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ppk ppk
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12 years ago
While electrical events in the ventricular contractile cell initiate contraction, intracellular second messengers modify ventricular contractility. Describe the second-messenger pathway that underlies the increase in ventricular contractility.
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Educator
12 years ago
Each of the effects on ventricular contractility are in some way related to changes in calcium or sensitivity to calcium. Hormones can alter contractility by their action on second-messenger systems. Epinephrine and norepinephrine binding to beta adrenergic receptors on the ventricular cell membrane increase the activity of the enzyme adenylate cyclase. Adenylate cyclase catalyzes the conversion of ATP to cyclic AMP (cAMP). cAMP increases the amount of calcium that enters the cell during the contractile cycle by enhancing the amount of calcium that can enter the cell through its sarcolemma calcium channels. This elevation in intracellular calcium will increase the interaction between actin and myosin by exposing more actin molecules through its binding to troponin. At the same time, calcium also triggers an increase in the release of calcium from the sarcoplasmic reticulum.
ppk Author
wrote...
Valued Member
On Hiatus
12 years ago
Each of the effects on ventricular contractility are in some way related to changes in calcium or sensitivity to calcium. Hormones can alter contractility by their action on second-messenger systems. Epinephrine and norepinephrine binding to beta adrenergic receptors on the ventricular cell membrane increase the activity of the enzyme adenylate cyclase. Adenylate cyclase catalyzes the conversion of ATP to cyclic AMP (cAMP). cAMP increases the amount of calcium that enters the cell during the contractile cycle by enhancing the amount of calcium that can enter the cell through its sarcolemma calcium channels. This elevation in intracellular calcium will increase the interaction between actin and myosin by exposing more actin molecules through its binding to troponin. At the same time, calcium also triggers an increase in the release of calcium from the sarcoplasmic reticulum.

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