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At least 19 recordsLinked to original sources
PubMed1969

The action of eledoisin on the peristaltic reflex of guinea-pig isolated ileum.

1. Low concentrations of eledoisin, acting from the serosal surface of the guinea-pig isolated ileum, had no effect on the peristaltic reflex, whereas in high concentrations it depressed or sometimes abolished this reflex.2. Eledoisin stimulated the peristaltic activity of the guinea-pig ileum subjected to continuously raised intraluminal pressure. This stimulatory effect could be produced regularly when the interval between additions of eledoisin was at least 20 min. When added at shorter intervals, tachyphylaxis to eledoisin developed, but its ability to promote peristaltic activity was restored by the addition of an anticholinesterase to the bath fluid. During tachyphylaxis to eledoisin, nicotine and dimethylphenylpiperazinium were unable to restore peristalsis.3. When the peristaltic reflex had been abolished by ganglion-blocking agents, morphine and morphine-like substances, or adrenaline, eledoisin restored the reflex. Eledoisin was much more effective in overcoming the blocking effect of hexamethonium, tetraethylammonium and azamethonium than that of nicotine or dimethylphenylpiperazinium.4. Eledoisin did not antagonize the inhibitory effects of atropine, hyoscine and hyoscine butylbromide.5. It is suggested that the stimulant effect of eledoisin may be due to a direct action on the smooth muscle and a release of acetylcholine from postganglionic nerve endings, but an effect on the intestinal ganglion cells cannot be excluded.

Animals↗
PubMed1986

Quantitative autoradiographic analysis of the distribution of binding sites for [125I]Bolton Hunter derivatives of eledoisin and substance P in the rat brain.

[125I]Bolton and Hunter eledoisin binds to a single class of non-interacting sites in rat cerebral cortex tissue sections with an apparent Kd of 9.9 nM and a Bmax of 244 fmol/mg protein. When concentrations of up to 23 nM [125I]Bolton and Hunter eledoisin were used, [125I]Bolton and Hunter eledoisin binding was specific, saturable and reversible. Kassinin, eledoisin and neurokinin B were more potent than substance P and neurokinin A in inhibiting the specific binding of [125I]Bolton and Hunter eledoisin to cerebral cortex tissue sections. These kinetic and pharmacological characteristics are consistent with results obtained from binding studies on cortical synaptosomes. When the localization of [125I]Bolton and Hunter substance P and [125I]Bolton and Hunter eledoisin binding sites were compared, differences in many areas of the brain were noted. Large differences were seen in the paraventricular and supraoptic hypothalamic nuclei, and in layers IV and V of the cerebral cortex, which were densely labeled by [125I]Bolton and Hunter eledoisin, but not by [125I]Bolton and Hunter substance P. In contrast, nuclei of the septum (diagonal band of Broca, septohippocampal nucleus, dorsal part of the lateral septal nucleus), the rostrodorsal part of the hippocampus and other discrete nuclei [endopyriform nucleus, anterior cortical amygdaloid nucleus, the vermis columns (9-10), the dorsal tegmental nucleus, the hypoglossal and ambiguus nucleus] had high levels of [125I]Bolton and Hunter substance P binding but were only labeled weakly by [125I]Bolton and Hunter eledoisin. Thus, the two ligands seem to label different sites, since these binding sites have different biochemical and pharmacological properties, and are localized in different anatomical structures.

Animals↗
PubMed1992

Ontogeny and characterization of [125I]Bolton Hunter-eledoisin binding sites in rat spinal cord by quantitative autoradiography.

The distribution and characteristics of [125I]Bolton Hunter-eledoisin binding sites in rat lumbar spinal cord were studied during postnatal development by in vitro receptor autoradiography. At three, six and 10 days of age, specific [125I]eledoisin binding was distributed throughout the dorsal and ventral horns of the spinal cord. In contrast, from day 24 onwards, specific binding of [125I]eledoisin was confined to superficial layers of the dorsal horn, with negligible amounts of specific binding in the ventral horn. [125I]Eledoisin binding to neonatal (three day) and adult (eight to 12 weeks) spinal cord sections was characterized using tachykinin agonists. In both dorsal and ventral horns of neonatal spinal cord, the rank order of potency of agonists indicated that the majority (64%) of specific [125I]eledoisin binding was to neurokinin-3 binding sites. The identity of the non-neurokinin-3 sites labelled by [125I]eledoisin remains to be determined. In adult rat spinal cord, [125I]eledoisin appeared to bind exclusively to neurokinin-3 binding sites. These results suggest that major changes take place in the localization of neurokinin-3 receptors during postnatal ontogeny of the rat spinal cord. These changes may reflect an important role for tachykinins in neuronal plasticity of the developing spinal cord.

Animals↗
PubMed1985

Effects of eledoisin on thyrotrophin secretion in rats.

The effect of peripheral administration of eledoisin on thyrotrophin-releasing hormone (TRH) and thyrotrophin (TSH) secretion in rats were studied. Eledoisin (500 micrograms/kg) was injected iv, and the rats were serially decapitated. TRH, TSH and thyroid hormone were measured by radioimmunoassay. The hypothalamic immunoreactive TRH (ir-TRH) content increased significantly after eledoisin injection, whereas its plasma concentration tended to decrease, but not significantly. Plasma TSH levels decreased significantly in a dose-related manner with a nadir at 40 min after the injection. Plasma thyroid hormone levels did not change significantly. Plasma ir-TRH and TSH responses to cold were inhibited by eledoisin, but the plasma TSH response to TRH was not affected. In the pimozide- or para-chlorophenylalanine-pretreated group, the inhibitory effect of eledoisin on TSH levels was prevented, but not in the L-dopa- or 5-hydroxytryptophan-pretreated group. These drugs alone did not affect plasma TSH levels at the dose used. The inactivation of TRH immunoreactivity by plasma or hypothalamus in vitro after eledoisin injection did not differ from that of controls. These findings suggest that eledoisin acts on the hypothalamus to inhibit TRH release, and its effects are modified by amines of the central nervous system.

Animals↗
PubMed1990

Sodium and water intake of sheep, rabbits and cattle during ICV infusion of eledoisin.

The present study reports the effects of ICV administered eledoisin, the most potent anti/dipsogenic member of the tachykinin family, in three species. Sheep with chronic parotid fistula lost daily 200-400 mmol sodium in 3-4 l of saliva. During ICV infusion of eledoisin, 2 to 50 ng/min, a decrease in sodium intake was observed. If water was withheld for 22 hours, sheep normally drank 5.4 l water on presentation. During ICV infusion of eledoisin, 50 ng/min, water intake increased significantly. Wild rabbits lost 5 mmol sodium in 50 ml of urine after injection of furosemide. During ICV infusion of eledoisin, 30 ng/min, a decrease in sodium intake and an increase in water drinking was observed. Cows prepared with parotid fistula had access to sodium solution every other day to replace salivary sodium loss. During ICV infusion of eledoisin, 50 and 150 ng/min, a decrease in sodium intake occurred, and water intake was unaffected. These results confirm that central administration of eledoisin specifically influences ingestive behaviour in mammals and draws attention to some species differences in the observed effects.

Animals↗
PubMed1962

Occurrence and some properties of eledoisin in extracts of posterior salivary glands of Eledone.

The posterior salivary glands of Eledone, alone among the tissues of this molluscan species, contain eledoisin, an endecapeptide with activity on blood vessels and extravascular smooth muscles. The salivary glands of Octopus vulgaris and O. macropus lack the polypeptide. Eledoisin is present, in amounts ranging from 20 to 160 mug/g fresh tissue, at all stages of growth and in every season; however, conspicuous differences in the eledoisin content were observed in different groups of animals. Eledoisin is fairly stable in intact salivary glands stored on ice. The most suitable solvent for its extraction is 70 to 80% methanol. Better results are also obtained with boiling diluted acetic acid, than with ethanol, whereas extraction with acetone gives unsatisfactory yields. Eledoisin is stable in neutral or slightly acid medium, but is rapidly destroyed by strong acids and even more rapidly by strong alkalis. It is quickly and completely inactivated by chymotrypsin, and somewhat more slowly and incompletely by trypsin. Carboxypeptidase is ineffective. Passage of crude salivary extracts of Eledone through an alumina column yields preparations of eledoisin which may be considered pure from a biological point of view.

Acetic Acid↗
PubMed1988

Comparison of the binding of radiolabelled neurokinin A and eledoisin in rat cortex synaptic membranes.

1. The binding of the 125I-Bolton Hunter (BH) conjugates of neurokinin A and eledoisin to synaptic plasma membranes prepared from rat cerebral cortex was investigated. 2. Saturation analyses indicated that both radioligands labelled a similar number of binding sites, but [125I]BH-eledoisin had a 7 fold higher affinity than [125I]BH-neurokinin A. 3. An identical pharmacological profile was apparent for both radioligands and tachykinin peptides inhibited the binding in the order: neurokinin B greater than BH-eledoisin greater than kassinin greater than L-363,851, eledoisin greater than substance P, neurokinin A greater than physalaemin greater than DiMeC7 greater than substance P methylester, indicating a profile consistent with the NK3-subtype of tachykinin receptors. 4. The binding of [125I]BH-neurokinin A and [125I]BH-eledoisin was equally sensitive to inhibition by the guanosine triphosphate (GTP) analogue, guanyly-5'-(beta-gamma-imido) diphosphate. 5. These results indicate that [125I]BH-neurokinin A and [125I]BH-eledoisin appear to label a common site in rat cerebral cortex synaptic plasma membranes with the characteristics of an NK3-receptor, and thus [125I]BH-neurokinin A is not a selective radioligand for the NK2-receptor.

Animals↗
PubMed1990

Eledoisin and lacrimal secretion in the rabbit.

Eledoisin has been tried as a possible treatment for dry eye based on the hypothesis that it pharmacologically stimulates tear secretion when topically applied to the eye. To determine if topically applied eledoisin pharmacologically stimulates orbital lacrimal secretion, the orbital lacrimal gland excretory duct of normal rabbits was cannulated, and eledoisin was applied topically with and without prior administration of proparacaine. To determine if topically applied eledoisin stimulated accessory lacrimal gland secretion, isotonic buffer with and without eledoisin was tested in a rabbit model with only accessory lacrimal tissue remaining after the administration of proparacaine. Topically applied eledoisin did not pharmacologically stimulate lacrimal secretion but rather increased lacrimal gland secretion only in non-anesthetized eyes through a sensory reflex mechanism that is blocked by proparacaine.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1978

Eledoisin, substance P and related peptides: intracranial dipsogens in the pigeon and antidipsogens in the rat.

The undecapeptide eledoisin caused vigorous and copious drinking within a minute or two of injection into the pigeon forebrain. Systemic injections of the same doses were ineffective. The relative efficacy of eledoisin and angiotensin II as dipsogens in the pigeon was similar to that of carbachol and angiotensin II in the rat. The related peptides eledoisin hexapeptide, physalaemin and substance P also caused some drinking, but they were less effective than eledoisin. In the rat none of these substances caused drinking. On the contrary eledoisin and substance P were found to depress angiotensin-induced drinking, but carbachol-induced drinking was not depressed to the same extent by these peptides. The preferential depression of angiotensin II-induced drinking resembles the effects of other vasoplegic drugs on this response in the rat, and may be related to the potent vasodilator properties of these peptides.

Angiotensin II↗
PubMed1975

The actions of bradykinin and eledoisin in the canine isolated kidney: relationships to prostaglandins.

1. The effects of two vasodilator polypeptides, bradykinin and eledoisin, were studied in isolated blood-perfused canine kidneys before and after administration of indomethacin, an inhibitor of prostaglandin synthesis, Bradykinin, but not eledoisin, releases renal prostaglandins. 2. Before administration of indomethacin, bradykinin decreased urinary osmolality and increased free qater clearance, whereas eledoisin did not affect the excretion of solute-free water. After administration of indomethacin, the renal vasodilator action of bradykinin was reduced but the vasodilator action of eledoisin was unaffected. 3. Fractional excretion of sodium was not affected by bradykinin before but was increased after administration of indomethacin. Reduction in glomerular filtration rate contributed to changes in sodium excretion produced by bradykinin and eledoisin. 4. The release of prostaglandins from the kidney by bradykinin amplifies the renal vasodilator action of the kinin and possibly mediates its effect on excretion of solute-free water.

Animals↗
PubMed1990

Chemoreceptor responses to substance P, physalaemin and eledoisin: evidence for neurokinin-1 receptors in the cat carotid body.

Substance P (SP) belongs to a group of peptides called tachykinins. Biological effects of SP are mediated by tachykinin receptors that have been classified as neurokinin-1 (NK-1), NK-2 and NK-3 subtypes. The aim of the present study is to elucidate the tachykinin receptor subtype(s) that mediate the excitatory effects of SP in the carotid body. For this purpose, we compared the carotid body responses elicited by SP with that of physalaemin and eledoisin. In other tissues, physalaemin exhibits equi or greater potency at NK-1 receptors and eledoisin exerts its effects more on NK-2 and NK-3 subtypes compared to SP. Experiments were performed on eight cats that were anaesthetized, paralyzed and artificially ventilated with room air. Close carotid body administration of SP and physalaemin produced dose-dependent augmentation of the chemoreceptor afferent activity. Chemoreceptor discharge, however, was unaffected by eledoisin. Compared to that by SP, the magnitude of excitation produced by physalaemin was the same at lower doses but significantly greater with the highest dose (100 nmol). The time course of the response induced by physalaemin, however, was the same as that by SP. The present results demonstrate that in the carotid body physalaemin is also either equi or relatively more potent than SP, whereas eledoisin has no effect on the chemoreceptor discharge. It is suggested that stimulation of the carotid body by SP is mediated by NK-1 but not NK-2 or NK-3 receptors.

Animals↗