AP151 LEC Short Essays 4

AP 151 LEC

What are the autorythmic cells? Do they need innervation to depolarize? Can you describe the action potential of these cells? Where are these cells located in the heart? Do they all depolarize at the same rate? What actions does the autonomic nervous system have on these cells?

Autorythmic cells are specialized cardiac cells that can spontaneously depolarize without innervation, setting the rhythm of the heart. They are located primarily in the SA node, AV node, and along the conduction pathways. Their action potential begins with a gradual depolarization from sodium influx, followed by calcium influx that triggers contraction, and repolarization through potassium efflux. These cells do not all depolarize at the same rate; the SA node sets the fastest pace, while others follow more slowly. The autonomic nervous system modulates its activity: sympathetic stimulation increases the depolarization rate to speed heart rate, while parasympathetic stimulation slows it to reduce heart rate.

Can you describe the different phases of the cardiac cycle? What is occurring? When are the different valves open? When do they close? Where are the heart sounds? 

The cardiac cycle has five main phases. Late diastole occurs when the heart is at rest; AV valves are open, semilunar valves closed, and blood passively fills the ventricles. During atrial systole, the atria contract, pushing the last 20% of blood into the ventricles; the AV valves remain open. Isovolumic ventricular contraction begins as the ventricles contract, the AV valves close, and the first heart sound (S1) is heard. In ventricular ejection, the semilunar valves open, the AV valves stay closed, and blood is pumped into the arteries. Finally, isovolumic ventricular relaxation occurs as the ventricles relax, the semilunar valves close, producing the second heart sound (S2), and the AV valves remain closed until the next filling phase.

When would you see the RAAS pathway activated? Can you describe the events of this pathway?

The RAAS pathway is activated when blood pressure is low, causing decreased stretch on specialized kidney cells, which release renin. Renin converts angiotensinogen, a liver-produced precursor, into angiotensin I. Angiotensin I is then converted to angiotensin II by ACE on the surface of the lungs. Angiotensin II has two major effects: it causes vasoconstriction, increasing total peripheral resistance, and it stimulates the adrenal cortex to release aldosterone, which promotes sodium and water reabsorption in the kidneys, increasing blood volume. Together, these effects raise blood pressure back toward homeostatic levels, and once pressure is normalized, renin release decreases.

What is the baroreceptor reflex, and how does it operate in regulating blood pressure? 

The baroreceptor reflex is a rapid feedback system that helps maintain blood pressure. Baroreceptors in the carotid sinus and aortic arch detect changes in arterial pressure and send signals to the medulla oblongata. The vasomotor center regulates total peripheral resistance, while the cardiac center adjusts heart rate and contractility. This reflex is more sensitive to decreases in blood pressure and responds best to sudden changes. When blood pressure falls, sympathetic activity increases to raise heart rate, contractility, and cause vasoconstriction, while increases in pressure trigger parasympathetic activity to lower these variables

Can you describe the process of signaling through a nuclear receptor? What are some hormones that can signal through this mechanism?

Signaling through a nuclear receptor begins when a lipid-soluble hormone, like a steroid or thyroid hormone, diffuses through the cell membrane and binds to a specific intracellular receptor in the cytoplasm or nucleus. The hormone–receptor complex then binds to hormone response elements on DNA, which activates or represses gene transcription. This process leads to changes in protein synthesis that alter cell function. Steroid hormones, such as cortisol, estrogen, and testosterone, as well as thyroid hormones, use this signaling mechanism. Overall, nuclear receptor signaling allows hormones to regulate gene expression and long-term cellular responses.

How might someone with hypothyroidism (low iodine) develop a goiter? How might someone with hyperthyroidism (Graves’ disease) also have a goiter? Please explain your answer using the feedback loop for thyroid hormone. 

In hypothyroidism caused by low iodine, the thyroid cannot produce enough T3 and T4. Low thyroid hormone levels fail to inhibit the hypothalamus and anterior pituitary, so TRH and TSH levels increase. The elevated TSH continuously stimulates the thyroid, causing it to enlarge and form a goiter. In hyperthyroidism, such as Graves’ disease, autoantibodies act as TSH agonists and chronically stimulate the thyroid independently of the feedback loop. This constant stimulation also enlarges the thyroid, producing a goiter, even though T3 and T4 levels are high.