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Lecture 5

BIOC33-34 Lecture 5.docx

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Department
Biology
Course
BIO120H1
Professor
Zachariah Campbell
Semester
Winter

Description
Lecture 5 – Regulation of Cardiac Output: Heart Rate and Stroke Volume 1. Exact summary of the last part of lecture 4 • Regulation of heart rate: sympathetic mechanisms • Regulation of heart rate: parasympathetic mechanisms 2. Quantifying Sympathetic and Parasympathetic “Tone” to the Heart: • It is possible to quantify the actual amount of the sympathetic and parasympathetic tone (input) influencing the heart o Parasympathetic stimulation activates muscarinic receptors on the heart o Sympathetic stimulation activates alpha and beta adrenoceptors on the heart, however, there are almost exclusively beta receptors  Alpha receptors are usually more common in blood vessels • We can pharmacologically manipulate these receptors to see how much sympathetic or parasympathetic innervation is affecting the heart at any given moment o Muscarinic receptors can be blocked with a drug called atropine, and we can block beta adrenoceptors with a drug called atenolol (sotalol)  If we block muscarinic receptors, heart rate will speed up  If we block the adrenergic receptors, heart rate will slow down o By comparing heart rate following sotalol or atropine treatment, and comparing it to resting heart rate, we can obtain a measure of the amount of sympathetic and parasympathetic tone to the heart • In the absence of any sympathetic or parasympathetic input, the pacemaker cells in the SA node usually depolarize around 100 times per minute, but resting heart rate is normally around 60-70 beats per minute o In other words, resting heart rate is lower than the endogenous rate of unaltered SA node depolarization  This means that in a normal person, something must be slowing the rate of pacemaker depolarization to produce the lower heart rate • This “something” is parasympathetic stimulation o The fact that resting heart rate is lower than resting (on its own) SA node depolarization means that parasympathetic stimulation must (in a normal person at rest) be more powerful than sympathetic stimulation • If the heart is beating at a fairly normal resting rate of 70 beats/minute, we can add sotalol (called a beta blocker) to block beta adrenergic receptors, reducing sympathetic tone o Heart rate will decrease to, for example, 50 beats/minute, and thus we know that person’s resting sympathetic tone is about 20 beats/minute o Beta blockers are also used in this manner to help with high blood pressure • To quantify the parasympathetic tone, we use a similar process, measure the resting heart rate and then add atropine, which blocks the muscarinic receptors on the heart o This raises heart rate, for example, to 100 beats/minute, which means that the resting parasympathetic tone is about 30 beats/minute o Atropine is a commonly used drug for manipulating heart rate and other parasympathetic systems 3. Other Cardiovascular-Related Output from the Brain: • There are other related outputs from the brain to the cardiovascular system, and vice versa • As well as the sympathetic and parasympathetic nerves going from the brainstem to the heart, there is sympathetic innervation of blood vessels (arteries and veins) o Norepinephrine is the neurotransmitter, it causes a constriction of the blood vessels (vasoconstriction) which raises total peripheral resistance and therefore increases blood pressure • Sympathetic stimulation of the adrenal gland causes the release of epinephrine and norepinephrine into the circulation • When we look at the effects of epinephrine on blood flow and pressure, we’ll see that its effects change from organ to organ, depending on the proportion of alpha to beta adrenoceptors o Generally, alpha receptors cause vasoconstriction while beta receptors cause vasodilation • What we haven’t looked at yet is input into the cardiovascular control centers o The most important input comes from baroreceptors (or pressure sensors) • There are 2 major populations of baroreceptors in the circulatory system: one in the aorta and one in the carotid arteries (in an area called the carotid sinus) o These sense arterial pressure and are very important for regulating overall blood pressure in the body • There are also feedback receptors in skeletal muscle that are also important in cardiac regulation and thought to play an important role in the control of breathing during exercise o As an aside, there is no known respiratory control system that can account for the increase in breathing that occurs during exercise 4. Stroke Volume (SV) Regulation: • How is stroke volume (ml of blood pumped per heart beat), the second part of the equation CO = HR x SV, regulated? o While regulation of heart rate was fairly simple, regulation of stroke volume is considerably more complex, with many more factors involved • 3 major factors will influence the regulation of stroke volume: o The force of ventricular contraction  Easy to modify, epinephrine and norepinephrine in the circulatory system adjust it, as does sympathetic innervation • Remember that the sympathetic stimulation of the heart not only enhances contraction but also speeds up ventricular relaxation as well, this gives the heart sufficient time to fill, which will affect stroke volume o The end diastolic volume  This is affected by many things such as muscular and respiratory pumps, but all of them will affect what is called preload or end diastolic pressure • Anything which alters the pressure of blood in the ventricles will affect end diastolic volume as well  Things that affect end diastolic pressure include atrial pressure (which is affected by venous pressure and the contraction of the atria) o The afterload (blood pressure) a) Regulation of Ventricular Contractility • The first of these factors which affect stroke volume is ventricular contractility o Sympathetic nerves innervate the cardiac myocytes (muscle cells) and release norepinephrine which acts on the cardiac cells by binding with beta receptors  Circulating adrenaline and noradrenaline from the adrenal gland can do the same thing o Binding of the catecholamines to the beta adrenoceptor activates a G protein-coupled system which activates adenylyl cyclase that produces cAMP, which then activates protein kinase-A o This in turn, will do 4 things:  First, it will open up calcium channels on the plasma membrane, allowing Ca2+ ions to flow into the cell  Second, it triggers further calcium release from the sarcoplasmic reticulum (SR) also by opening calcium channels  Third, it facilitates the binding together of actin and myosin fibers which is required for muscle contraction  Fourth, it phosphorylates the calcium ATPase on the SR membrane allowing for rapid confiscation of calcium when the heart is relaxing • This is important because it allows the heart to spend more time in diastole and therefore have more time to fill o (look at the slide on page 5) the slide shows that phosphorylation of the myosin hed causes it to enter the high energy state which is required for contraction  The following slide illustrates that calcium binds to troponin which causes a conformational change in tropomyosin • This change causes tropomyosin to move off the myosin-binding site on actin allowing for actin and myosin to bind together and form the crossbridges required for muscle contraction b) Afterload and Stroke Volume • The final factor involved in stroke volume regulation is afterload which is the pressure that the ventricles must work against during the ventricular ejection phase of the heart cycle o In other words, afterload is aortic blood pressure (on the left side of the heart) and pulmonary artery pressure (on the right side of the heart)  If afterload increases, then stroke volume will decrease • The effect of decreasing afterload is a decrease in end-systolic volume and a decrease in end- diastolic volume although the decrease in end diastolic volume is less than the decrease in end systolic volume o As both EDV and ESV decrease (with decreases in afterload) stroke volume increases
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