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Biomedical subjects

A Johns

Publications and source records attributed to A Johns.

At least 109 records · Page 6Linked to original sources

The effect of magnesium-free solutions on the responses of the guinea pig urinary bladder to adenosine 5'-triphosphate and nerve stimulation.

Exposure of the guinea pig urinary bladder to magnesium-free Krebs-Henseleit type solution for 60 min led to an increase in the responses of the tissue to added adenosine 5'-triphosphate (ATP). The responses of the tissue to histamine were unaffected. The atropine-resistant contractions due to nerve stimulation were potentiated at frequencies above 4 Hz when the response of the tissue was 60% of its maximum response. This would suggest that, although ATP does contribute to the responses of the tissue at high frequencies, it is not the transmitter of the noncholinergic nerves present in the bladder.

Adenosine Triphosphate↗

Effect of the external concentrations of potassium and sodium on the release of (--)-[3H]noradrenaline from the adrenergic nerves of the rat vas deferens.

The effect of the external concentrations of sodium and potassium on the nerve-induced release of (--)-[3H]noradrenaline from the adrenergic nerves of the rat vas deferens has been investigated. Increasing the external potassium concentration above 5 mM decreased the amount of noradrenaline released, while reducing the external potassium concentration below 5 mM had no significant effect on the induced release of noradrenaline. Decreasing the external sodium concentration below 75 mM progressively decreased the release of noradrenaline. It is concluded that the amplitude of the action potential is optimum for release at the normal resting membrane potential, and only decreasing the amplitude of the action potential alters the amount of transmitter released per nerve impulse.

Animals↗

The effect of theophylline on the responses of the guinea-pig urinary bladder to nerve stimulation, adenosin 5' triphosphate and histamine.

The effects of theophylline (10(-5)M, 10(-4)M and 10(-3)M) on the contractile responses of the guinea-pig urinary bladder to nerve stimulation, adenosin 5' triphosphate (ATP) and histamine have been investigated. Contractile responses were unaffected by 10(-5)M and 10(-4)M therophylline but were significantly reduced by 10(-3)M theophylline. Since responses to histamine were reduced to a similar extent as responses to ATP, it is suggested that theophylline is not a specific antagonist of ATP in this tissue and that the ATP receptors in the bladder differ from those in other smooth muscle preparations.

Adenosine Triphosphate↗

Effect of indomethacin on atropine-resistant transmission in rabbit and monkey urinary bladder: evidence for involvement of prostaglandins in transmission.

The effects of 2.9 x 10(-5)M atropine and 2.8 x 10(-6)M indomethacin on responses of rabbit and monkey detrusor muscle to transmural stimulation were investigated. Response to transmural stimulation were partially inhibited by atropine. Indomethacin caused further inhibition in the presence of atropine, but did not alter responses to acetylcholine. Prostaglandins E2 and F2alpha contracted rabbit and monkey detrusor. It is suggested that prostaglandins are liberated during stimulation of excitatory nerves to the rabbit and monkey detrusor, and contribute to the resultant contractile response.

Acetylcholine↗

Inhibition of spontaneous contractility of the human and the rabbit fallopian tube by potassium.

Spontaneous contractions of circular and longitudal muscle of the ampulla and isthmus of human and rabbit Fallopian tubes were recorded isometrically. Addition of K+ to tissue in K+-free medium always caused immediate inhibition of spontaneous contractility. K+-induced inhibition was prevented by ouabain and reversed by removal of K+. It is suggested that K+ caused inhibition of contractility by activating electrogenic Na+ pumping with resultant hyperpolarization of the muscle cells.

Animals↗

The potentiating effects of 4-aminopyridine on adrenergic transmission in the rabbit vas deferens.

The effects of 4-aminipyridine on adrenergic transmission in rabbit vas deferens were investigated. 10(-5)-10(-3) M 4-aminopyridine markedly potentiated the sustained, secondary contractile response to transmural stimulation and significantly increased the amount of (+/-)-|3H]-metaraminol released at 5 Hz, but had little effect on responses to exogenous (-)-noradrenaline. 10(-5)-10(-4) M 4-aminopyridine did not significantly alter the accumulation or efflux of (-)-[3H]-noradrenaline in rabbit heart. It is suggested that 4-aminopyridine potentiated responses of rabbit vas deferens to transmural stimulation mainly by increasing transmitter release, possibly as a result of prolongation of the action potential. Responses to transmural stimulation were also potentiated by by 2- and 3-aminopyridine and by 3,4-diaminopyridine but not by pyridine, aniline, 4-dimethylaminopyridine, 4-aminoethylpyridine or 2-aminopyrimidine.

Animals↗

Effect of rubidium on responses of rabbit vas deferens to transmural stimulation and to noradrenaline.

The effects of 2 mM RbCl on adrenergic transmission in rabbit vas deferens were investigated. Rubidium, but not potassium, markedly potentiated the sustained, secondary contractile response to transmural stimulation at 2--16 Hz. This effect was not abolished by indomethacin. Significant spontaneous desensitization to (--)-noradrenaline occurred, but this was prevented by the addition of 2 mM RbCl or KCl. Addition of 2 mM RbCl, but not of 2 mM KCl, significantly increased the amount of [3H] (+/-)-metaraminol released on transmural stimulation at 5 Hz, without affecting the uptake of [3H] (+/-)-metaraminol over a 30 min period. It is suggested that rubidium mainly potentiated responses of rabbit vas deferens to transmural stimulation by increasing transmitter release, possibly as a result of prolongation of the action potential.

Animals↗

Postjunctional supersensitivity of the rat vas deferens and gap junctions.

Tissues from the duodenum and vas deferens of Sprague-Dawley rats were examined of the rat vas deferens and gap junctions. Can. J. Physiol. Pharmacol. 54, 412-416. by electron microscopy after glutaraldehyde fixation and postosmication. Gap junctions (nexuses) were readily demonstrated in the duodenum in both control and reserpine treated animals (1.0 mg/kg per day for 7 days). Honever, gap junctions could not be demonstrated in vas deferens. It is concluded that the postjunctional supersensitivity and spontaneous activity induced by reserpine in vas deferens, does not result from the formation of gap junctions.

Animals↗

Cell contacts and distribution of nerves in the smooth muscle of estrogen-dominated rabbit oviduct.

The types of cell-to-cell contacts and the relationship between the nerve endings and the smooth muscle of the estrogen-treated rabbit oviduct have been investigated. The cell contacts most consistently found in the oviduct were simple appositions, with a 20-nm cell separation, which occasionally included a more dense region, and interdigitations of muscle cell processes with the same separation distances. Very rarely, wider intermediate contacts were present. Gap junctions (nexuses) were absent. It seems likely that simple appositions and interdigitations form the low resistance pathway for conduction of electrical activity. Nerves containing small dense-cored vesicles were present both within and near muscle bundles; they were rarely found close to smooth muscle cells.

Animals↗

The mechanism of action of dicyclomine hydrochloride on rabbit detrusor muscle and vas deferens.

Dicyclomine inhibited responses of rabbit detrusor muscle to transmural stimulation more than atropine or lidocaine, and also inhibited responses to acetylcholine and to KCl. Responses of rabbit vas deferens to noradrenaline and transmural stimulation were inhibited by dicyclomine. Dicyclomine was as potent a local anesthetic as lidocaine, as determined by the guinea-pig wheal test. 45Ca++ exchange in the rabbit detrusor, measured by the lanthanum methods, was not altered by atropine, lidocaine or dicyclomine. It is concluded that dicyclomine not only acts as an anticholinergic agent but also impairs excitation-contraction coupling and release of transmitter from autonomic nerves.

Acetylcholine↗

Characteristics of responses of isolated human fallopian tube to transmural stimulation and to sympathomimetic amines.

The responses of circular and longitudinal muscle of human fallopian tube to transmural stimulation and sympathomimetic amines have been investigated. It was found that tissues from the earlier part of the menstrual cycle (i.e., estrogen dominant) were less responsive to all stimuli than those from the middle or late phase of the cycle. Although excitatory alpha responses of ampulla and isthmus could be observed, the predominant response of ampulla and isthmus, in all phases of the menstrual cycle, to (--)-noradrenaline and transmural stimulation was inhibition of spontaneous activity. The inhibitory response to transmural stimulation, was abolished by tetrodotoxin and guanethidine. The inhibitory responses to transmural stimulation and (--)-noradrenaline were reversed by propranolol. These findings show that the response of tissues to transmural stimulation resulted from release of noradrenaline from adrenergic nerves, and subsequent action on inhibitory beta adrenergic receptors.

Electric Stimulation↗

The inhibitory effects of prostaglandin E1 on guinea-pig ureter.

Prostaglandin E1 (PGE1) hyperpolarized the smooth muscle cells of guinea-pig ureter in normal Krebs solution and was without effect on ureters depolarized in KCl Krebs, PGE1 inhibited both electrically induced contractions and K+-induced contractures of the ureters. Conditions that favored greater tension development by the ureters, namely, high [K+] or high [Ca-2+] reduced the inhibitory effects of PGE1 on the K+-induced contractures. Depolarization of guinea-pig ureter with KCl Krebs led to an increase in radio-calcium content of the tissue over a 30 min loading period. This increase in the tissue's radio-calcium content was further increased by PGE1 but not by theophylline, PGE1 was found to have no effect on either total calcium content or the calcium efflux from the tissue. It is suggested that PGE1 exerts its inhibitory action by increasing calcium sequestration at the inner surface of the cell membrane.

Animals↗