Biomedical subjects

E E Daniel

Publications and source records attributed to E E Daniel.

At least 109 records · Page 6Linked to original sources

PubMed1994

Sensitivity to protein kinase C inhibitors of nicardipine-insensitive component of high K+ contracture in rat and guinea-pig aorta.

1. In the rat and guinea-pig aorta, we observed that the contraction to hypertonically-added K+, unlike the isotonic K(+)-induced contraction, was only partially sensitive to nicardipine (0.1, 1 and 10 microM), an L-type Ca2+ channel blocker and occurred in Ca(2+)-free medium containing 50 microM EGTA. We have characterized this nicardipine-insensitive hypertonically-added K+ contraction. 2. The contraction induced by an equi-osmolar concentration of mannitol was similar in size to that evoked by hypertonically-added K+. 3. When the tissue was depleted of its internal Ca2+ stores with various agents such as phenylephrine (10 microM) cyclopiazonic acid (30 microM), thapsigargin (1 microM) or ryanodine (30 microM), or by incubation in Ca(2+)-free medium over 30 min, little effect was observed on the high K+ contracture in the presence of L-type Ca2+ channel blockade. 4. Phentolamine (10 microM) or indomethacin (10 microM) did not reduce the contraction induced by high K+. 5. Application of a protein kinase C inhibitor, H7 (10, 30 and 100 microM) or calphostin C (1 microM), reduced the high K+ contraction but not that caused by an equi-osmolar concentration of mannitol. 6. The data suggest that hypertonic K(+)-induced contraction differs from that caused by hypertonicity or depolarization per se and invokes membrane enzyme activation.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1994

Investigation of alpha 1-adrenoceptor subtypes in canine aorta, using alkylating agents.

The ability of putative selective irreversible ligands SZL-49 (1-(4-amino-6,7-dimethoxy-2,5-diene-2-carbonyl)) and CEC (chlorethylclonidine), for alpha 1A and alpha 1B adrenoceptor subtypes, respectively, to affect alpha 1-adrenoceptors of canine aorta microsomal membranes was investigated. These membranes contain an apparently homogeneous population of [3H]prazosin binding sites. SZL-49, like phenoxybenzamine, abolished all binding of [3H]prazosin. CEC abolished 75% of the prazosin binding sites under the most stringent conditions we applied. However, the remaining 25% of binding sites was identical in affinity for prazosin with control membranes, and competition studies of other subtype-selective ligands revealed unchanged ability to complete against CEC-sensitive and -insensitive sites. We concluded that SZL-49 and CEC are not alpha 1A- and alpha 1B-adrenoceptor selective under in vitro conditions. Our data led to the hypothesis that canine aortic membranes contain exclusively alpha 1B-adrenoceptors but that current tools for identifying alpha 1-adrenoceptor subtypes proved inadequate in vitro in this study.

Adrenergic alpha-1 Receptor Antagonists↗

PubMed1994

Tachykinin-mediated increase in motility acts independently of vasoactive intestinal polypeptide release in the canine ileum.

Tachykinins induce motor activity in the canine ileum, and their mechanism of excitation may include inhibition of the release of a nonadrenergic, noncholinergic inhibitor, for which vasoactive intestinal polypeptide (VIP) is a candidate. Both substance P and neurokinin A produced a dose-dependent increase in ileal contractility with no significant change in VIP output. The highly selective NK1 agonist [Sar9, Met(O2)11]substance P and the highly selective NK2 agonist [Nle10]neurokinin A (4-10) also increased motor activity in the absence of any change in VIP released. These data suggest that the tachykinins produce motor activity in the canine ileum via a mechanism that does not involve changes in VIP output but may involve excitation through both NK1 and NK2 receptors.

Animals↗

PubMed1994

Ultrastructure of interstitial cells of Cajal in the canine distal esophagus.

The ultrastructure of canine distal esophagus was studied focusing on interstitial cells of Cajal (ICC) and their relationships to nerves and muscle. The distal esophagus consisted of two muscle layers composed of intertwining skeletal and smooth muscle bundles. The ICC formed an interconnecting network and were an integral part of these structures. The ICC communicated with one another and with adjacent smooth muscle cells through numerous gap junctions. The morphology of individual ICC resembled that observed in other gut regions. All interstitial cells were densely innervated. The highest density of ICC, just proximal to the lower esophageal sphincter, coincided with the previously reported highest incidence of occurrence of electrical slow wave type action potentials. Examination of a large number of structural associations of ICC led us to conclude that in the distal esophagus, two networks of ICC and nerves exist, one associated with the inner muscle layer, another associated with the outer muscle layer. These networks are not sheet-like structures, such as the network of ICC in the myenteric plexus or deep muscular plexus of the small intestine, but are three dimensional and are interspersed throughout both muscle layers. The networks do not extend into Auerbach's plexus. The main branches of the networks run along the long axis of the esophagus and seem ideally suited to facilitate communication in this direction. These observations suggest that esophageal interstitial cells are structurally organized in such a manner that they may play a role in pacemaking and neural control of esophageal motility.

Animals↗

PubMed1994

Ultrastructural localization of nitric oxide synthase in canine small intestine and colon.

The ultrastructural distribution and subcellular localization of nitric oxide synthase (NOS) immunoreactivity and its possible colocalization with vasoactive intestinal polypeptide (VIP) and substance P in the muscularis externa in canine ileum and colon were studied by using polyclonal antisera raised against VIP, substance P, and cerebellar NOS. Immunogold staining, with or without silver enhancement, was carried out directly on ultrathin sections using single and two-faced double immunogold methods. NOS immunoreactivity was observed in nerve profiles in myenteric plexus and circular muscle layer. Immunoreactivity was occasionally detected in smooth muscle cells and interstitial cells of Cajal. The double immunostaining revealed NOS and VIP in the same nerve varicosities but never in the same organelles. NOS was localized in electron-dense material of undetermined nature, whereas VIP was associated with large granular vesicles. Substance P and NOS were never found in the same nerves. These results indicate that NOS is present in the enteric nerves containing VIP but in different organelles and that nitric oxide release probably does not occur by an exocytotic mechanism.

Amino Acid Oxidoreductases↗

PubMed1994

Characterization of galanin receptor in canine small intestinal circular muscle synaptosomes.

We used 125I-galanin (porcine) as ligand to study the galanin receptors in circular muscle and deep muscular plexus from canine small intestine. Specific binding sites were found in both nerve and muscle membranes. On synaptosomal membranes, the equilibrium binding study showed a high-affinity (dissociation constant, Kd = 1.1 +/- 0.13 nM; maximum binding capacity, Bmax = 244 +/- 2.1 fmol/mg) binding site. The specific binding of 125I-galanin to nerve membrane was inhibited by galanin or NH2-terminal galanin fragments but not by the COOH-terminal fragment. Computer analysis suggested a two-site model (inhibitor constants, Ki1 = 0.02 +/- 0.005 nM and Ki2 = 1.05 +/- 0.3 nM) for competition by galanin-(1-29). Kinetic and competition studies using guanosine 5'-O-(3-thiotriphosphate) or pertussis toxin (PTX) suggested that the high-affinity binding site involved a PTX-sensitive G protein which acted to slow dissociation of bound galanin from the receptor. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis of the galanin receptor complex revealed a radioactive band at 50 kDa. We conclude that, in canine small intestine, galanin may act as an inhibitory neuromodulator by a PTX-sensitive G protein-coupled interaction of galanin and its specific receptor on enteric nerve synaptosomes.

Animals↗

PubMed1994

Galanin receptor in plasma membrane of canine small intestinal circular muscle.

High-affinity binding sites for galanin were identified and characterized in plasma membrane of circular muscle from canine small intestine using 125I-radioiodinated synthetic porcine galanin. Scatchard analysis indicated a high-affinity binding site on plasma membrane with a dissociation constant (Kd) of 0.58 nM and a binding capacity of 389 fmol/mg. Unlabeled galanin or NH2-terminal galanin fragments competitively inhibited the binding of 125I-galanin in a concentration-dependent manner, whereas the COOH-terminal fragment was inactive. Computer analysis of competitive binding data suggested a two-site model with a high-affinity (inhibitor constant, Ki = 0.01 nM) and a low-affinity (Ki = 2.8 nM) binding site. Guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S) enhanced the dissociation of bound 125I-galanin. Cholera toxin (CTX) and GTP gamma S abolished the activity of the high-affinity binding site, leaving the low-affinity binding site. We conclude that galanin may act as an neurotransmitter to inhibit canine small intestinal smooth muscle contraction by interaction with a CTX-sensitive G protein-coupled specific receptor on muscle membrane. This receptor showed different G protein coupling from a synaptosomal receptor previously described in the same tissue preparations.

Animals↗

PubMed1994

Role of nitric oxide-related inhibition in intestinal function: relation to vasoactive intestinal polypeptide.

This study examined the role of nitric oxide (NO) in tonic inhibition of motor activity in isolated, perfused canine ileal segments. Brief addition of N omega-nitro-L-arginine methyl ester (L-NAME) to the perfusate caused, after a delay, a concentration-dependent persistent increase in tonic and phasic activity of circular muscle. This increased motor activity was prevented or reversed by addition of L- but not D-arginine to the perfusate. Removal of Ca2+ or addition of 10(-7) M omega-conotoxin (GVIA) to the perfusate markedly reduced this response. The motor activity induced by L-NAME was accompanied by loss of distal inhibition and enhanced excitation to low-frequency field stimulation. L-NAME infusion significantly reduced tonic vasoactive intestinal polypeptide (VIP) output, sodium nitroprusside increased VIP output, but L-arginine infusion did not restore VIP output. Atropine (10(-7) M) and/or hexamethonium (10(-4) M) reduced the motor response to L-NAME by 75%. Atropine reduced and hexamethonium nearly abolished VIP output. We conclude that there is tonic Ca(2+)-dependent NO output from perfused intestinal segments dependent on nerves with N-Ca channels, that NO acts to inhibit muscle directly and by inhibiting release of excitatory mediators, and that this output is the primary inhibitory determinant of contractile activity.

Acetylcholine↗

PubMed1994

Relaxation oscillator and core conductor models are needed for understanding of GI electrical activities.

This review examines the applicability of modeling of intestinal electrical activities (slow waves or pacesetter potentials) by coupled relaxation oscillator models, in comparison to a "multidimensional model" based on core conductor theory. We briefly review the relaxation oscillator model and correct some misunderstandings. We point out that new insights about the role of networks of interstitial cells of Cajal in intestinal pacemaking require reconsideration of the mechanisms producing oscillations, the coupling between oscillators, and how the oscillator network is coupled to the driven cells. Recent advances in relaxation oscillator models allow the production of pacemaking pacemaking activity, which can be selectively varied as to waveform, frequency, and occurrence of silent periods. Core conductor models do not produce pacemaking activity or permit this flexibility. We point out that many of the criticisms leveled against relaxation oscillator models relate to studies made in simplified in vitro systems constrained by extensive dissection. Such systems do not adequately reflect the in vivo systems. We conclude that a full understanding of control of electrical (and mechanical) events in the gastrointestinal tract requires that better understanding of relaxation oscillator models growing out of recent research be combined with improved applications of core conductor theory to multidimensional models.

Animals↗

PubMed1994

Neural and myogenic effects of leukotrienes C4, D4, and E4 on canine bronchial smooth muscle.

The leukotrienes (LTs), referred to as the slow-reacting substance of anaphylaxis (SRS-A), are reported to have little or no activity in the canine airway. The objective of this study was to determine whether LTC4, LTD4, and LTE4 (10(-10)-10(-7) M) play a role in neuromuscular control of third- to fifth-order canine bronchi. In the presence of 1 microM indomethacin (Indo), canine bronchial smooth muscle contracted and was depolarized in a concentration-dependent manner by LTC4 or LTD4 but not by LTE4. LTC4 and LTD4 concentration-response curves were not significantly affected when conducted in the presence of any of the following: 10(-7) M propranolol (beta-adrenoceptor antagonist), 10(-6) M chlorpheniramine (H1-receptor antagonist), 10(-6) M ketanserin (nonselective 5-hydroxytryptamine receptor antagonist), 10(-7) M atropine (muscarinic receptor antagonist), and 10(-6) M tetrodotoxin (sodium channel blocker). LTC4 and LTD4 also potentiated electrical field-stimulated (EFS) excitatory junction potentials (EJPs), suggesting a possible prejunctional enhancement of acetylcholine release. In the absence of Indo, no postjunctional responses to LTC4 and LTD4 occurred. Endogenous prostaglandin E2 (PGE2) and 6-keto-PGF1 alpha (a stable metabolite of PGI2) levels from canine bronchi were significantly reduced by Indo. In the presence of Indo, addition of > or = 10(-8) M of PGE2 suppressed contractions to LTC4 and LTD4. These data suggest that the decrease in PGE2 and PGI2 production by Indo is sufficient to unmask the excitatory postjunctional actions of LTC4 and LTD4 on bronchial smooth muscle. Serine borate (45 mM; an inhibitor of gamma-glutamyl transpeptidase, which prevents the conversion of LTC4 to LTD4) increased selectively the contractile activity of LTC4. L-Cysteine (3 mM; an inhibitor of an aminopeptidase, which prevents the conversion of LTD4 to LTE4) enhanced the contractile responses to LTD4. Serine borate increased the amplitude and duration of EFS contractions and potentiated the amplitude of EFS EJPs; the last effects were prevented by nordihydroguaiaretic acid. These and other studies suggest that LTs are synthesized by canine bronchi and have receptors on canine bronchial smooth muscle but that contractions to LTC4 and LTD4 in the canine airway are usually not observed because of the presence of inhibitory prostanoids (PGE2 and PGI2). We suggest that decreases in PGE2 and PGI2 in models of airway disease in combination with increases in LTC4, LTD4, and thromboxane A2 may contribute to airway hyperresponsiveness in vitro.

6-Ketoprostaglandin F1 alpha↗

PubMed1994

NK1 receptors mediated release of 6-keto-PGF1 alpha from the ex vivo perfused canine ileum.

The purpose of this study was to determine the effects of tachykinins on prostanoid production by the dog ileum and to characterize the tachykinin receptor(s) responsible for the principal eicosanoid shown to be released, 6-keto-PGF1 alpha. Substance P, the selective NK1 receptor agonist [Sar9,Met(O2)11]substance P and neurokinin A caused concentration-dependent production of 6-keto-PGF1 alpha; neurokinin A was least potent. The selective NK2 agonist [Nle10]neurokinin A(4-10) had no effect. The selective NK1 antagonist CP-96,345 (10(-7) M), blocked 6-keto-PGF1 alpha release from substance P (10(-7) M), [Sar9,Met(O2)11]substance P (10(-7) M) and neurokinin A (10(-7) M). Although the putative NK2 antagonist MEN 10207 (10(-7) M) partially blocked the 6-keto-PGF1 alpha release induced by neurokinin A (10(-7) M), we conclude that all these peptides acted primarily on NK1 receptors to induce 6-keto-PGF1 alpha. Additional experiments suggest that a major site of production of 6-keto-PGF1 alpha in the canine ileum may be the vasculature, but these experiments do not exclude other sources such as intestinal muscle for this prostanoid. Calcium-free Krebs' solution partially reduced the release of 6-keto-PGF1 alpha to substance P (10(-7) M), implying that extracellular calcium helps support tachykinin-induced production of 6-keto-PGF1 alpha. Blockade of synthesis of another vasoactive mediator, endothelium-derived relaxing factor (nitric oxide), by N omega-L-arginine methyl ester) did not alter substance P-induced release of 6-keto-PGF1 alpha.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗

PubMed1994

L-type calcium channels may fill directly the IP3-sensitive calcium store.

The relationship between inositol-1,4,5-trisphosphate-sensitive Ca2+ stores and Ca2+ entry through potential-dependent L-type Ca2+ channels was examined using whole-cell voltage-clamp technique in cells of longitudinal muscle layer of guinea-pig ileum. It was found that heparin (10(-10) mol/l) in the pipette rapidly inhibited the current through L-type Ca2+ channels. Neither an inhibitor of the sarcoplasmic reticulum Ca2+ pump (cyclopiazonic acid) nor blockers of Ca(2+)-induced Ca2+ release (ryanodine or ruthenium red) affected the Ca2+ current. The failure of heparin to affect Ca(2+)-currents through L-type Ca2+ channels in cells from circular muscle of the same organ suggested that heparin had no direct effect on L-type Ca2+ channels. Thus the inhibition of the latter in heparin-loaded cells from the longitudinal layer is supposed to be Ca(2+)-dependent due to the overfilling of the inositol-1,4,5-trisphosphate-sensitive Ca2+ store.

Animals↗

PubMed1994

Effects of Panax notoginseng saponins on receptor-operated Ca2+ channels in vascular smooth muscle.

The effects of saponins of Panax notoginseng (PNGS) on the alpha-adrenoceptor agonists-induced contractile responses and Ca2+ movement were studied in dog mesenteric artery (MA) and saphenous vein (SV). PNGS reduced the contractions and the 45Ca influx (from 0.36 +/- 0.03 to 0.14 +/- 0.05 mumol.g-1 wet strip) induced by phenylephrine (Phe) without effect on KCl-induced contraction and 45Ca influx which were nearly completely inhibited by nifedipine 0.1 mumol.L-1. PNGS did not change the 45Ca efflux induced by Phe and the Kd value (from 0.76 +/- 0.04 to 0.72 +/- 0.15 nmol.L-1) for [3H]prazosin binding on the microsomal membrane isolated from MA. Our results indicate that PNGS selectively inhibits Ca2+ entry through receptor-operated Ca2+ channel.

Adrenergic alpha-Agonists↗

PubMed1994

Identification of mechanisms and sites of actions of mu and delta opioid receptor activation in the canine intestine.

Perfusion with ([N-Me-Phe3,D-Pro4]morphiceptin (PL017)), [D-Pen2,5]enkephalin (DPDPE) and MEt5 and Leu5 enkephalin induced circular muscle contractions and decreased immunoreactive vasoactive intestinal polypeptide (VIP) venous output in canine ileal segments. Motility and VIP responses to PL017 were abolished by the mu antagonist CTAP (D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2) and unchanged by the delta antagonist ICI 174,864 ([N,N-dially-Tyr1,Aib2,3]Leu-enkephalin) which abolished DPDPE motility and VIP responses. The VIP response to DPDPE was unchanged by CTAP, which reduced motility responses, suggesting a DPDPE interaction with endogenous mu opioids, at a mu/delta(complexed) receptor. ICI 174,864 abolished Met5 and Leu5 enkephalin motility responses and Leu5 enkephalin VIP responses while CTAP was ineffective on Leu5 enkephalin motility responses or on both enkephalin VIP responses. CTAP increased Met5 enkephalin motility responses suggesting mu actions to inhibit excitatory nerves. ICI 174,864 reduced Met5 enkephalin VIP output decrements requiring CTAP addition for abolition, suggesting actions at mu/delta(complexed) receptors. Inhibition of nitric oxide synthase with N-omega-L-arginine methyl ester (L-NAME) abolished delta opioid and reduced by 30% mu opioid motility responses, leaving the VIP response intact. Hexamethonium and atropine abolished tonic VIP output, leaving intact motility responses to PL017 and DPDPE. Subsequently L-NAME eliminated delta opioid and reduced by 1/3 mu opioid motility responses. All opioids reduced the NO-mediated IJPs in myenteric plexus-free ileal circular muscle. Thus mu or delta opioids inhibit both NO and VIP release but removal of NO, not VIP, disinhibits circular muscle motility.

Amino Acid Sequence↗

PubMed1994

Amplification of 5-hydroxytryptamine-induced contractile responses via 5-hydroxytryptamine receptors and alpha-adrenoceptors in dog mesenteric artery and vein.

The interactions between 5-hydroxytryptamine (5-HT) and both serotonergic and alpha adrenoceptors were investigated by using isolated dog mesenteric vascular rings mounted in tissue baths for the measurement of isometric contraction. In the mesenteric artery, 5-HT elicited concentration-dependent contractions, producing 46.5% of the KCl maximal response. At low concentrations, the 5-HT-induced contraction was effectively inhibited by 10(-6) M methysergide and by 10(-6) M ketanserin, but was prazosin-resistant. At high 5-HT concentrations, the contractile response was effectively antagonized by 10(-7) M prazosin. The presence in the medium of 20 mM KCl, which increased resting tension less than 10% of the KCl maximal response, markedly enhanced the responses to 5-HT primarily at concentrations lower than 10(-5) M. These amplified responses were methysergide-sensitive, but prazosin- and ketanserin-resistant. In the mesenteric vein, exposure to 5-HT caused an extremely small contraction, producing 5.2 +/- 4.3% of the KCl maximal response. In the presence of 20 mM KCl, which had small contractile effects, 5-HT produced a biphasic concentration-response curve. Methysergide (10(-6) M) and 10(-6) M ketanserin effectively inhibited the responses to low concentrations of 5-HT, and only 10(-7) M rauwolscine effectively blocked the responses to high concentrations of 5-HT. In the dog mesenteric artery, our data suggest that addition of threshold concentrations of KCl enhanced the contractile response to 5-HT through amplification of 5-HT1-like receptor-mediated responses. In the dog mesenteric vein, KCl enhanced 5-HT responses via amplification of both 5-HT2 receptor- and alpha-2 adrenoceptor-mediated responses.

Animals↗

PubMed1994

Properties of the LP-805-induced potassium currents in cultured bovine pulmonary artery endothelial cells.

The actions of 8-tert-butyl-6,7-dihydropyrolo[3,2-e]-5- methylpyrazolo[1,5-a]pyrimidine-3-carbonitrile (LP-805) on membrane K+ currents in cultured bovine pulmonary artery endothelial cells were investigated using the patch-clamp technique. In the whole-cell voltage clamp experiments, with 11 mM ethylene glycol bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) in the pipette, membrane currents revealed only an inwardly rectifying K+ current, and no outward current could be observed at depolarized potentials. Using a pipette solution containing 0.3 mM EGTA, outward K+ current was present in response to depolarizing voltage steps from a holding potential of -60 mV. LP-805 (1-10 microM) significantly increased outward K+ currents in a concentration-dependent manner. The increase of this K+ current was inhibited by 5 mM tetraethylammonium and 5 mM tetrabutylammonium to a level less than the control. Partial recovery occurred on washout. However, the increase of outward K+ current by 10 microM LP-805 was unaffected by 5 mM 4-aminopyridine and 1 microM glibenclamide. LP-805 (1-10 microM) significantly decreased the inwardly rectifying K+ current in a concentration-dependent manner. In cell-attached patches, inward single K+ currents were recorded at negative membrane potentials, and single channel conductance was 23 +/- 2 pS (n = 5). No outward current could be observed at positive potentials. LP-805 (10 microM) inhibited the inwardly rectifying K+ currents. Thus LP-805 inhibits inwardly rectifying K+ currents but activates outward Ca(++)-dependent K+ currents in bovine pulmonary artery endothelial cells.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Aminopyridine↗

PubMed1993

Characterization of [3H]ryanodine binding sites in smooth muscle of dog mesentery artery.

The ryanodine receptor has been widely demonstrated to be a Ca2+ release channel in both skeletal and cardiac muscle. Ryanodine also functionally affects Ca2+ release from an intracellular pool of smooth muscle. In the present study, both high and low affinity ryanodine binding sites are identified in dog mesenteric artery (with Kd 5 nM and 269 nM, respectively). [3H]ryanodine binding is not correlated with the density of innervation in different smooth muscles. This study provides direct evidence of the presence of ryanodine binding sites in dog mesentery artery. These ryanodine binding sites are of smooth muscle origin.

Animals↗

PubMed1993

PYY: a neuropeptide in the canine enteric nervous system.

This study re-examined the anatomical locations of PYY in the canine gastrointestinal tract. Immunohistochemical studies with two relatively selective PYY antisera demonstrated PYY-LI immunoreactivity in nerve cell bodies and nerve fibres in the intestinal and gastric myenteric plexus and the intestinal submucosal plexus and in nerve fibres of the intestinal deep muscular plexus. Immunoreactive PYY-LI was also present in ileal endocrine cells. All PYY-LI immunoreactivity was completely abolished by pre-incubation of the antibodies with synthetic PYY but was unaltered by pre-incubation with synthetic NPY. Individual synaptosomal preparations obtained from canine intestinal and gastric myenteric plexus, and intestinal deep muscular plexus and submucous plexus, contained considerable quantities of PYY-LI which, on reverse-phase HPLC, co-eluted with a synthetic canine/porcine PYY standard. In contrast, isolated myenteric ganglia from rat and guinea pig did not contain detectable amounts of PYY-LI. These studies demonstrate that PYY is not confined to distal intestinal endocrine cells in the dog but is also an enteric neuropeptide with maximal concentrations being present in the intestinal myenteric plexus.

Animals↗