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Beta1-Gs.html
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<html>
<head>
<META HTTP-EQUIV="Content-Type" CONTENT="text/html; charset=iso-8859-1">
<META NAME="Author" CONTENT="Michael B. Bolger">
<META NAME="Classification" CONTENT="educational">
<META NAME="Description" CONTENT="For Students in the Level III Therapeutics III Course at USC School of Pharmacy">
<META NAME="KeyWords" CONTENT="autonomic pharmacology nervous system drug receptor">
<TITLE>beta1-Adrenergic Receptor</TITLE>
</head>
<body>
<H3>beta1 - Adrenergic Receptors (NE)</H3>
<IMG SRC="images/Beta1-Gs.jpg" WIDTH=600 HEIGHT=431 Target="_top">
<P><u>Activation of adenylyl cyclase by agonists that bind to beta1-adrenergic receptors</u>.<br>
Binding to beta1-adrenoceptors stimulates adenylyl cyclase by
activating the stimulatory G protein, Gs, which leads to the dissociation of its
alpha subunit charged with GTP. This alpha subunit directly activates adenylyl cyclase,
resulting in an increased rate of synthesis of cAMP. These catalytic
units also phosphorylate the cAMP response element binding protein (CREB), which modifies
gene expression.<br>
beta1-adrenergic receptors cause <b>actions in the heart</b> in the following manner:<br>
<ul>
<li>Heart SA node: increase in heart rate.
<li>Heart AV node: increase in automaticity and conduction velocity
<li>Heart Atria and Ventricles: increase in contractility and conduction velocity
<li>Kidney: increased Renin Secretion
</ul>
<P>
Adapted from Figure 9-2: StatRef Online Library: Basic and Clinical Pharmacology 8th ed. (2001)<br>
by Michael Bolger, 8/24/04<br>
Copyright(c) 2001 The McGraw Hill Companies, Inc. All rights reserved
<P>
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<i>Last updated 8/26/01</i><br>
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