Observations on an isolated, innervated preparation of rat urinary bladder

TL;DR: The innervation of the feline bladder and urethra was studied by a histochemical fluorescence technique and the use of peripheral nerve stimulations in combination with different blocking agents to observe a change in adrenergic innervation.

TL;DR: A detailed account of the early developments and current status of purinergic signalling is presented and the current knowledge on purinoceptors, their distribution and role in signal transduction in various tissues in physiological and pathophysiological conditions is summarized.

TL;DR: The results suggest that the insensitivity of the rat bladder to ATP is due to its rapid degradation to AMP and adenosine and support the hypothesis that the bladder receives a purinergic excitatory innervation.

TL;DR: The observations suggest that the inhibition by conotoxin of the Ca2+ influx required for excitation‐secretion coupling in autonomic nerve terminals is not absolute, and can be overcome by repeated stimulation or by raising theCa2+ concentration.

TL;DR: The experiments to be described have been concerned with the effect of vagus stimulation in the isolated heart and auricles of the rabbit and the action of cocaine, of hexamethonium and of the cardiac glycoside ouabain was studied.

TL;DR: In the intestine corroborative evidence provided by anticholinesterases and by botulinum toxin strongly suggests that the nerve endings concerned are cholinergic, and therefore supports the theory put forward by Dale and Gaddum that this type of atropine-resistance is due to "proximity" of the nerves endings to the effector cells.

TL;DR: The tissue in the neighborhood of the post-ganglionic sympathetic fibers (this tissue most probably being the terminations of the fibers themselves) can take up noradrenaline from the blood or from the surrounding fluid, and it is probably also derived from the nordrenaline released into the blood stream by the adrenaline medulla.