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The effects of calmidazolium, carbachol and membrane permeable derivatives of cGMP (dipalmitoyl cGMP and 8-Bromo cGMP) on the longitudinal internal resistivity (Ri) were studied in the rabbit atiial trabeculae by means of electrophysiological recording techniques and histological planimetry. Calmidazolium as well as carbachol decreased Ri whereas cGMP-derivatives enhanced this resistivity. The effect of calmidazolium suggested that calmodulin reduced the cell coupling under control conditions. Carbachol decreased the Ca-inward current, and probably it prevented the calmodulin activation. The action of the nucleotides showed that cGMP did not mediate the cholinergic effect on the cell coupling. The possible interaction between calmodulin and cGMP was discussed.
Acetylcholine (ACh), a well known animal neurotransmitter was isolated from tissues of Pharbitis nil using five different methods. Its presence in plant extract was confirmed by infrared spectroscopy and mass spectrometry. For quantitative estimation of ACh in P. nil seedlings pyrolysis-gas chromatography was applied. The presence of ACh was found in all organs of the examined plant: seeds, shoot apex, cotyledons, leaves, shoots and roots. However, the highest level of the investigated substance was noted in the youngest growing parts. In 5-day-old etiolated seedlings they were cotyledons, whereas in 14 day-old green plants - shoot apex and young leaves.
The aim of the study was to examine the changes in the density of VAChT (marker of acetylcholine present)-, NPY-, VIP-, SOM-, SP- and nNOS-immunoreactive (IR) nerve terminals and co-localization of VAChT with the above-mentioned neurotransmitters after the occurrence of dexamethasone (DXM)-induced ovarian cysts in gilts. DXM administration led to an increase in the density of VAChT/SP-, VAChT/nNOS- and NPY-IR nerve terminals around the cystic walls. In DXM-treated animals an elevated number of VAChT- and SP-IR nerve endings was found close to the tertiary follicles. Moreover, in the gilts receiving DXM the density of NPY-IR nerve endings (that simultaneously co-localized VAChT) was high near the interstitial gland. An increase in the number of VAChT/SP- and VIP-IR nerve fibers around the medullar arteries (A) was observed in cystic ovaries, while the number of VAChT-IR nerve endings near the cortical A was lowered after DXM application. Furthermore, nerve fibers containing VAChT were absent around veins in the whole ovary of DXM-treated animals. After DXM injections, an increase in the number of VAChT/SP- and VAChT/nNOS-IR nerve endings in the cortical, as well as VIP- and nNOS-IR (co-existing with VAChT), nerve terminals in the medullar part of the autonomic ground plexus (GP) was present. However, the administration of DXM led to a drop in the density of SOM-positive nerve endings (also VAChT-IR) in the medullar subdivision of the GP. The present study shows that in the porcine ovaries with DXM induced cysts the pattern of cholinergic innervation, as well as the co-localization of VAChT and NPY, VIP, SOM, SP or nNOS, were changed. Data obtained also suggest that acetylcholine and the above-mentioned neurotransmitters effecting the functioning (steroidogenic activity, blood flow) of the polycystic ovaries may have a significant influence on the course of this pathological status.
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Muscarinic receptor subtypes in the alimentary tract

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Acetylcholine is a transmitter in preganglionic autonomic and postganglionic parasympathetic nerves and a non-neuronal paracrine mediator in the alimentary tract. Acetylcholine is involved in the control of almost any function within these organ systems, and almost every cell type expresses multiple muscarinic receptor subtypes. Although muscarinic receptors at non-neuronal effector cells commonly are of the M3 subtype, the population usually consists of a mixture of muscarinic receptor subtypes often co-acting postsynaptically. However, the pattern of heterogeneity of varies between different tissues. The population in gland parenchymal tissue often consists of a mixture of M1 and M3 receptors, smooth muscle tissue of the gut of M2 and M3, blood vessels of M1, M3, M4 and M5 and neuronal cells of M1 and M4. Nitric oxide production, effects on inflammation and proliferation may involve M1, M3 and M5 receptors. Muscarinic receptors expressed on nerve terminals may indirectly modulate the responses by inhibition or facilitation of neuronal transmission in the autonomic nervous system. The present review describes signalling mechanisms, expression and functional effects of muscarinic receptors in salivary glands and in the gastrointestinal tract.
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Central and peripheral neural control of pancreatic exocrine secretion

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Efferent vagal impulses act on the exocrine pancreas via pancreatic ganglia, where the impulses are modulated and modified, and terminate via postganglionic fibers at the acinar cells. Acinar muscarinic receptors of the subtype M1 play an important role for the mediation of the stimulatory vagal influences on pancreatic exocrine secretion. In dogs, a potentiative interaction exists between the two most important mediators of the pancreatic exocrine response to intraduodenal stimuli, efferent vagal impulses and CCK. In contrast to humans and rats, in which all action of CCK on pancreatic enzyme output is vagally mediated, CCK acts in dogs in part as a classical humoral factor independent of the cholinergic system. Although several peptides found in pancreatic nerve cell bodies or fibers can stimulate or inhibit pancreatic exocrine secretion, their physiological importance in the neural control of the exocrine pancreas needs to be further evaluated.
In the present paper the influence of the rat C-terminal fragment [Tyr°]CGRP(28-37) (Ct-CGRP) was compared with the influences of noradrenaline (NA) and acetylcholine (ACh), respectively on isolated pig uterine artery (UA). It was shown that Ct-CGRP (10 -8 mol/1) caused contraction of UA, similar to NA (10-7 mol/1) action. ACh addition before Ct-CGRP treatment inhibited the action of this peptide. ACh administration after Ct-CGRP pretreatment negated the action of this peptide, whereas Ct-CGRP given before and after NA treatment caused additive contractile reactions of UA. Moreover, it was also shown that susceptibility of UA reaction on Ct-CGRP was higher in the postovulatory phase than in other phases of the oestrous cycle. But the effect of Ct-CGRP addition in NA pretreatment vessels as well as the influence of NA added after Ct-CGRP pretreatment were more marked in the luteal phase than in pre- and postovulatory phases of the cycle. Furthermore it was showed that CGRP (10 -9 mol/1) caused very strong dilatation of UA, equal to the reaction observed after ACh (10-8 mol/1) treatment. We concluded that Ct-CGRP in contrast to the whole molecule of calcitonin gene-related peptide (CGRP) caused vasocontractile activity in the isolated pig uterine artery. This effect was synergistic with NA action and was inhibited by ACh.
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