Cardiac output: intrinsic, neural and endocrine effects
Heart – a Double Pump
The cardiovascular system, the body’s pressurized blood re-circulation system is powered by a double pump. It is composed of two filling and two pumping chambers, the atria and the ventricles. The right ventricle, a low-pressure output system drives blood into the thin walled arteries of the lung, the pulmonary arteries.
In the lung carbon dioxide, a waste product of metabolism is removed from blood and oxygen is added. Oxygenated blood returns to the left chambers of the heart through the pulmonary veins and is pumped by the left ventricle into the aorta with sufficient force to carry it to distant parts of the body.
The model for building tension by cycling of actin and myosin cross bridges is the same for cardiac muscle and skeletal muscle. However, cardiac muscle is organized somewhat differently. Unlike straight-line skeletal muscle cells with their many nuclei per cell, cardiac muscle cells contain only one nucleus that is located centrally and the cells are branched.
Myosin filaments are fewer and thicker in cardiac muscle than in skeletal muscle. Cardiac muscle has larger T-tubules that do not form triads with the sarcoplasmic reticulum. Protein structures called intercalated discs tie cardiac muscle cells to each other creating a network. Ease of movement of ions and other material within the network is aided by the presence of gap junctions between cells.
There are two types of muscle cells in the heart, contracting muscle cells and conducting muscle cells. Contracting muscle cells make up most of the atria and ventricles and generate the force and pressure required to eject blood.
The conducting muscle cells, in blue, contribute little to the generation of force. Their function is to spread action potentials that trigger muscle contraction over the entire heart. Click on the image for a larger view.
In the image 1. Sinoatrial (SA) Node; 2. Atrial Ventricular (AV) Node; 3. Bundle of His; 4. Left Bundle Branch; 5. Left Posterior Fascicle; 6. Left Anterior Fascicle; 7. Left Ventricle; 8. Ventricular Septum; 9. Right ventricle.
Cardiac Muscle Electrical Activity
Contraction of cardiac muscle requires action potentials like skeletal muscle. But, in the heart action potentials originate in the conducting muscle cells rather than at a neuron synapse. Muscle cell action potentials use the same type of chemistry as neuron and skeletal muscle action potentials. A review of action potentials can be found at “Neurons: Where Does Their Electricity Come From?”
There are some differences however between heart and skeletal muscle action potentials. Heart muscle action potentials last much longer, 150-300 milliseconds compared to 1-2 milliseconds for skeletal muscle. Heart muscle action potentials display variable shape because of the participation of voltage-gated chloride [Cl–] and calcium [Ca++] channels in addition to the sodium [Na+] and potassium [K+] channels used by skeletal muscle and neurons.
The time course and shape of action potentials differs among ventricle, atrium, and pacemaker muscle. Yet, in all cases it is the amount of Ca++ entering during an action potential that governs the force generated and the pace of heart pumping. This is because entering Ca++ is the trigger in heart muscle that releases stored calcium from the sarcoplasmic reticulum, which in turn initiates cross bridge formation between actin and myosin filaments and muscle shortening. Click on the image above to see it larger.
The primary pacemaker cells of the human heart are located at the sinoatrial [SA] node. Other conducting muscle cells with pacemaker capability exist along the tract of conducting muscle from the SA node to the tip of the ventricles. But it is the fastest pacemaker, the SA node that normally determines heart rate.
Inward flowing ions during a pacemaker potential spread through muscle gap junctions to activate the tract of conducting muscle cells.
Likewise, contracting muscle cells along the conducting tract are brought to threshold triggering their action potentials. The timing of the spread of action potential ions through the conducting tract and into contracting muscle brings large areas of contracting muscle to threshold simultaneously.
Frank-Starling Law of the Heart
Pressure in the arteries depends upon the force of ventricular contraction and the amount of blood ejected. The Frank-Starling Law of the heart states that the volume of blood ejected by the ventricle depends upon the volume present at the end of the filling period. This relationship between stretch of heart muscle during filling and force of contraction ensures that the amount of blood ejected by the heart matches venous return to the heart.
Unlike skeletal muscle, increasing cardiac muscle length increases sensitivity of troponin-C to Ca++. This means that cross bridges between actin and myosin occur at lower concentrations of Ca++. Stretching of cardiac muscle also increases the amount of Ca++ released from sarcoplasmic reticulum stores when the next action potential arrives.
Autonomic Control of Blood Pressure
Blood is driven through the vascular system of arteries and veins by the difference in blood pressure between the arterial and venous sides of the circulation. Mean arterial pressure, the driving force behind blood flow is maintained at a set point of about 100 mm Hg [millimeters of mercury] by a continuously active neural feedback loop.
Baroreceptor Reflex Afferent to brain Stem
Neural sensory receptors for blood pressure, baroreceptors, are located in the walls of the aortic arch and the carotid sinus. The carotid sinus is where the common carotid bifurcates into the internal carotid artery and the external carotid artery to the brain and face, respectively.
Baroreceptors are neuron afferents that respond to pressure and mechanical stretch of the arteries. They fire constantly and are particularly sensitive to the rate of change of arterial pressure. Their firing rate increases with increased arterial stretch and decreases with decreased pressure or arterial stretch.
Baroreceptor afferent signals travel to the brain stem in cranial nerve IX, the glossopharyngeal nerve [carotid sinus afferent], and cranial nerve X, the vagus nerve [aortic arch afferent]. Their destination is the nucleus tractus soltaris in the brain stem which is also constantly active. This brain nucleus interprets changes in firing rates of the baroreceptor afferent and changes its own firing rate accordingly.
Sympathetic & Parasympathetic Efferent Activity
The nucleus tractus solataris signals to the cardiovascular centers in the brain stem that control sympathetic and parasympathetic activity. Efferent sympathetic neurons synapse first in the spinal cord, then in the spinal ganglion and finally in the heart. Efferent parasympathetic neurons travel back to the heart in the vagus nerve.
The sympathetic and parasympathetic brain centers work in a coordinated fashion to move blood pressure back to the mean arterial pressure set point of about 100 mmHg. Increased sympathetic activity, induced by low pressure in the large arteries, increases heart rate and contractility of cardiac muscle. It restricts blood flow to surface arterioles and mobilizes increased venous return. The net result is increased cardiac output and a rise in pressure in the large arteries.
Parasympathetic firing of the vagus nerve, in response to high pressure in the large arteries, decreases rate and contractility of the heart. A corresponding decrease in sympathetic activity opens blood flow at the peripheral arterioles. The net result is decreased cardiac output and a fall in pressure in the large arteries.
Preservation of Blood Volume
Another component of maintaining an acceptable mean arterial pressure is preserving sufficient blood volume. Preservation of blood volume requires a response of the endocrine system to supplement the reflex response of the neural baroreceptors.
Insufficient Blood Volume
When blood volume is low there is insufficient venous return and decreased arterial pressure. To regain volume and pressure the vasculature must increase its water and salt [Na+] content. Increasing blood water and Na+ is accomplished by the kidney nephrons.
When the kidney senses that Na+ is too low in the filtrate flowing into the distal tubules of the nephrons, an indicator of low blood pressure due to low volume, it secretes a molecule named renin into the blood of the peritubular capillaries. Low filtrate Na+ indicates low blood volume because water follows Na+ due to osmotic pressure gradients created by Na+ molecules.
Renin sets in motion the serial conversion of blood molecules to form a hormone named angiotensin II. Angiotensin II has several effects. At the glomerulus it boosts the filtration rate. It decreases the diameter of the efferent arteriole hindering blood flow out of the glomerulus, thereby further increasing pressure in the capillaries.
Angiotensin II also improves reabsorption of Na+ and water at the proximal convoluted tubule and stimulates release of another hormone named aldosterone from the adrenal gland, which sits on top of the kidney. Aldosterone works to augment the action of angiotensin II.
Aldosterone’s effect is at the distal tubule and collecting duct of the nephron. There it promotes re-absorption of Na+ into the surrounding blood capillaries. Water is drawn to the blood by the osmotic gradient created by the increase in blood Na+. Blood volume and blood pressure are returned to normal augmenting the sympathetic response of the large artery baroreceptors.
High Blood Volume
When blood expands to a greater than normal volume, pressure in the large arteries and in the atria of the heart rises. Large artery baroreceptors change their activity and the cardiovascular control centers in the brain stem respond. In addition, mechanical stretch of the wall of the atrium causes release of a hormone from cardiac muscle cells named atrial natriuretic peptide [ANP].
ANP travels to the kidney and increases the kidney’s blood filtration rate by altering the diameter of the glomerular arterioles. With higher filtration pressure, more water and Na+ move into the nephrons’ tubules. Large amounts of Na+ in the distal tubules decreases renin secretion by the kidney.
In turn, angiotnesin II and aldosterone secretion shuts down. In the absence of those hormones, ANP works to decrease Na+ and water re-absorption at the distal tubules and collecting ducts. Urinary Na+ and water increase and blood volume decreases.
ANP activity augments the drop in sympathetic and increase in parasympathetic activity initiated by the baroreceptor reflex of the large arteries. ANP causes relaxation of smooth muscle of the arterioles and venules by inhibiting basal release of sympathetic norepinephrine, which opens blood flow to the surface.
A Common Theme in Physiology
Although the heart is autonomous with regard to regular pacing of its contractions and therefore its blood output, it still depends greatly on fine tuning of its operation by the nervous, renal and endocrine systems. The interdependence of the nervous, cardiovascular and endocrine systems is a common theme in physiology.
Action potential and renal physiology are found at:
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Margaret Thompson Reece PhD, physiologist, former Senior Scientist and Laboratory Director at academic medical centers in California, New York and Massachusetts and CSO at Serometrix LLC is now CEO at Reece Biomedical Consulting LLC.
Dr. Reece is passionate about helping students, online and in person, pursue careers in life sciences. Her books “Physiology: Custom-Designed Chemistry” (2012), “Inside the Closed World of the Brain” (2015) and the workbook (2017) companion to her online course “30-Day Challenge: Craft Your Plan for Learning Physiology” are written for those new to life science.More about her books can be found at amazon.com/author/margaretreece.
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