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PubMed1991

Endothelin modulation of neuroeffector transmission in smooth muscle.

In a series of muscle preparations, the peptides endothelin-1 (ET-1) and endothelin-3 (ET-3) were investigated for effects on basal muscle tone, responses to transmural nerve stimulation, and release of [3H]norepinephrine or [3H]acetylcholine. ET-1 and ET-3 contracted rat vas deferens and guinea pig ileum, ET-1 being the most potent. In the guinea pig taenia coli, ET-1 induced a relaxation whereas ET-3 was almost without relaxing effect. In the rat vas deferens, ET-1 and ET-3 enhanced contractile responses to nerve stimulation, whereas the nerve-induced release of [3H]norepinephrine was inhibited by ET-1 but not by ET-3. Contractions to exogenous ATP were increased by ET-1 whereas contractions to norepinephrine were not. In the guinea pig ileum, nerve-induced contractions were inhibited by ET-1 and ET-3 as was acetylcholine release, whereas contractions to exogenous acetylcholine were enhanced by ET-1. The inhibition of nerve-induced contractions by the endothelins was not affected by treatment with 8-(p-sulfophenyl)theophylline, BW755C, or indomethacin. The relaxation by ET-1 in the guinea pig taenia coli was not affected by treatment with NG-monomethyl-L-arginine, BW755C, or indomethacin. In conclusion, ET-1 exerted a stimulatory postjunctional effect and concomitantly an inhibitory prejunctional effect on adrenergic and cholinergic neurotransmission. Also, ET-3 exerted a stimulatory postjunctional effect, whereas a prejunctional inhibitory effect of ET-3 only was evident on cholinergic neurotransmission. Blockade of the production of nitric oxide or arachidonic acid metabolites or application of an adenosine antagonist did not alter the effects of ET-1 or ET-3.

Acetylcholine↗
PubMed1988

Presynaptic P1-purinoceptors in jejunal branches of the rabbit mesenteric artery and their possible function.

1. Excitatory junction potentials (EJPs) evoked by nerve stimulation with fifteen pulses at 1 Hz were recorded from smooth muscle cells of the rabbit isolated mesenteric artery. The effects of P1-purinoceptor agonists and antagonists, as well as of substances which interfere with the inactivation of endogenous adenosine, were tested. 2. Adenosine and its analogues depressed the EJPs in the train in a concentration-dependent manner. The percentage inhibition of the first EJP and that of the later ones was similar; some early EJPs, however, were inhibited more markedly. The rank order of potency of the agonists was (-)-N6-(R-phenylisopropyl)-adenosine (R-PIA) congruent to 5'-N-ethylcarboxamidoadenosine (NECA) greater than (+)-N6-(S-phenylisopropyl)-adenosine (S-PIA) greater than adenosine. The respective IC40 values (the concentrations producing 40% inhibition of the first EJP in the train) were 0.018, 0.028, 0.83 and 4.7 mumol/l. 3. Three methylxanthines, namely 8-phenyltheophylline (1, 10 mumol/l), 8-cyclopentyltheophylline (0.1, 1 mumol/l) and 8-(p-sulphophenyl)-theophylline (100 mumol/l), antagonized the effect of R-PIA (0.1 mumol/l). When given alone they also enhanced the amplitudes of all EJPs in the train. The percentage facilitation of the first EJP and that of the later ones was similar. Some early EJPs, however, were potentiated more markedly. 8-Phenyltheophylline was less potent than 8-cyclopentyltheophylline both in preventing the action of R-PIA and in enhancing the EJPs. A concentration (100 mumol/l) of 8-(p-sulphophenyl)-theophylline, which strongly antagonized the R-PIA effect, produced only a moderate facilitation of EJPs. 4. S-(p-nitrobenzyl)-6-thioguanosine (10 mumol/l) both depressed the EJPs, and enhanced the inhibitory effect of adenosine. Adenosine deaminase (10 micrograms/ml) caused some potentiation of EJPs; this action was prevented by a concentration (10 mumol/l) of deoxycoformycin, which had no effect of its own. AH21-132 (10 mumol/l) enhanced all EJPs in the train. 5. None of the above substances influenced the resting membrane potential of the smooth muscle cells. In addition, R-PIA (0.1 mumol/l) did not change the depolarization induced by noradrenaline (3 mumol/l). 6. We suggest that the axon terminals of postganglionic sympathetic neurones in the rabbit mesenteric artery possess P1-purinoceptors of the A1-type. The activation of these presynaptic receptors by endogenous adenosine may inhibit the release of the main neuroeffector transmitter, which is probably ATP.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed2000

Vagal ganglionic and nonadrenergic noncholinergic neurotransmission to the ferret lower oesophageal sphincter.

In the present study we aimed to discretely characterise ganglionic and neuroeffector transmission to the ferret lower oesophageal sphincter (LOS) using a novel preparation of LOS muscle with intact vagal innervation in conjunction with isolated LOS muscle strips. In this way we could compare vagally mediated LOS relaxation with that of enteric inhibitory motorneurones which were directly stimulated. Preparations of LOS muscle, with or without attached vagus nerves, were dissected from adult ferrets and maintained under preload in organ baths, where LOS muscle developed spontaneous tone. LOS relaxations in response to vagal stimulation (0.5-5 Hz, 30 V) were recorded, alone and following pretreatment with tetrodotoxin (TTX), hexamethonium (Hex), Hex and atropine and NG-nitro-L-arginine (L-NNA). Direct activation of enteric inhibitory motorneurones was performed via electrical field stimulation (EFS). Vagal stimulation elicited frequency-dependent relaxations of the LOS that were abolished by tetrodotoxin (1 microM) and markedly reduced following L-NNA pretreatment (100 microM), but unaltered following pretreatment with the selective VIP or PACAP receptor antagonists VIP (10-28) or PACAP (6-38), respectively (each at 5 microM). The potent NOS inhibitor S-methyl-L-thiocitrulline (100 microM) inhibited LOS relaxation to the same degree at 5 Hz. Hex alone (500 microM) reduced maximal relaxation by 50%; in combination with atropine (2 microM), relaxation was almost abolished. In isolated LOS muscle strips, neither VIP (10-28) nor PACAP (6-38) altered EFS-induced relaxation. Taken together, these results suggest ganglionic neurotransmission to the ferret LOS occurs mainly through a combination of nicotinic and muscarinic receptors and utilises nitroxidergic enteric inhibitory motorneurones to relax the LOS. Moreover, LOS relaxation due to direct activation of inhibitory motorneurones also utilises primarily nitric oxide and other as yet undefined neurotransmitters. Neither VIP nor PACAP are involved in vagally mediated or direct enteric neuronally stimulated LOS relaxation in the ferret.

Acetylcholine↗