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Biomedical subjects

J Koley

Publications and source records attributed to J Koley.

27 records · Page 2Linked to original sources
PubMed1984

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.

Adenosine Triphosphate↗
PubMed1984

Positive inotropic effect of nicotine on electrically evoked contraction of isolated toad ventricle.

The mechanism of the responses of nicotine on electrically evoked contractions of the isolated spirally cut toad ventricle was investigated. Nicotine produced a concentration-dependent positive inotropic effect of the ventricle. Prior administration of propranolol, hexamethonium, hemicholinium-3 or guanethidine failed to antagonize the positive inotropic effect of nicotine, thus ruling out the possibility of the nicotine effect being mediated through activation of beta-adrenoceptors, ganglionic activation, presynaptic liberation of acetylcholine and liberation of norepinephrine from the sympathetic nerve endings respectively. The positive inotropic effect is probably mediated through mobilisation of calcium since prior incubation with verapamil--the calcium transport blocker, EDTA, which chelates the extracellular calcium and calcium-free Ringer prevented the positive inotropic effect of nicotine. These results suggest that the positive intropic effect of nicotine may presumably be due to the facilitating effects of nicotine on Ca++ exchange or mobilisation of membrane bound Ca++.

Animals↗
PubMed1982

Visceral receptors and their afferents in the caudal mesenteric nerve of the duck.

1. The behaviour and reactivities of visceral receptors to different mechanical and chemical stimuli in simple unit preparations from the caudal mesenteric nerve of adult ducks were studied to examine the physiological roles of such receptors. 2. In total, 83 single unit activities were recorded from the caudal mesenteric nerve. 3. Receptors were grouped according to their locations in different layers of the rectum as (i) over the branching points of the blood vessel or in the serosal layer, (ii) in the muscle layer or (iii) in the mucous membrane of the rectum. 4. All the receptors, both spontaneous and non-spontaneous, responded to mechanical probing. Receptors of the muscle layer responded to distension also and showed a slowly-adapting nature. Most of the receptors of the other two groups were of the rapidly-adapting type. 5. Conduction velocity ranged from 0.76 to 34.6 m/s. 6. Sympathetic afferent fibres from the hind gut ascend along the intestinal nerve and join the caudal mesenteric nerve via the colonic ganglion.

Animals↗
PubMed1977

Effects of bradykinin mediated by autonomic efferent nerves.

Intra-arterial injections of bradykinin cause increases in blood pressure and increased impulse rates in single sympathetic efferent fibres. The peptide also causes one or more large bladder contractions, which are associated with increased impulse rates in pelvic nerve efferent fibres whose spontaneous discharges are temporally associated with increases in intravesical pressure. These induced increases in pelvic nerve discharge and intravesical pressure could be abolished or greatly reduced by interference with conduction in pathways which mediate reflex bladder contractions. It is concluded that bradykinin has little direct action on the bladder, and that the large contractions which result from its administration are mediated by the central nervous system.

Action Potentials↗
PubMed1977

The effects of bradykinin on afferent units in intra-abdominal sympathetic nerve trunks.

The effects of intra-arterial injections of bradykinin on afferent discharges in the splanchnic and hypogastric nerves have been studied. All units which were excited by the peptide were mechanosensitive. Following i.a. bradykinin, the slowly adapting mechanoreceptors associated with the bladder showed increased discharge rates which appear to be related to changes in intravesical pressure. When the effects of bradykinin on the bladder were blocked by cord cooling, the afferents were not excited. It is concluded that bradykinin causes discharges in the slowly adapting mechanoreceptors around the bladder because it causes bladder contractions, and not because of any chemosensitivity of the nerve ending.

Action Potentials↗
PubMedDate not supplied

Effect of ATP on smooth muscle of toad urinary bladder.

Adenosine 5'-triphosphate (ATP), at a dose range of 1.8 to 116 microM, produced an initial phasic contraction followed by a rhythmic contraction in urinary bladder smooth muscle of the toad (Bufo melanostictus). Acetylcholine produced a rhythmic contraction which was antagonized by atropine (1.5 microM) and potentiated by neostigmine (1.7 microM), indicating activation of muscarinic receptors. However, both phasic and rhythmic components of ATP contraction were atropine-resistant. Quinidine (26-264 M) abolished the responses to ATP and acetylcholine, while indomethacin (28 microM) and theophylline (55 microM) antagonized only the acetylcholine responses. Repeated application of alpha, beta-methylene ATP desensitized the receptors and completely abolished contraction. ATP did not produce a phasic contraction in alpha, beta-methylene ATP-desensitized tissue, indicating that both ATP and its alpha, beta-methylene analogue occupy the same receptor site for phasic contraction. On the other hand, the rhythmic contraction induced by ATP remained unaffected in alpha, beta-methylene ATP-treated tissue. The phasic contraction in response to ATP can be blocked by verapamil (4 microM), but rhythmic contraction can only be abolished by a high concentration of verapamil (16 microM). Moreover, ATP produced no response in Ca+(+)-free or EGTA-containing solution, showing thereby that contractile responses to ATP are dependent upon extracellular Ca(+)+. These results indicate that the phasic component is a P2x-receptor-activated response while the rhythmic component might be an opening of calcium ion channels, either by depolarization of the membrane or by some unknown mechanism.

Acetylcholine↗