius in the medullary area of the brainstem, where inhibitory interneurons affect sympathetic outflow. Increased firing of baroreceptor nerves causes a reduction in sympathetic outflow in the sympathetic efferent fibers. Decreases in sympathetic and increased in parasympathetic nerve activity to the heart reduce contractility and HR, which decreases BP. This baro reflex is highly effective at rapidly controlling BP during short term perturbations, such as postural changes. This exhibits a rapidly adapting control mechanism which normalizes BP

Diagram of neural control of the circ

CNS IX & X cranial nerves

Corotid & aortic

Chemo & Baro receps

Vagus nerve

SA node

HEART CO Art Pr = CO x TPR

Blood vs ( TPR)

Signals from the arch of the aorta are transmitted through the vagus nerve( 10th cranial nerve) in to the same areas in the medulla

Of the response baroreceptors to pressure above 60mmHg they respond progressively and more rapidly and reach a maximum at about 180mmHg. Aortic baroreceptors operate starting at pressures of 30mmHg or higher.

The baroreceptor feedback mechanism functions most effectively in the pressure range where its most needed.

The baroreceptors respond extremely rapidly to changes in arterial pressure and the rate of impulse firing increase during systole and decrease during diastole. The baroreceptors respond much more to a rapidly changing pressure than to a stationary pressure

DECREASED arterial pressure arterial wall stretch less sensory nerves from the corotid sinus(sinus nerve) and from the aortic arch(depressor nerve) become less active and send fewer impulses. Upon receiving fewer impulses from the baroreceptors (signaling fall in pressure), the CV centers respond by exciting sympathetic nerves and by inhibiting parasympathetic nerves. These factors below contribute to a compensatory raising of blood pressure back to normal.

    1. increased HR (increased CO)
    2. increased strength of contraction (stroke volume so that CO increased
    3. a general increased constriction of arterioles, which increases resistance(but not in brain or heart)
    4. increased vaso constriction in veins raises venous return to ht as it redistributes blood, shifting it from the venous reservoir to the arterial side of the circulation.

The best known of the nervous mechanisms for arterial pressure control is the baroreceptor reflex. This reflex is initiated by stretch receptors (baro and presso). 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 to normal level

Reflex initiated by the baroreceptors 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

  1. Vasodilation of the veins and arterioles through out the peripheral circulatory system
  2. Decreased HR an decreased strength of contraction

Therefore excitation of the baroreceptors by pressure in the arteries reflexly causes the arterial pressure to decrease because of a decrease in peripheral resistance ad a decrease in CO.

ABP is controlled by a negative feedback of itself , and similar feedback mechanisms exist for peripheral resistance, CO,

describe in words and charts or graphs the following functional characteristics of the CAROTID BARORECEPTOR REFLEX:

The baroreceptors will reset themselves in 1 to 2 days to whatever pressure level they are exposed. If the pressure rises from the normal value of 100 to 160, extreme numbers of baroreceptor impulses are at first transmitted. During the next few seconds, the rate of firing diminishes considerably; then it diminishes much more slowly during the next 1 to 2 days, at the end of which time the rate will have returned essentially to the normal level despite the fact that the art pressure now remains at 160. This "resetting" of the reflex prevents it from functioning as a control system for art pressure changes that last longer than a few days at a time.

describe in words the EFFECTS OF SYMPATHETIC NERVOUS SYSTEM STIMULATION on peripheral vascular resistance, heart rate, myocardial contractility, venous compliance, venous pressure, cardiac filling pressure, and cardiac output, and relate these effects to the OVERALL CONTROL OF ARTERIAL PRESSURE

The SNS will cause an increase in heart rate, conduction velocity, excitability, and contractility. Contractility is affected by more Ca++ entering thus more cross-bridges can form. TPR will be increased. Venous compliance will decrease but venous pressure will increase. Cardiac filling pressure or preload will be increased from the veins sending more back to the heart thus stroke volume will increase which signifies an increase in CO. Together all these things will increase the MSAP.

Somatosympathetic reflex is the pressor response to stimulation of somatic afferent nerves.

The most important part of the ANS for regulation of the circulation is the SNS. The PSNS is also important in contributing to regulation of heart function.

The hypothalamus releases ADH which acts on the kidney to increased water re-absorption from the renal tubules, thereby increased blood volume and hence ABP. ADH also constricts blood vessels

SNS See Guyton for anatomy of the circulation and SNS pp 210.

SNS innervation of blood vs The SNS innervates small arteries and arterioles which allows for increased resistance decreased flow of blood to tissues. Innervation of veins allows SNS to decreased the volume of veins alter the volume of the peripheral circulatory system which translocates blood into heart plays a mojor role in the regulation of CV function.

SNS innervation of the heart SNS stim increased the activity of the heart increased HR & enhancing strength of pumping.

Describe in words the EFFECTS OF SYMPATHETIC NERVOUS STIMULATION on:

  1. peripheral vascular resistance - increases it
  2. heart rate is accelerated by SNS via this list as seen in Ganong
  1. decreased activity of baroreceptors in the arteries, Lt ventricle and pulm circ
  2. increased acitivity of atrial stretch receptors
  3. inspiration
  4. excitement
  5. anger
  6. most painful stimuli
  7. hypoxia
  8. exercize
  9. norepinephrine
  10. epinephrine
  11. thyroid hormones
  12. fever
  13. bainbridge reflex not a stretch mediated reflex, its an increased HR in response to infusion of bld or NS in anesthetized animals.

Heart rate is slowed by:

  1. increased activity of baroreceptors in the arteries, lt ventricle, and pulm circ
  2. expiration
  3. fear
  4. grief
  5. stimulation of pain fibers in trigeminal nerve
  6. increased intracranial pressure
  7. myocardial contractility - increased
  1. venous compliance - decreased
  2. venous pressure - decreased
  3. cardiac filling pressure - ???????
  4. and cardiac output - increased

relate these effects to the OVERALL CONTROL OF ARTERIAL PRESSURE- the key factors that regulate systemic BP are

  1. peripheral resistance( as mediated through blood vessel constriction vasoconstriction) and CO (ht stroke vol x HR, usu 5-6 L/m) An increas in either of these factors will increase ABP. INCREASED peripheral resistance increased ABP by impeding bld flow, resulting in backup of bld in the arteries, where ABP is measured. Resistance increased mainly thru vaso constriction, particularlly at the arteriolar level. ABP may increase thru friction due to increased blood viscosity as well.
  2.  CO determines the size of the bolus ejected into the arterial system, which stretches the arterial walls raising ABP significantly during systole. This local pressure is transmitted down the vascular tree, because blood moves from a higher pressure area to a lower pressure area. If CO were seerely diminished or absent there would be a tiny or no pressure gradient to drive the flow of blood.

Increased CO2 & H+ levels ( as might occur with low BP and decreased tissur perf) affect the brainstem and stimulate the vasomotor center to increased sympathetic output, thereby increased ABP systemically

compare and contrast the effects of alpha1,alpha2, and 1 blockade on arterial blood pressure:  

 

Normal effect on blood pressure

Blockade/effect on pressure

alpha1

Vasoconstricts blood vessels

Vasodilates blood vessels

alpha2

Reduces SNS activity by effecting peripheral resistance. Makes the receptors think they dont need as much SNS stimulation thus allowing vasodilation to occur.

Increases SNS activity to block them, allows more vasoconstriction.

beta1

Found on the heart. To stimulate will increase SNS activity so will increase heart rate, contractility that will increase MSAP.

To block these receptors will decrease CO and HR thus decreasing MSAP.

The brain stem and hypothalamus contain blood pressure regulating centers.

  1. the brainstem contains a vasomotor center (influenced by numerous other areas of the nervous system), which increased blood pressure by firing sympathetic nerve messages.
  2. The sympathetic nerves release Norepinephrine, which stimulates alpha 1 receptors on the peripheral blood vessels vasoconstriction, and also stimulates beta 1 receptors on the heart muscle increased CO via increased SV and HR. The veins are also vasoconstricted. Sympathetic nerves also stimulate the adrenal medulla to sec Norepinephrine and epinephrine, which travel systemically. This nor causes vasoconstriction, and the epinephrine causes vasoconstriction when it acts on alpha 1 receptors, and vasodilation when it acts on blood vessels beta 2 receptors( most notably in the skeletal muscle and the heart. This beta 2 stimulation by epinephrine ensures perfusion to heart and skeletal muscle in flight or fight.
  3. Sympathetic nerves stimulate beta 1 receptors on cardiac muscle (SA & AV) increased HR, AV conduction, and contractility with a net increased CO.
  4. Sympathetic nerves stimulate beta 1 receptors on the granular cells of the kidney to cause renin secretion. Renin initiates a chain reaction that results in the production of angiotension II & aldosterone( stimulates Na reabsorption and passively water which increased pressure and increased blood volume) , which are both powerful vasoconstriction.

LOCATION AND EFFECTS OF STIMULATION OF ADRENERGIC RECEPTORS

 

ALPHA 1 RECEPTORS

Arterioles and Veins:
  Constriction( epi & NE)

Glands:
  Decreased sec

Eye:
  Constriction of radial musc

Intestine:
  Decreased motility

ALPHA 2 RECEPTORS

CNS Post-synaptic terminals:
  Decreased sympathetic outflow form brain

CNS Pre-synaptic terminals: 
  nor release

Beta Islet Cells of Pancreas:
  Decreased sec

BETA 1 RECEPTORS

Heart:
  Increased HR
  Increased Contractility
  Increased conduction velocity
  Increased automaticity

Kidney:
  Increased renin sec 

BETA 2 RECEPTORS

Trachea & bronchioles:
  Dilation

Pregnant/non-pregnant Uterus:
  Relaxation

Arterioles (no beta 2 receptors in skin or brain):
  Dilation (epi)

describe using words and diagrams the OVERALL SEQUENCE OF RESPONSES in the cardiovascular system to suddenly moving from a SUPINE to a STANDING position (or from a horizontal position to a 60 degree head-down tilt on a tilt-table):  In changing from a laying to standing position, creates gravitational forces on the blood initially. The weight of our blood creates different pressures at different heights in our bodies. The blood becomes redistributed in the veins, as much as 600cc. The cardiac output therefore falls which causes decreased stretch on the baroreceptors activation of sympathetic and inhibition of the parasympathetic occurs. (MSAP is determined by the balance of blood flowing into the arteries (CO) and blood flowing out (arteriolar drainage) the compensation mediated response via the baroreceptor reflex include vasoconstriction of veins to help replenish arterial volume, increased CO (increased inflow), and decreased outflow - increased arteriolar resistance. These mechanisms raise fluid level toward normal

Immediately on standing, the arterial pressure in the head and upper part of the body tends to fall, and marked reduction of this pressure can cause loss of consciousness. The falling pressure at the baroreceptors elicits an immediate reflex, resulting in strong sympathetic discharge throughout the body, and this minimizes the decrease in pressure in the head and upper body. The sequence would include a strong vasoconstriction of the arteries and SMAs thus maintaining present blood volume and a strong vasoconstriction of the veins which will decrease their compliance and increase their pressure thus sending the blood available back up to the heart to counteract the fallen amt in the upper body. Standing up will make you utilize your leg muscles, which will help squeeze the blood in the veins back up to the heart. Feet down on a tilt table is a more passive move and doesnt include this assistance from muscular contraction thus more blood pools and one can faint.

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