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

Abstract

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.