# CALCIUM MOVEMENTS IN EXCITATION-CONTRACTION COUPLING

> **NIH NIH R01** · RUSH UNIVERSITY MEDICAL CENTER · 1990 · $119,394

## Abstract

The transduction of action potential to muscle contraction (EC coupling) is
an example of fast communication between cell membrane events and metabolic
state.  As in many systems, the central messenger of this coupling is
calcium, which in muscle is released from the Sarcoplasmic Reticulum (SR)
to activate contractile proteins.  Our goal is to understand quantitatively
these Ca movements.

The release channels of the SR are controlled by changes in potential at
the plasma and T-tubular membrane in an ill-understood way, involving a
voltage sensor in the T-tubular membrane and an unknown mechanism of
communication between voltage sensor and release channel (T-SR coupling).
We can measure the main variables of the EC coupling steps:  charge
movement currents associated to the voltage senor, the rapid change in
myoplasmic [Ca] and Ca flux through the release channel.  The transverse
tubular membrane of muscle has a ('slow') CA channel, of no known
functional role, in large numbers.  Our results suggest that the slow Ca
channel is intimately related to charge movement and Ca release.  We plan
to study charge movement, seeking a unified model of its many described
componennts to clarify its relationship to CA release.  We will compare in
detail the pharmacology of the slow Ca channel and the EC coupling events
to test the hypothesis that the slow Ca channel is involved in EC
coupling.  If this is the case a role in T-SR coupling will be sought for
the Ca channel and the current carried by the channel.  We will study the
slow Ca channel reconsituted in artificial bilayer membranes to
characterize its properties in better defined ionic conditions.  We will
compare the merits of three proposed mechanism of T-SR coupling:  a
mechanical link, calcium, and IP3 as a transmitter.  This will be done by
introducing changes in the intracellular medium that selectively interfere
with the proposed mechanisms, including a fast Ca buffer and a blocker of
IP3 metabolism.

Release of Ca and its removal by proteins and the SR pump are the main
fluxes involved in Ca regulation.  Progress in the study of one flux
generates and requires more knowledge about the other.  The relationship
between CA removal fluxes and an intrinsic optical signal generated by the
muscle will be studied.  The Ca binding protein pravalbumin will be
introduced into muscle fibers to test its role in the intrinsic signal and
in the process of removal that eventually closes the cycle of calcium
movements.

## Key facts

- **NIH application ID:** 3156413
- **Project number:** 5R01AR032808-08
- **Recipient organization:** RUSH UNIVERSITY MEDICAL CENTER
- **SAM.gov UEI:** C155UU2TXCP3
- **Principal Investigator:** Eduardo Rios
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1990
- **Award amount:** $119,394
- **Award type:** 5
- **Project period:** 1983-07-01 → 1991-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3156413

## Citation

> US National Institutes of Health, RePORTER application 3156413, CALCIUM MOVEMENTS IN EXCITATION-CONTRACTION COUPLING (5R01AR032808-08). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3156413. Licensed CC0.

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