G Proteins and Smooth Muscle Ca* L-type Ca** channel • The overall effect of Beta 2 agonism in the bronchioles is relaxation due to the Muscarinic 3 SR Ca** (Gq-R Beta 2 activation of cAMP and inhibition of MLCK IP3 Ca* (Gs-R) CM Са"-см CAMP Gi-R MLC ATP MLCK MLCP Relaxation Contraction Rho- kinase CGMP Gq-R NO

Human Anatomy & Physiology (11th Edition)
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Chapter1: The Human Body: An Orientation
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PLEASE EXPLAIN PATHWAYS IN LAYMAN'S TERMS. 

# G Proteins and Smooth Muscle

## Diagram Overview

This diagram illustrates the complex interactions between signaling pathways involved in the contraction and relaxation of smooth muscle, specifically focusing on G proteins. 

### Key Components:

- **L-type Ca++ Channel**: Allows calcium ions (Ca++) to enter the cell, contributing to muscle contraction.
- **Sarcoplasmic Reticulum (SR)**: Stores Ca++ ions; their release is facilitated by the molecule IP3.
- **Muscarinic 3 Receptor (Gq-R)**: Activates the pathway that increases intracellular Ca++, promoting muscle contraction.
- **Beta 2 Receptor (Gs-R)**: Activates cyclic AMP (cAMP), leading to relaxation by inhibiting myosin light chain kinase (MLCK).
- **Gi-R**: Involved in inhibiting cAMP production.

### Pathways:

1. **Contraction Pathway**:
   - Ca++ influx through L-type Ca++ channels and release from the SR.
   - Ca++ binds with calmodulin (CM), forming the Ca++-CM complex.
   - This complex activates MLCK, phosphorylating myosin light chains (MLC), resulting in contraction.

2. **Relaxation Pathway**:
   - cAMP production is activated by the Beta 2 receptor (Gs-R), inhibiting MLCK.
   - Nitric oxide (NO) stimulates cGMP production, activating myosin light chain phosphatase (MLCP), enhancing relaxation.
   - Rho-kinase can inhibit MLCP, modulating the contraction/relaxation balance.

### Notes:

- The diagram highlights how Beta 2 agonism in bronchioles results in relaxation through cAMP activation and MLCK inhibition.
- Relaxation and contraction are tightly regulated through a balance of these signaling molecules and pathways.

This illustration is integral for understanding the molecular basis of smooth muscle physiology and the therapeutic targeting of these pathways in respiratory diseases.
Transcribed Image Text:# G Proteins and Smooth Muscle ## Diagram Overview This diagram illustrates the complex interactions between signaling pathways involved in the contraction and relaxation of smooth muscle, specifically focusing on G proteins. ### Key Components: - **L-type Ca++ Channel**: Allows calcium ions (Ca++) to enter the cell, contributing to muscle contraction. - **Sarcoplasmic Reticulum (SR)**: Stores Ca++ ions; their release is facilitated by the molecule IP3. - **Muscarinic 3 Receptor (Gq-R)**: Activates the pathway that increases intracellular Ca++, promoting muscle contraction. - **Beta 2 Receptor (Gs-R)**: Activates cyclic AMP (cAMP), leading to relaxation by inhibiting myosin light chain kinase (MLCK). - **Gi-R**: Involved in inhibiting cAMP production. ### Pathways: 1. **Contraction Pathway**: - Ca++ influx through L-type Ca++ channels and release from the SR. - Ca++ binds with calmodulin (CM), forming the Ca++-CM complex. - This complex activates MLCK, phosphorylating myosin light chains (MLC), resulting in contraction. 2. **Relaxation Pathway**: - cAMP production is activated by the Beta 2 receptor (Gs-R), inhibiting MLCK. - Nitric oxide (NO) stimulates cGMP production, activating myosin light chain phosphatase (MLCP), enhancing relaxation. - Rho-kinase can inhibit MLCP, modulating the contraction/relaxation balance. ### Notes: - The diagram highlights how Beta 2 agonism in bronchioles results in relaxation through cAMP activation and MLCK inhibition. - Relaxation and contraction are tightly regulated through a balance of these signaling molecules and pathways. This illustration is integral for understanding the molecular basis of smooth muscle physiology and the therapeutic targeting of these pathways in respiratory diseases.
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Before proceeding with the query we must know the following terms-

Beta 2 agonists- They are also known as Beta-2 adrenergic receptor agonists and involve those drugs that are used for the treatment and management of bronchial asthma and COPD  (chronic obstructive pulmonary disease).

Beta-2 adrenergic receptor- This receptor binds to adrenaline (epinephrine) and activates G-proteins, adenylyl cyclase, cAMP, and L-type calcium channels.

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