Target type: biologicalprocess
The process in which an SA node cardiac muscle cell membrane potential changes in the direction from the positive membrane potential at the peak of the action potential towards the negative resting potential. [GOC:BHF, GOC:dph, GOC:mtg_cardiac_conduct_nov11]
Membrane repolarization during sinoatrial (SA) node cell action potential is a crucial step in regulating heart rate and rhythm. It occurs after the peak of the action potential, when the membrane potential rapidly transitions from a positive value back towards the resting potential. Here's a detailed explanation of the process:
1. **Sodium Channel Inactivation:** As the action potential reaches its peak, sodium channels responsible for the rapid depolarization phase begin to inactivate. This means that they close, preventing further influx of sodium ions.
2. **Calcium Channel Deactivation:** The influx of calcium ions through L-type calcium channels, which contributes to the plateau phase of the action potential, starts to decline. This is due to both the inactivation of these channels and the decrease in the driving force for calcium entry as the membrane potential becomes more negative.
3. **Potassium Channel Activation:** The key players in repolarization are potassium channels, particularly the delayed rectifier potassium channels (IKr) and the inward rectifier potassium channels (IK1). These channels open in response to the membrane depolarization and allow potassium ions to flow out of the cell.
4. **Outward Potassium Current:** The efflux of potassium ions through these channels creates an outward potassium current, which drives the membrane potential back towards the negative resting potential. This outward current counteracts the inward currents carried by sodium and calcium ions.
5. **Repolarization Rate:** The rate of repolarization is influenced by the kinetics of the potassium channels involved. The faster the channels open and close, the faster the repolarization.
6. **Resting Potential:** As the potassium current continues, the membrane potential eventually reaches the resting potential. This marks the end of the action potential and the beginning of a new cycle.
7. **Role of the Funny Current (If):** While not directly involved in repolarization, the funny current (If) plays a significant role in the subsequent depolarization phase, contributing to the spontaneous firing of the SA node.
In summary, membrane repolarization during SA node cell action potential is a carefully orchestrated process that relies on the inactivation of sodium and calcium channels, the activation of potassium channels, and the resulting efflux of potassium ions. This process ensures the rapid and efficient recovery of the membrane potential, allowing the SA node to maintain its pacemaker function and regulate heart rhythm.'
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| Protein | Definition | Taxonomy |
|---|---|---|
| Potassium voltage-gated channel subfamily A member 5 | A voltage-gated potassium channel subunit KCNA5 that is encoded in the genome of human. [] | Homo sapiens (human) |
| Compound | Definition | Classes | Roles |
|---|---|---|---|
| N-(2-aminoethyl)-5-chloro-1-naphthalenesulfonamide | naphthalenes; sulfonic acid derivative | ||
| 5-methoxypsoralen | 5-methoxypsoralen : A 5-methoxyfurocoumarin that is psoralen substituted by a methoxy group at position 5. 5-Methoxypsoralen: A linear furanocoumarin that has phototoxic and anti-inflammatory properties, with effects similar to METHOXSALEN. It is used in PUVA THERAPY for the treatment of PSORIASIS. | 5-methoxyfurocoumarin; organic heterotricyclic compound; psoralens | hepatoprotective agent; plant metabolite |
| flecainide | flecainide : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of 2,5-bis(2,2,2-trifluoroethoxy)benzoic acid with the primary amino group of piperidin-2-ylmethylamine. An antiarrhythmic agent used (in the form of its acetate salt) to prevent and treat tachyarrhythmia (abnormal fast rhythm of the heart). Flecainide: A potent anti-arrhythmia agent, effective in a wide range of ventricular and atrial ARRHYTHMIAS and TACHYCARDIAS. | aromatic ether; monocarboxylic acid amide; organofluorine compound; piperidines | anti-arrhythmia drug |
| lidocaine | lidocaine : The monocarboxylic acid amide resulting from the formal condensation of N,N-diethylglycine with 2,6-dimethylaniline. Lidocaine: A local anesthetic and cardiac depressant used as an antiarrhythmia agent. Its actions are more intense and its effects more prolonged than those of PROCAINE but its duration of action is shorter than that of BUPIVACAINE or PRILOCAINE. | benzenes; monocarboxylic acid amide; tertiary amino compound | anti-arrhythmia drug; drug allergen; environmental contaminant; local anaesthetic; xenobiotic |
| nifedipine | Nifedipine: A potent vasodilator agent with calcium antagonistic action. It is a useful anti-anginal agent that also lowers blood pressure. | C-nitro compound; dihydropyridine; methyl ester | calcium channel blocker; human metabolite; tocolytic agent; vasodilator agent |
| sertindole | sertindole : A phenylindole that is 1H-indole which is substituted on the nitrogen by a p-chlorophenyl group, at position 5 by chlorine, and at position 3 by a piperidin-4-yl group, which is itself substituted on the nitrogen by a 2-(2-oxoimidazolidin-1-yl)ethyl group. | heteroarylpiperidine; imidazolidinone; organochlorine compound; organofluorine compound; phenylindole | alpha-adrenergic antagonist; H1-receptor antagonist; second generation antipsychotic; serotonergic antagonist |
| 4'-methoxyflavone | 4'-methoxyflavone: from seeds of Psoralea corylifolia (Fabaceae); structure in first source | ether; flavonoids | |
| senicapoc | senicapoc: a Gardos channel blocker; structure in first source | ||
| quinidine | quinidine : A cinchona alkaloid consisting of cinchonine with the hydrogen at the 6-position of the quinoline ring substituted by methoxy. Quinidine: An optical isomer of quinine, extracted from the bark of the CHINCHONA tree and similar plant species. This alkaloid dampens the excitability of cardiac and skeletal muscles by blocking sodium and potassium currents across cellular membranes. It prolongs cellular ACTION POTENTIALS, and decreases automaticity. Quinidine also blocks muscarinic and alpha-adrenergic neurotransmission. | cinchona alkaloid | alpha-adrenergic antagonist; anti-arrhythmia drug; antimalarial; drug allergen; EC 1.14.13.181 (13-deoxydaunorubicin hydroxylase) inhibitor; EC 3.6.3.44 (xenobiotic-transporting ATPase) inhibitor; muscarinic antagonist; P450 inhibitor; potassium channel blocker; sodium channel blocker |
| (2'-(benzyloxycarbonylaminomethyl)biphenyl-2-carboxylic acid 2-(2-pyridyl)ethylamide) | biphenyls | ||
| acacetin | 5,7-dihydroxy-4'-methoxyflavone : A monomethoxyflavone that is the 4'-methyl ether derivative of apigenin. | dihydroxyflavone; monomethoxyflavone | anticonvulsant; plant metabolite |
| clathrodin | clathrodin: structure given in first source; isolated from marine sponges of the genus Agelas | ||
| oroidin | oroidin: from marine sponges of the genus Agelas; structure in first source | pyrroles; secondary carboxamide | metabolite |
| hymenidin | hymenidin: serotonergic receptor antagonist from Okinawan marine sponge Hymeniacidon; structure given in first source | ||
| a 1899 | A 1899: a TASK-1 potassium channel blocker; structure in first source | ||
| [[(1S,2S,5R)-5-methyl-2-propan-2-ylcyclohexyl]-phenylphosphoryl]benzene | monoterpenoid |