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PubMed1993

Effects of halothane on beta-adrenoceptors and M-cholinoceptors in human myocardium: radioligand binding and functional studies.

We investigated whether a postsynaptic sensitization by halothane for beta-adrenoceptor-mediated effects occurs in diseased human myocardium. In addition, we hoped to achieve further insights into the cellular mechanism and, in particular, the role of M-cholinoceptors and beta-adrenoceptors. The experiments were performed on isolated, electrically driven atrial and ventricular preparations and membranes isolated from human hearts obtained at cardiac surgery. Halothane concentration-dependently reduced binding of [3H]quinuclidinylbenzilate ([3H]QNB) to M-cholinoceptors but had no effect on equilibrium saturation binding of 125-iodocyanopindolol (125I]Cyp) to beta-adrenoceptors. High-and low-affinity states of agonist binding of carbachol to M-cholinoceptors were not affected, but halothane inhibited high-affinity binding of isoprenaline to beta-adrenoceptors. In contrast, halothane augmented the potency and efficacy of the positive inotropic effect of isoprenaline in atrial and ventricular myocardium. The "direct" negative inotropic effect in atrial and the "indirect" negative inotropic effect in ventricular myocardium by M-cholinoceptor stimulation with carbachol was unchanged by halothane. We conclude that in human atrial and ventricular myocardium a sensitization to catecholamines is induced by halothane, the mechanism of which is likely to be located at the postsynaptic level of the sympathetic neuroeffector junction. Facilitated coupling of beta-adrenoceptors or an uncoupling of M-cholinoceptors with reduced negative inotropic effects of agonist does not play a role. We showed that sensitization of this system apparently is due to direct actions of halothane on the G-protein-coupled adenylate cyclase complex.

Catecholamines↗
PubMed1982

Labelled-replica techniques: post-shadow labelling of intramembrane particles in freeze-fracture replicas.

Three methods are described for direct post-fracture, post-shadow labelling of individual classes of intramembrane particles (IMPs) in freeze-fracture replicas of biological membranes. The P-face IMPs corresponding to the acetylcholine receptor complexes (AChRs) of vertebrate neuroeffector junctions are identified by post-replication labelling with ferritin-antibody complexes and with neurotoxin-biotin-avidin-colloidal gold affinity ligands. (The freeze-etch nomenclature of Branton et al., 1975, is used in this report.) These post-shadow labelling techniques resemble conventional en bloc labelling techniques except that the labelling reagents must penetrate a thin but discontinuous layer of platinum superimposed on the molecules of interest. In the 'sectioned labelled-replica technique', the replicated and labelled tissues are stained, embedded in plastic and sectioned parallel to the replica-tissue interfaces. In the direct 'labelled-replica techniques', the replicated and labelled samples are freeze-dried or critical point dried, the labelled surfaces are stabilized by carbon coating, and the underlying tissues are dissolved, allowing the labelled-replicas to be examined as conventional freeze-fracture replicas. The unshadowed side of each AChR IMP is shown to retain sufficient biochemical information to permit both immunospecific and neurotoxin specific labelling despite formaldehyde fixation, freezing, fracturing, platinum shadowing, and thawing in aqueous media. A new mixed ferricyanide-osmium staining method reveals electron opaque structures spanning the membrane bilayer in the same size, number and distribution as the labelled IMPs. These experiments demonstrate the feasibility of identifying individual IMPs in freeze-fracture replicas and may allow the identification of specific membrane lesions in human disease.

Animals↗
PubMedDate not supplied

Differential blocking effects of prazosin and yohimbine on pressor responses to neuronally released and exogenously administered noradrenaline in the pithed rat.

The effects of prazosin and yohimbine on pressor responses to sympathetic nerve stimulation and intravenous injections of noradrenaline, phenylephrine and clonidine were examined in pithed rats to determine the postjunctional location of alpha 2-adrenoceptors in the vascular smooth muscle. Prazosin antagonized the pressor responses to phenylephrine and to sympathetic nerve stimulation more effectively than the responses to noradrenaline and to clonidine. Yohimbine antagonized the pressor responses to noradrenaline and to clonidine more effectively than the responses to sympathetic nerve stimulation and to phenylephrine. These results suggest that alpha 2-adrenoceptors as well as alpha 1-adrenoceptors produce vasoconstriction in the rat vasculature and support the hypothesis that alpha 1-adrenoceptors are predominantly located within the neuroeffector junction in contrast to an extrajunctional location of alpha 2-adrenoceptors.

Animals↗
PubMed1998

Presynaptic adrenergic facilitation of parasympathetic neurotransmission in sympathectomized rat smooth muscle.

1. Parasympathetic innervation of rat eyelid tarsal smooth muscle normally inhibits sympathetic neurotransmission prejunctionally without significant direct postjunctional effects. Following surgical sympathectomy, parasympathetic stimulation elicits smooth muscle contraction. This study examined the relative contributions of cholinergic and adrenergic mechanisms mediating these contractions. 2. Electrical stimulation of the superior salivatory nucleus, which activates tarsal muscle parasympathetic nerves, elicited large contractions at 2 days postsympathectomy, which were abolished by atropine and were decreased by 65 % by alpha1-adrenoceptor blockade or spinal cord transection. 3. Contractions in response to direct cholinergic stimulation by bethanechol at 2 days postsympathectomy were increased following spinal cord transection (C2) and suppressed by the alpha1-adrenoceptor agonist phenylephrine, indicating that adrenoceptors on smooth muscle attenuate cholinergic contractions. However, phenylephrine infusion enhanced contractile responses to parasympathetic stimulation. 4. Reverse transcription-polymerase chain reaction revealed alpha1D-adrenoceptor mRNA within pterygopalatine ganglia. 5. At 5 weeks and 14 months postsympathectomy, adrenergic facilitation was significantly less than at 2 days, whereas prazosin-insensitive muscarinic contraction was increased. 6. We conclude that degeneration of sympathetic innervation is followed rapidly by adrenoceptor-mediated prejunctional enhancement of parasympathetic nerve-smooth muscle neurotransmission, which occurs prior to neuroeffector junction formation as determined previously by electron microscopy. Subsequently, noradrenergic enhancement is diminished as cholinergic neurotransmission becomes established.

Animals↗
PubMed1977

Atropine resistance and muscarinic receptors in the rat urinary bladder.

The action of an anticholinesterase and an antimuscarinic drug upon nerve-induced contractions of the rat urinary bladder were examined during transmural stimulation at 20 Hz. Responses were graded in magnitude by limiting the duration of the stimulus trains. 2 Responses of low magnitude produced by short stimulus trains were unchanged by atropine; however, maximal responses resulting from long stimulus trains were diminished in magnitude and shortened in duration. 3 Responses of small magnitude elicited by short stimulus trains involve muscarinic receptors in close proximity to the neuroeffector junction and are resistant to atropine. 4 Maximal responses elicited by long stimulus trains involve 'junctional' muscarinic receptors as well as receptors located at the periphery of the junction; the 'extrajunctional' receptors are blocked by atropine. 5 Responses of low magnitude produced by short stimulus trains were unaffected by echothiophate; however, the duration of maximal responses resulting from the long stimulus trains was extended. 6 The inhibition of cholinesterase did not increase the occupation of muscarinic receptors by the transmitter; however, after large quantities of transmitter were released by the long stimulus trains the association between the receptors and acetylcholine was prolonged.

Animals↗
PubMed1979

Attenuation by bradykinin of adrenergically-induced vasoconstriction in the isolated perfused kidney of the rabbit: relationship to prostaglandin synthesis.

1 In the isolated kidney of the rabbit perfused with oxygenated Tyrode solution, we studied the effect of bradykinin on the vasoconstriction evoked by sympathetic nerve stimulation (3Hz, 1 ms) and by injections of noradrenaline (50 to 75 ng) in the presence and in the absence of indomethacin (1 microgram/ml), an inhibitor of prostaglandin biosynthesis. Prostaglandin E(PGE)-like material in the renal effluent was measured by bioassay after extraction with organic solvents and separation by thin layer chromatography. 2 Bradykinin in concentrations of 10 to 100 ng/ml reduced the vasoconstrictor response to sympathetic nerve stimulation and to injected noradrenaline. Also, the peptide (1 to 10 ng/ml) increased the basal release of PGE-like material and the release induced by sympathetic nerve stimulation. 3 Indomethacin, 1 microgram/ml, diminished the inhibitory effect of bradykinin on the vasoconstrictor response to nerve stimulation, minimized the reduction of the noradrenaline-induced vasoconstriction caused by bradykinin (100 ng/ml), and abolished the release of PGE-like material. 4 This study indicates that bradykinin reduces the renal vascular reactivity to adrenergic stimuli and suggests that part of the action of the kinin at the vascular adrenergic neuroeffector junction in the rabbit kidney depends upon the biosynthesis of renal prostaglandins.

Animals↗
PubMed1983

Microelectrode recording of the effects of agonists and antagonists on alpha-adrenoceptors on rat somatic nerve terminals.

The effects of apomorphine, catechol, clonidine, isoprenaline, (-)-and (+/-)-noradrenaline, phenylephrine, pyrogallol and xylazine were investigated on the frequency and amplitude of miniature endplate potentials (m.e.p.ps) and, with the exception of apomorphine, catechol and pyrogallol, on the amplitude of endplate potentials (e.p.ps) in the rat phrenic nerve diaphragm preparation. Clonidine, (-)-noradrenaline, phenylephrine and xylazine (each at 1.5 X 10(-5)M) increased m.e.p.p. frequency but not amplitude. The other drugs were ineffective, except isoprenaline (1.5 X 10(-5)M) which enhanced m.e.p.p. amplitude but not frequency. The increase in m.e.p.p. frequency was inhibited by phentolamine, prazosin and yohimbine (each 1.5 X 10(-9)M). Prazosin and yohimbine alone each reduced m.e.p.p. frequency but failed to abolish m.e.p.ps even at high concentrations (10(-3)M). Clonidine, (-)-noradrenaline, phenylephrine and xylazine (each 3 X 10(-6)M) enhanced e.p.p. amplitude; this enhancement was blocked by prazosin and by yohimbine (each 3 X 10(-6)M). In preparations fatigued by prolonged continuous nerve stimulation (5 Hz, 0.05 ms for 30 min), (-)-noradrenaline (3.3 X 10(-4)M) restored m.e.p.p. frequency. The results indicate that adrenoceptors on somatic nerve terminals interact with both alpha 1- and alpha 2-agonists and antagonists and show different characteristics from those at autonomic neuroeffector junctions. The alpha-adrenoceptors on somatic nerve terminals may have an ancilliary physiological role in influencing but not controlling transmitter release.

Adrenergic alpha-Antagonists↗
PubMed1988

Subtypes of muscarinic receptor on cholinergic nerves and atrial cells of chicken and guinea-pig hearts.

1. Electrically driven chicken and guinea-pig atria were used to investigate the negative inotropic effects of the muscarinic agonists methacholine and acetylcholine (ACh). The release of ACh from isolated hearts into the perfusate in response to (preganglionic) vagal or (pre- and postganglionic) field stimulation was bioassayed on the guinea-pig ileum or determined by labelling with [3H]-choline. 2. Concentration-response curves for the negative inotropic effect of methacholine were shifted to the right by pirenzepine in various concentrations (0.03 to 10 mumol l-1). The pA2 values were 7.76 in chicken atria and 6.53 in guinea-pig atria. Pirenzepine and atropine antagonized the negative inotropic response to 0.3 mumol l-1 ACh. The half-maximally effective concentrations (IC50) of pirenzepine (Pz) and atropine were 40 and 5.4 nmol l-1 in chicken atria and 330 and 3.5 nmol l-1, respectively, in guinea-pig atria. Thus, the respective potency ratios (IC50Pz/IC50atropine) were 7.4 and 94.3 in the two species. 3. Pirenzepine in low concentrations increased the release of unlabelled and 3H-labelled ACh from isolated hearts evoked by vagal and field stimulation only in chicken, but not in guinea-pigs. The half-maximally-effective concentration of pirenzepine was about 30 nmol l-1 in the chicken heart, whereas, in the guinea-pig heart, an increased release was observed at 300 nmol l-1. 4. (+)-Tubocurarine [(+)-Tc; 100 mumol l-1] reduced the release of ACh evoked by (preganglionic) vagal stimulation to a (+)-Tc-resistant release of about 30%. The time-course of the neuronal release of [3H]-ACh was markedly altered: the onset was delayed and the termination was extended beyond the period of stimulation (1 min or 5s) by several seconds. The (+)-Tc-resistant release was nearly abolished by 30 nmol l-1 pirenzepine. 5. In conclusion, the pre- and post-synaptic muscarinic receptors of the parasympathetic neuroeffector junction of the heart both belong to the M1-subtype in the chicken and to an M2-subtype in the guinea-pig. Block of the nicotinic ganglionic transmission in the chicken heart by (+)-Tc unmasked a muscarinic transmission, which presumably was mediated through M1-receptors stimulating a low and prolonged postganglionic release of ACh.

Acetylcholine↗
PubMed1990

Cardiac beta-adrenoceptor binding characteristics with age following adrenal demedullation.

1. The role of adrenal medullary catecholamines in the regulation of cardiac function becomes more important when adrenergic neural influences in the heart are decreased. Since adrenergic nervous input to the heart decreases with age, it would be expected that catecholamine influence on cardiac neuroeffector junction would increase. 2. Fischer-344 rats of 6-, 12- and 24-months were adrenal demedullated or sham-operated and the animals were killed at the end of two weeks. beta-Adrenoceptors were studied in the membrane preparations from the ventricles of rat hearts. [125I]-iodopindolol was used as the radioligand. The density of beta-receptors (Bmax), dissociation constant (KD) and the ratio of cardiac beta-adrenoceptor subtypes were studied. The relative percentages of beta-receptor subtypes were determined by use of ICI 89,406 (beta 1-selective antagonist) and ICI 118,551 (beta 2-selective antagonist). 3. In 24-month-old animals which were adrenal demedullated, hydrocortisone replacement was employed for one week; the animals were killed one week later. 4. The data indicate that there was a diminution of the Bmax following adrenal demedullation at all ages but that the ratios of beta 1: beta 2-adrenoceptors remain the same as in the controls (67:33). The effect of adrenal medullary catecholamines on cardiac beta-receptor binding characteristics did not seem to be influenced by age.

Adrenal Medulla↗
PubMed1994

Demonstration of the neurotransmitter role of calcitonin gene-related peptides (CGRP) by immunoblockade with anti-CGRP monoclonal antibodies.

1. Monoclonal antibodies (MAbs) against rat alpha-calcitonin gene-related peptide (alpha CGRP) were produced. Those which bound CGRP in a radioimmunoassay and inhibited the binding of 2-[125I]-iodohistidyl10-CGRP in a receptor binding assay were selected for immunoblockade experiments. 2. The effect of MAbs on CGRP inhibition of electrically stimulated contractions of the rat isolated vas deferens was characterized. Four out of 11 MAbs tested shifted the concentration-response curve of CGRP to the right compared with vehicle or irrelevant MAb control. MAb C4.19 produced equipotent blockade of rat alpha CGRP and rat beta CGRP and was chosen for further studies. MAb C4.19 had no pharmacologically significant effect on the concentration-response relationship of isoprenaline, rat beta-endorphin or somatostatin. 3. We demonstrated that the pharmacological response to CGRP in the presence of MAb C4.19 could be predicted when the dissociation constant and concentration of binding sites of the antibody were known. Comparison of experimental and computer simulated data showed good agreement for EC50 and maximum effect of CGRP in the presence of MAb C4.19. 4. Capsaicin at 1 microM inhibited the electrically stimulated contractions by 60.8% (95% confidence interval 51.8% to 69.9%). This effect was significantly attenuated by MAb C4.19 to 26.0% (95% confidence interval 15.2% to 36.8%; P < 0.003). 5. The immunoblockade of exogenous and endogenous CGRP described here, together with complementary evidence from other studies, strongly suggest that CGRP has a major neurotransmitter role at the neuroeffector junction of the rat vas deferens.

Animals↗
PubMed1994

Beta-adrenoceptors mediate inhibition of [3H]-acetylcholine release from the isolated rat and guinea-pig trachea: role of the airway mucosa and prostaglandins.

1. Rat or guinea pig isolated tracheae were labelled with [3H]-choline to measure evoked tritium outflow, which reflects neuronal release of [3H]-acetylcholine. Tritium outflow was evoked either by electrical stimulation of the extrinsic vagal nerve (rat tracheae) or by 27 mM potassium (guinea pig tracheae). 2. In rat tracheae isoprenaline (0.01, 0.1 microM) inhibited evoked [3H]-acetylcholine release, whereas beta 2-adrenoceptor-selective agonists (fenoterol, formoterol, salbutamol) were ineffective. 3. The inhibitory effect of isoprenaline was abolished under the following conditions: (i) presence of propranolol (1 microM) or of the beta 1-selective antagonist CGP 20712 A (0.1 microM); (ii) removal of the mucosa at the start of the experiments; (iii) blockade of cyclooxygenase activity by 3 microM indomethacin. 4. In rat isolated tracheae prelabelled with [3H]-arachidonic acid, isoprenaline (0.1 microM) but not formoterol (0.01 microM) enhanced the outflow of [3H]-prostaglandins (PGD2, PGE2). This effect was blocked by 0.1 microM CGP 20712 A. 5. In guinea pig tracheae electrical stimulation of the extrinsic vagal nerve did not cause a constant release of [3H]-acetylcholine, but 27 mM potassium elicited a reproducible release of [3H]-acetylcholine. In this species both isoprenaline (0.1 microM) and formoterol (0.01 microM) inhibited evoked [3H]-acetylcholine release. Inhibition was abolished under the following conditions: (i) presence of propranolol (1 microM) or of the beta 2-selective antagonist ICI 118551 (0.3 microM); (ii) removal of the mucosa at the start of the experiments; (iii) blockade of cyclooxygenase activity by 3 microM indomethacin. 6. In conclusion, the present experiments have demonstrated that activation of beta-adrenoceptors localized in the mucosa mediates inhibition of [3H]-acetylcholine release from the neuroeffector junctions of the pulmonary, parasympathetic nerves most probably by the liberation of inhibitory prostaglandins from the airway mucosa. The adrenoceptor subtype involved differs in rat (beta 1 subtype) and guinea pig (beta 2 subtype) airways.

Acetylcholine↗
PubMed1995

Inhibition of relaxations to nitrergic stimulation of the mouse anococcygeus by duroquinone.

1. The role of copper/zinc superoxide dismutase (Cu/Zn SOD) in protection of nitrergic neurotransmission in the mouse anococcygeus was investigated by use of duroquinone (DQ), which generates superoxide anions within tissues via reduction by flavoprotein enzymes. 2. In control anococcygeus muscles, DQ (10-100 microM) produced concentration-related inhibition (-log IC40 = 4.41) of relaxations to exogenous nitric oxide (NO; 15 microM). Nitrergic relaxations induced by field stimulation (10 Hz; 10 s train) were much less affected, 100 microM DQ reducing nitrergic relaxations by only 14 +/- 6%. 3. Following incubation with the Cu/Zn SOD inhibitor, diethyldithiocarbamate (DETCA; 3 mM; 45 min incubation; 10 min washout), the inhibitory effects of DQ on relaxations to NO were potentiated (-log IC40 = 5.22), and clear, concentration-related inhibitions of nitrergic relaxations were now observed (-log IC40 = 4.54). In both cases, these inhibitions were partially reversed by Cu/Zn SOD (250 u ml-1). In DETCA-treated tissues, DQ (100 microM) also reduced relaxations to sodium nitroprusside (1 microM) and S-nitroso-glutathione (30 microM), but potentiated those to 8-Br-cyclic GMP (100 microM). 4. Neither hydroquinone (HQ: 100 microM) nor 1,4-benzoquinone (BQ: 100 microM), both of which reduced responses to exogenous NO, inhibited relaxations induced by field stimulation in DETCA-treated tissues. Indeed, when added during DQ-induced inhibition of nitrergic relaxations, both HQ and BQ produced partial reversal of the block. 5. DQ had no effect on the detection of superoxide anions estimated via the xanthine:xanthine oxidase chemiluminescence assay, or of authentic NO as measured by a chemical microsensor. However, the detection of both superoxide anions and NO in these assays was inhibited by inclusion of either HQ or BQ. 6. The results support the proposal that nitrergic transmission in the peripheral nervous system is protected by Cu/Zn SOD activity in the region of the neuroeffector junction, and this may explain the lack of effect of superoxide anion generating drugs such as DQ. Such an explanation does not hold for either HQ or BQ, which appear to be acting directly as free radical scavengers in these experiments.

Animals↗
PubMed1987

Muscle sympathetic activity and venous plasma noradrenaline concentrations during static exercise in normotensive and hypertensive subjects.

Peroneal muscle sympathetic activity (MSA) was recorded during 2 min of isometric handgrip at 30% of maximal power and correlated with plasma levels of noradrenaline (NA) in venous blood from the contralateral forearm in 16 normotensive subjects and 15 previously untreated patients with essential hypertension. Resting values for MSA and NA were similar in the two groups and there was a significant positive correlation between the level of MSA (expressed either as bursts per 100 heart beats or bursts min-1) and the concentration of NA. Changes of MSA and NA during handgrip were similar in both groups. When monitored every minute in a subgroup of the material (n = 12), the number of sympathetic bursts min-1 increased maximally by 23% and total MSA (bursts min-1 X mean burst amplitude) by 67% during the second minute of handgrip. The maximal increase of venous NA concentrations was 21% and occurred 2 min later, probably reflecting a slow wash-out of NA from the neuroeffector junctions. It is concluded that: there is no difference in MSA between normotensive and hypertensive subjects at rest or during isometric handgrip, MSA is an important determinant of the concentration of NA in forearm venous plasma, and the relative change of the venous plasma NA concentration during isometric handgrip is considerably smaller than the change in total MSA.

Adult↗
PubMed1990

Neuropeptide Y receptor subtypes, Y1 and Y2.

Heterogeneity among NPY (and PYY) receptors was first proposed on the basis of studies on sympathetic neuroeffector junctions, where NPY (and PYY) can exert three types of action: 1) a direct (e.g., vasoconstrictor) response; 2) a postjunctional potentiating effect on NE-evoked vasoconstriction; and 3) a prejunctional suppression of stimulated NE release; the two latter phenomena are probably reciprocal, since NE affect NPY mechanisms similarly. It was found that amidated C-terminal NPY (or PYY) fragments, e.g., NPY 13-36, could stimulate selectively prejunctional NPY/PYY receptors, which were termed Y2-receptors. Consequently, the postjunctional receptors which were activated poorly by NPY/PYY fragments, were termed Y1-receptors. Later work has indicated that the Y2-receptor may occur postjunctionally in selected sympathetic effector systems. The central nervous system appears to contain a mixture of Y1- and Y2-receptors as indicated by functional as well as binding studies. For instance, NPY and NPY 13-36 produced diametrically opposite effects on behavioral activity, indicating the action of the parent peptide on two distinct receptors. Cell lines, most importantly neuroblastomas, with exclusive populations of Y1- or Y2-receptors, have been characterized by binding and second messenger studies. In this work, selective agonists for the two receptor subtypes were used. Work of many investigators has formed the basis for subclassifying NPY/PYY effects being mediated by either Y1- or Y2-receptors. A preliminary subclassification based on effects of NPY, PYY, fragments and/or analogs is provided in Table 6. It is, however, to be expected that further receptor heterogeneity will be revealed in the future. It is argued that mast cells possess atypical NPY/PYY receptors. The histamine release associated with stimulation of the latter receptors may, at least in part, underlie the capacity of NPY as well as of short C-terminal fragments to reduce blood pressure. Fragments, such as NPY 22-36, appear to be relatively selective vasodepressor agents because of their weak vasopressor properties.(ABSTRACT TRUNCATED AT 400 WORDS)

Calcium↗
PubMed1986

Molecular forms of acetylcholinesterase in mammalian smooth muscles.

A comparative study of the molecular forms of acetylcholinesterase (AChE) was made in various smooth muscles (intestine, vas deferens, ciliary body, iris, nictitating membrane retractor, ureter, arteries, anococcygeus muscles) of some mammals (cat, guinea-pig, rat, rabbit, mouse), seeking for a correlation between the presence of 16 S (asymmetric, tailed) form of AChE in smooth muscles and their type of innervation defined by morphological criteria, as well as by the nature of the main neurotransmitters involved in their neuroeffector junctions. Contrary to previous assertions, many smooth muscles contain 16 S AChE, although all those examined here exhibited a proportion clearly less than that of striated muscles. There are large species-specific and individual variations in the percentage of 16 S AChE. The highest percentages of 16 S AChE were found in ciliary and iris muscles, which are provided with an individual (= multiunit) cholinergic innervation. The vas deferens muscles, which are also individually, but noradrenergically innervated contain practically no 16 S AChE. In the muscles having a fascicular (= unitary) innervation, the differences are striking: 16 S AChE is in rather high amount in intestine muscle layers, whereas it is very low or virtually absent in ureter or arterial muscles. Thus, the type of innervation is not clearly involved in the amount of 16 S AChE present in smooth muscles. As for the nature of neurotransmitter a clear correlation exists only in the case of individual innervation, in which only one neurotransmitter is involved or largely predominant.

Acetylcholinesterase↗
PubMed2002

ATP as a cotransmitter in sympathetic nerves and its inactivation by releasable enzymes.

ATP and norepinephrine (NE) are cotransmitters released from many postganglionic sympathetic nerves. In this article, we review the evidence for ATP and NE cotransmission in the rodent vas deferens with special attention to the mechanisms involved in removing the cotransmitters from the neuroeffector junction. Although the clearance of NE is well understood (e.g., the primary mechanism being reuptake into the nerves), the clearance of ATP is just beginning to be explained. The general belief has been that ATP is metabolized by cell-fixed ecto-nucleotidases. It now seems, however, that when ATP is released from nerves as a transmitter there is a concomitant release of nucleotidases that rapidly degrade ATP sequentially to ADP, AMP, and adenosine, thereby terminating the action of ATP. In the guinea pig vas deferens, there appear to be at least two enzymes, one that converts ATP to ADP and ADP to AMP (an ATPDase) and a second enzyme that converts AMP to adenosine (an AMPase). An important feature of this process is that the transmitter-metabolizing nucleotidases are released into the synaptic space as opposed to being fixed to cell membranes. A preliminary characterization of these enzymes suggests that the releasable ATPDase exhibits some similarities to known ectonucleoside triphosphate/diphosphohydrolases, whereas the releasable AMPase exhibits some similarities to ecto-5'-nucleotidases.

Adenosine Triphosphate↗
PubMed1974

Failure of beta-adrenergic receptor blockade to prevent arrhythmias induced by sympathetic nerve stimulation.

Cardiac arrhythmias produced by electrical stimulation of the ventrolateral cardiac sympathetic nerve in dogs were not blocked by the combined administration of propranolol and practolol in amounts that completely blocked cardiac beta-adrenergic receptors. Blockade of cardiac alpha-adrenergic receptors, as well as cardiac cholinergic receptors, also had no influence on the arrhythmias. These results suggest that the adrenergic neuroeffector junction is fundamentally different from any hitherto described, differing perhaps in the neurotransmitter involved or in the nature of the receptor.

Adrenergic alpha-Antagonists↗
PubMed1995

Tick salivary gland physiology.

The multifunctional, morphologically complex salivary glands are essential to the biological success of ticks and are intricately involved in the transmission of pathogens. They are innervated, and there is convincing evidence that dopamine is a neurotransmitter at the neuroeffector junction controlling fluid secretion. As feeding progresses, the rate of salivary fluid secretion increases greatly, enabling the ixodid tick to concentrate the bloodmeal by returning excess water and ions to the host. Saliva in feeding ticks is rich in bioactive components and exhibits a range of pharmacological properties. Factors identified in saliva or salivary glands include cement to help anchor the mouthparts to the host, various enzymes and inhibitors, histamine agonists and antagonists, prostaglandins, antihemostatic factors, and immuno-modulating factors. A secretion from the salivary glands allows ticks to absorb water from the air during the lengthy periods off their hosts. The physiology of this remarkable organ provides a striking example of strategies that have evolved to meet the challenge of a unique parasitic life style.

Animals↗