The effects of nicotine on spontaneous contractions of cat urinary bladder in situ

• Published in: British journal of pharmacology 1984-10, Vol.83 (2), p.347-355
• Main Authors: Koley, Biswanath, Koley, Juthika, Saha, Joy Krishna
• Format: Article
• Language: English
• Subjects: Adenosine Triphosphate - pharmacology; Adrenalectomy; Animals; Atropine - pharmacology; Autonomic Nervous System - drug effects; Biological and medical sciences; Blood Pressure - drug effects; Cats; Epinephrine - pharmacology; Fundamental and applied biological sciences. Psychology; Guanethidine - pharmacology; Hemicholinium 3 - pharmacology; Hexamethonium Compounds - pharmacology; Isoproterenol - pharmacology; Muscle Contraction - drug effects; Muscle Denervation; Muscle, Smooth - drug effects; Nicotine - pharmacology; Norepinephrine - pharmacology; Phentolamine - pharmacology; Phenylephrine - pharmacology; Physostigmine - pharmacology; Propranolol - pharmacology; Quinidine - pharmacology; Spinal Cord - physiology; Urinary Bladder - drug effects; Vertebrates: urinary system
• ISSN: 0007-1188; 1476-5381
• DOI: 10.1111/j.1476-5381.1984.tb16494.x

1 Nicotine and dimethyl‐phenylpiperazinium (DMPP) increased intravesicular pressure and then transiently depressed the spontaneous activity of the urinary bladder in chloralose anaesthetized cats. 2 Adrenaline (5–10 μg kg−1), noradrenaline (5–20 μg kg−1) and isoprenaline (40–50 μg kg−1) which depressed spontaneous urinary bladder activity, were antagonized by the β‐receptor blocking agent propranolol (1 mg kg−1). Phenylephrine (10–30 μg kg−1) was ineffective on the urinary bladder though it increased the systemic blood pressure. This latter effect was blocked by the α‐receptor blocking agent phentolamine (2 mg kg−1). 3 Acetylcholine (2–8 μg 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 μg kg−1) treatment. 4 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. 5 The increased intravesicular pressure induced by nicotine (20–40 μg kg−1) or DMPP (50–100 μg 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 μg kg−1), hemicholinium 3 (2 mg kg−1) or atropine (1 mg kg−1) were also unable to affect the response to nicotine. 6 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 (C1–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 atropine‐resistant 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.