The response to atropine, hexamethonium, nicotine, emepronium bromide and some adrenergic compounds has been studied on the urinary bladder of the rabbit and the cat. It was shown that atropine caused a very small or no reduction in the response to electrically stimulated parasympathetic nerves in the urinary bladder of the rabbit. In the cat a dose dependent blockade was obtained after atropine administration. The stimulating response was abolished by hexamethonium or nicotine, suggesting that there are nicotinic receptors in the parasympathetic pathway. It is possible that the parasympathetic nerves running to the rabbit urinary bladder end in such nicotinic receptors on the effector cells in the detrusor muscle. Emepronium bromide, a potent anticholinergic compound, used clinically as a urological drug, was found to block the stimulatory response, which was interpreted as an effect on parasympathetic nicotinic receptors. Experiments with isoprenaline, adrenaline and noradrenaline showed that there are adrenergic α‐ and β‐receptors in the urinary bladder of the rabbit.
ROTHLIN showed in 1923 that the fall in blood pressure caused by stimulation of the depressor nerves in, the rabbit was greatly diminished by ergotamine. HEYMANS and REGNIERS (1929) studied the effect of ergotamine on the sinus reflexes and found that while the vasomotor reflexes from the sinus region were suppressed by ergotamine (0.25 nig ergotamine tartrate pr kg) in the dog, the cardio-inhibitory reflexes persisted or were even temporarily reinforced. Using smaller doses, 0.1-0. I 5 mg/kg in the cat, WRIGHT (1930) was able t o state that the vasomotor reflexes from the sinus were abolished, though the dose of ergotamine was not sufficient to suppress the effect of injected adrenaline or else block the peripheral vasomotor mechanism. On the other hand central asphyxia was still active i n producing a rise in blood-pressure. He therefore drew the conclusion that ergotamine inhibited the central transmission of impulses on the afferent side of the vasomotor centre. HEYMANS, REGNIERS and BOUCKAERT (1930), in a continuation of their previous study, showed that when 0.26 mg ergotamine tartrate per kg was injected into a dog, the head of which was perfused by another dog, occlusion and opening of the common carotids leading to the perfused head had no effect on the blood pressure of the rest of the body. The animal was in this case insensitive even t o injected adrenaline, however. 04 the other hand a similar dose of ergotarnine injected into the
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