Ganglionic stimulating drugs

The answer is d. (Hardman, pp 142—M3.) ACh will stimulate both muscarinic and nicotinic receptors. Skeletal muscle contraction is mediated through NM receptors, and ganglionic stimulation is an effect of NN receptors All of the other effects listed in the question occur following muscarinic receptor activation and will be blocked by atropine and scopolamine, both of which are muscarinic receptor antagonists. Skeletal muscle contraction will not be affected by these drugs rather, a neuromuscular blocker (e.g., tubocurarine) is required to antagonize this effect of ACh. 

Levamisole (and its racemate tetramisole) leads to worm paralysis by ganglionic stimulation via acetylcholine. It is curious that the drug produces a depolarizing neuromuscular blockade in vertebrates. Levamisole is used in ascariasis outside the United States. The drug also is said to have immunostimulant properties, and it has been approved in the United States (1990) for such indications. As a thymomimetic in mice it tends to restore T-cell immune responses to normal. 

Dopamine is found in every sympathetic neuron and ganglion in the CNS. As a drug, and in addition to stimulation of dopaminergic receptors, dopamine indirectly stimulates both a- and )3-adrenoreceptors. Dopamine also causes a release of endogenous norepinephrine. The mechanism of action is based on the excitatory effect on )3-adrenoreceptors (in low and moderate doses), as well as on a-adrenoreceptors (in large doses). It has a positive inotropic effect on the heart, increases blood supply, selectively widens renal and mesenteric blood vessels, does not elevate blood pressure, and slightly increases the frequency of heartbeats. 

Agonist 1 increases HR, presumably through direct activation of cardiac P receptors because the effect is blocked by propranolol but is not influenced by the alpha blocker (prazosin), the ganglion blocker (trimethaphan), or blockade of M receptors (atropine). Only two of the listed drugs directly activate cardiac receptors epinephrine and norepinephrine. For NE, any direct cardiac stimulation is counteracted by reflex bradycardia resulting from the increase in mean BP via its activation of a, receptors in blood vessels (it has no effects... 

---