Atropine in the strictest sense does not an inhibit the action of acetylcholine (i.e. it does not cause any changes in the activity/structure of acetylcholine itself). It is an antagonist to acetylcholine receptors, thus competing with acetylcholine for binding sites and increases the amount of acetylcholine needed to reach Kd, as can be seen on a graded dose-response curve.

Atropine acts on only muscarinic acetylcholine receptors (turbocurare works on nicotinic acetylcholine receptors). Skeletal muscle only works through nicotinic acetylcholine receptors, so atropine would do little to stop the uncontrolled spasms associated with organoflourophosphates (nerve gas). Atropine would counteract the effects of nerve gas on smooth muscle (muscarinic receptors), but these contractions are slow and would not be spasmodic.

The primary therapeutic effect of atropine in the event of nerve gas poisoning is the prevention of heart failure. Acetylcholine acts through muscarinic receptors in the heart to slow down heart rate. Thus, addition of atropine stimulates an increase of heart rate, preventing heart failure.

Muscarinic acetylcholine receptors are pervasive throughout the body, including the GI tract, urinary tract, and sweat glands. Antagonism of these receptors by atropine causes GI malfunction (lack of GI and bladder tone causes constipation and the the inability to urinate, respectively). Inactivation of muscarinic sweat receptors causes a decreased secretion of sweat. All of these side effects make atropine therapy extremely unpleasant for the patient. Thus, atropine is unpopular as a clinical therapeutic, and is reserved for more extreme uses (such as nerve gas poisoning).