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. They 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 phases that coordinate heart filling and pumping. During late diastole, the heart is relaxed, the AV valves are open, the semilunar valves are closed, and blood flows passively into the ventricles. Atrial systole follows, where the atria contract and push the final 20% of blood into the ventricles while the AV valves stay open. Next, isovolumic ventricular contraction begins as the ventricles contract, the AV valves close, producing the first heart sound (S1), and pressure rises until the semilunar valves open for ventricular ejection. Finally, in isovolumic ventricular relaxation, the semilunar valves close, creating the second heart sound (S2), the AV valves remain closed, and the cycle resets for 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 diffuses through the cell membrane because it does not need a surface receptor. Once inside, the hormone binds to its intracellular receptor located in either the cytoplasm or directly in the nucleus. The hormone–receptor complex then dimerizes and attaches to specific hormone response elements on the DNA, allowing it to activate or suppress gene transcription. These transcription changes alter protein synthesis, producing slower but long-lasting physiological effects in the cell. Steroid hormones such as cortisol, estrogen, and testosterone, along with thyroid hormones, use this nuclear receptor signaling pathway.

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 functional T3 and T4, reducing negative feedback on the hypothalamus and anterior pituitary. As a result, TRH and TSH levels rise, and the excess TSH—being a trophic hormone—continuously stimulates the thyroid, causing it to enlarge and form a goiter. In hyperthyroidism, such as Graves’ disease, autoantibodies act as agonists to the TSH receptor and chronically stimulate the thyroid gland independent of feedback control. This overstimulation causes excessive T3 and T4 production and the symptoms of hyperthyroidism. Despite high thyroid hormone levels, the constant stimulation again enlarges the thyroid, producing a goiter through a different mechanism.