Question

12 pts - If a heart is removed from the body, its beat rate actually speeds up until sugar reserves dwindle.  

• Discuss how the SA [sinoatrial-pacemaker] node cells manipulate ions at their surface to rhythmically contract.  Be specific about pumps, transporters, and channels.  Make sure your explanation includes setup and recovery back to set-up. Be specific about how the Action Potential passes down the length of the cardiac cell and from one cell to the next.

• Then discuss how the body’s parasympathetic nervous system slows this rate down to a more normal ~65 beats/minute [if the heart is still “hooked up”].  Be clear about all the roles for the various channels, pumps, receptors and allosteric secondary messengers in both normal contraction and slowed contraction. How is the above story manipulated?

• How does the sympathetic system do the opposite and speed the heart up?

Answer 1

The action potential initiated by the SA node travels along the conduction system and spreads out to excite the “working” atrial and ventricular muscle fibers, called contractile fibers. There are following steps which take place during action potential.

Depolarization. Unlike autorhythmic fibers, contractile fibers have a stable resting membrane potential that is close to 90 mV. When a contractile fiber is brought to threshold by an action potential from neighboring fibers, its voltage-gated fast Na channels open. These sodium ion channels are referred to as “fast” because they open very rapidly in response to a threshold-level depolarization. Opening of these channels allows Na in flow because the cytosol of contractile fibers is electrically more negative than interstitial fluid and Na concentration is higher in interstitial fluid. Inflow of Na down the electrochemical gradient produces a rapid depolarization. Within a few milliseconds, the fast Na channels automatically inactivate and Na inflow decreases.

Plateau. The next phase of an action potential in a contractile fiber is the plateau, a period of maintained depolarization. It is due in part to opening of voltage-gated slow Ca2 channels in the sarcolemma. When these channels open, calcium ions move from the interstitial fluid (which has a higher Ca2concentration) into the cytosol. This inflow of Ca2 causes even more Ca2 to  pour out of the sarcoplasmic reticulum into the cytosol through additional Ca2 channels in the sarcoplasmic reticulum membrane. The increased Ca2 concentration in the cytosol ultimately triggers contraction.

Several different types of voltage-gated K Channels are also found in the sarcolemma of a contractile fiber. Just before the plateau phase begins, some of these K channels open, allowing potassium ions to leave the contractile fiber.

Therefore, depolarization is sustained during the plateau phase because Ca2 in flow just balances K outflow. The plateau phase lasts for about 0.25 sec, and the membrane potential of the contractile fiber is close to 0 mV.
By comparison, depolarization in a neuron or skeletal muscle fiber is much briefer, about 1 msec (0.001 sec), because it lacks a plateau phase

Repolarization. The recovery of the resting membrane potential during the repolarization phase of a cardiac action potential resembles that in other excitable cells. After a delay (which is particularly prolonged in cardiac muscle), additional voltage-gated Kchannels open.

Outflow of Krestores the negative resting membrane potential (90 mV). At the same time, the calcium channels in the sarcolemma and the sarcoplasmic reticulum are closing, which also contributes to repolarization.

Parasympathetic nerve impulses reach the heart via the right and left vagus (X) nerves. Vagal axons terminate in the SA node, AV node, and atrial myocardium. They release acetylcholine, which decreases heart rate by slowing the rate of spontaneous depolarization in autorhythmic fibers. As only a few vagal fibers innervate ventricular muscle, changes in parasympathetic activity have little effect on contractility of the ventricles.

Sympathetic neurons extend from the medulla oblongata into the spinal cord. From the thoracic region of the spinal cord, sympathetic cardiac accelerator nerves extend out to the SA node, AV node, and most portions of the myocardium. Impulses in the cardiac accelerator nerves trigger the release of norepinephrine, which binds to beta-1 (1) receptors on cardiac muscle fibers.

This interaction has two separate effects: (1) In SA (and AV) node fibers, norepinephrine speeds the rate of spontaneous depolarization so that these pacemakers fire impulses more rapidly and heart rate increases; (2) incontractile fibers throughout the atria and ventricles, norepinephrine enhances Ca2entry through the voltage-gated slow Ca2channels, thereby increasing contractility.