The effects of nicotine on spontaneous contractions of cat urinary bladder in situ.
Nicotine and dimethyl-phenylpiperazinium (DMPP) increased intravesicular pressure and then transiently depressed the spontaneous activity of the urinary bladder in chloralose anaesthetized cats. Adrenaline (5-10 micrograms kg-1), noradrenaline (5-20 micrograms kg-1) and isoprenaline (40-50 micrograms kg-1) which depressed spontaneous urinary bladder activity, were antagonized by the beta-receptor blocking agent propranolol (1 mg kg-1). Phenylephrine (10-30 micrograms kg-1) was ineffective on the urinary bladder though it increased the systemic blood pressure. This latter effect was blocked by the alpha-receptor blocking agent phentolamine (2 mg kg-1). Acetylcholine (2-8 micrograms kg-1) caused a marked fall in systemic blood pressure, which was potentiated by physostigmine, but failed to produce any response on the intravesicular pressure even after physostigmine (50-100 micrograms kg-1) treatment. ATP (2 mg kg-1) produced an increase in intravesicular pressure accompanied by a fall in systemic blood pressure. The increased intravesicular pressure was antagonized by quinidine (20 mg kg-1); however, the fall in blood pressure remained unaltered. The increased intravesicular pressure induced by nicotine (20-40 micrograms kg-1) or DMPP (50-100 micrograms kg-1) was not affected by phentolamine (2 mg kg-1), propranolol (1 mg kg-1) or guanethidine (15-20 mg kg-1). Physostigmine (50-100 micrograms kg-1), hemicholinium 3 (2 mg kg-1) or atropine (1 mg kg-1) were also unable to affect the response to nicotine. Hexamethonium (1 mg kg-1), reduced the amplitude of spontaneous bladder contractions and quinidine (20 mg kg-1) abolished the effect of nicotine. 7 Bilateral sectioning of the cervical sympathetic or hypogastric nerves did not alter the effect of nicotine or DMPP. Higher spinal cord transection (Cl-C2) blocked the spontaneous, as well as the nicotine- and DMPP-induced, contractions of the bladder. 8 It is concluded that the increase in intravesicular pressure induced by nicotine is atropineresistant and is not mediated either through adrenergic or cholinergic mechanisms. It is probable that a purinergic mechanism is involved, via the activation of P2-receptors present in the urinary bladder.
D000255:Adenosine Triphosphate / Q000494:pharmacology; D000315:Adrenalectomy; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001341:Autonomic Nervous System / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects; D002415:Cats; D004837:Epinephrine / Q000494:pharmacology; D006145:Guanethidine / Q000494:pharmacology; D006426:Hemicholinium 3 / Q000494:pharmacology; D006584:Hexamethonium Compounds / Q000494:pharmacology; D007545:Isoproterenol / Q000494:pharmacology; D009119:Muscle Contraction / Q000187:drug effects; D009121:Muscle Denervation; D009130:Muscle, Smooth / Q000187:drug effects*; D009538:Nicotine / Q000494:pharmacology*; D009638:Norepinephrine / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D010830:Physostigmine / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D011802:Quinidine / Q000494:pharmacology; D013116:Spinal Cord / Q000502:physiology; D001743:Urinary Bladder / Q000187:drug effects*
D006584:Hexamethonium Compounds; D010656:Phenylephrine; D006426:Hemicholinium 3; D009538:Nicotine; D001285:Atropine; D000255:Adenosine Triphosphate; D010830:Physostigmine; D011433:Propranolol; D011802:Quinidine; D007545:Isoproterenol; D009638:Norepinephrine; D004837:Epinephrine; D010646:Phentolamine; D006145:Guanethidine