Class Notes (806,520)
New Zealand (287)
Physiology (14)
PHSL232 (9)
Lecture 3

Lecture 3.docx

5 Pages
Unlock Document

University of Otago
Regis Lamberts

Objectives:  The process and the responsible cellular structures involved in the calcium handling within the cardiomyocytes  Electro-mechanical interaction leading to excitation-contraction coupling, process of excitation-contraction coupling, and physiological consequences of the calcium plateau phase in the ventricular cell  Basics of cardiac metabolism Cardiac Muscle:  SA nodes depolarise spontaneously  propagation of depolarisation wave along specific pathways  Reaches muscle; propagates further, made easy by gap junctions in intercalated discs Depolarisation Wave:  Electrical signal via ions will be transposed into a mechanical activity: overlap in time  Depolarisation  influx of Ca+2 contraction  Repolarisation  decrease of Ca2+  relaxation Excitation-Contraction Coupling: I. Calcium Entry: depolarisation enters gap junctions a. Depolarisation enters gap junctions i. Reaches threshold b. Na+ influx  membrane potential rises  voltage gated ca2+ channels open and Ca2+ moves down its concentration gradient, into the cell c. Cell membrane depolarises: membrane potential rises reaches threshold of L-type Ca2+ channels = DHB receptor L-type Ca2+ channels open  calcium enters the cell from the ECF i. Entering Ca2+ ions trigger release of Ca2+ from intracellular stores in the SR (via the ryanodine receptor (RYR)) NB: There is a higher concentration of calcium both in the ECF and the SR, than intracellularly ii. RYR are calcium release channels, of which the density is greatest near L-type Ca2+ channels, and the distance between the two channels is very short. iii. This process is called Calcium-Induced Calcium Release d. Ca2+ concentration rises 10-100 fold (ECF 2mM, Cytosol 0.1- 1microM, SR 1mM) i. L-type calcium channels are responsible for the release of 25% of calcium entry into the cell, while the other 75% comes through RYR from the SR ii. This keeps the membrane potential higher II. Contraction: a. Ca2+ binds to troponin C in troponin complex b. Tropomyosin moves, actin-myosin interaction c. Tension developed III. Relaxation: end of contraction caused by decrease in Ca2+ concentration a. SR Calcium (ATP-ase) Pump (SERCA) i. ATP dependent active transport ii. Pumps cytoplasmic Ca into the SR (75%) iii. SERCA activated/regulated by phospholamban (PLB) iv. PLB protein is phosphorylated then stimulates Ca2+ uptake b. Sodium-Calcium Exchanger (SCX) i. Na+-Ca2+ exchange pump, driven by the low Na+ concentration inside the cell- for every ONE Ca2+ pumped out, THREE Na+ enter the cell c. Ca2+ ATPase i. Cell membrane ATP dependent pump (1%) ii. Requires Na+ gradient: Na+ moves in as Ca2+ moves out Contraction  Large complex of proteins involved  Troponin/tropomyosin act as regulators  TnC – Troponin C: Ca
More Less

Related notes for PHSL232

Log In


Don't have an account?

Join OneClass

Access over 10 million pages of study
documents for 1.3 million courses.

Sign up

Join to view


By registering, I agree to the Terms and Privacy Policies
Already have an account?
Just a few more details

So we can recommend you notes for your school.

Reset Password

Please enter below the email address you registered with and we will send you a link to reset your password.

Add your courses

Get notes from the top students in your class.