Curariform drugs can cause paralysis of skeletal muscle through different modes of action depending on their molecular properties and the properties of muscle and the myoneural junction. These drugs can be divided into at least three basic types based on their chemical and pharmacological properties: Type I depolarizers that have affinity for acetylcholine receptors and high intrinsic activity, Type II cholinolytics that are competitors with low intrinsic activity, and Type III non-competitors that have affinity for non-acetylcholine receptors and are non-competitive antagonists of acetylcholine. Gradual changes in molecular configuration of these drugs can cause gradual changes between types via intermediates with changing intrinsic activity and affinities.
Curariform drugs can cause paralysis of skeletal muscle through different modes of action depending on their molecular properties and the properties of muscle and the myoneural junction. These drugs can be divided into at least three basic types based on their chemical and pharmacological properties: Type I depolarizers that have affinity for acetylcholine receptors and high intrinsic activity, Type II cholinolytics that are competitors with low intrinsic activity, and Type III non-competitors that have affinity for non-acetylcholine receptors and are non-competitive antagonists of acetylcholine. Gradual changes in molecular configuration of these drugs can cause gradual changes between types via intermediates with changing intrinsic activity and affinities.
Curariform drugs can cause paralysis of skeletal muscle through different modes of action depending on their molecular properties and the properties of muscle and the myoneural junction. These drugs can be divided into at least three basic types based on their chemical and pharmacological properties: Type I depolarizers that have affinity for acetylcholine receptors and high intrinsic activity, Type II cholinolytics that are competitors with low intrinsic activity, and Type III non-competitors that have affinity for non-acetylcholine receptors and are non-competitive antagonists of acetylcholine. Gradual changes in molecular configuration of these drugs can cause gradual changes between types via intermediates with changing intrinsic activity and affinities.
Curariform drugs may have a different mode of action in blocking
neuromuscular transmission and thus in causing paralysis of skeletal muscle.
This mode of action depends on the molecular properties of the drug and on the inherent properties of muscle and myoneural junction.
On basis of their chemical and pharmacological properties, curariform drugs
have to be divided into at least three basic types.
Type I, the cholinomimetics or depolarizers, which have affinity to the ACh-
receptors in the myoneural junction and which as well as ACh have a high intrinsic activity (e.g. suxamethonium).
Type II, the cholinolytics, curarimimetics or competitors, which have affinity
towards the same receptors as Type I drugs but which have a very low intrinsic activity (e.g. D-tubocurarine). Type III, the “non-competitors”, which have affinity towards other than ACh- receptors and which are non-competitive antagonists of ACh (e.g. Prestonal).
The features of these basic types were studied on the isolated frog's rectus abdominis muscle and the nerve-muscle preparation of the cat and the chicken.
Gradual changes in the molecular configuration of curariform drugs cause
gradual changes in the intrinsic activity and the affinitie with consequently gradual changes from the one type to the other via intermediates or mixed type