Describe symptoms for the following disorders or mutations with respect to non-c

Question

Describe symptoms for the following disorders or mutations with respect to non-contractile cardiac muscle in the SA node:

An autoimmune disorder that directs antibodies toward nicotinic AChRs, increasing their affinity for ACh.

An autoimmune disorder that directs antibodies toward muscarinic AChRs, increasing their affinity for ACh.

An autoimmune disorder that directs antibodies toward acetylcholine esterase, rendering this enzyme to be non-functional.

Decreased activity of adrenal glands, decreasing the basal level of epinephrine secreted into the bloodstream under normal conditions.

A mutation that shifts the threshold for L-type Ca2+ channel activation to more positive voltages.

A mutation that shifts the threshold for T-type Ca2+ channel activation to more negative voltages.

A mutation that causes troponin to unbind tropomyosin and actin in response to a depolarized membrane potential instead of unbinding in response to Ca2+.

A mutation that increases the rate at which myosin hydrolyzes ATP.

Explanation / Answer

These two effects of acetylcholine are due to two different receptors: nicotinic and muscarinic.

Binding of acetyl choline to nicotinic receptor causes excitation in the skeletal muscles.

If acetylcholine binds to the muscarinic receptor, this interaction inhibits the adenylyl cyclase activity. The cAMP production leads to reduced activation of cAMP-dependent protein kinase; this reduces the heart rate, and contraction strength.

An autoimmune disorder that directs antibodies toward nicotinic AChRs, increasing their affinity for Ach - non-contractile cardiac muscle in the SA node shows faster rhythm, thus heart rate increases.

An autoimmune disorder that directs antibodies toward muscarinic AChRs, increasing their affinity for Ach – Actually muscarinic receptors show negative effect on heart rate, this mutation results in slower rhythm, thus heart rate decreases.

An autoimmune disorder that directs antibodies toward acetylcholine esterase, rendering this enzyme to be non-functional – Ach binds continuously to the receptors, so this mutation will result in increased heart rate.

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