PACAP and nitric oxide inhibit contractions in the proximal intestine of the atlantic cod, Gadus morhua

2000 ◽  
Vol 203 (3) ◽  
pp. 575-583 ◽  
Author(s):  
C. Olsson ◽  
S. Holmgren
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Intestinal Motility ◽  
Gadus Morhua ◽  
Atlantic Cod ◽  
Inhibitory Response ◽  
Nitric Oxide Donor ◽  
The Mean ◽  
Proximal Intestine ◽  
Spontaneous Contractions

The possible inhibitory roles of pituitary adenylate cyclase-activating polypeptide (PACAP), vasoactive intestinal polypeptide (VIP) and nitric oxide in the control of intestinal motility were investigated in the Atlantic cod, Gadus morhua. Circular and longitudinal smooth muscle preparations developed spontaneous contractions that were inhibited by atropine (10(−)(5)mol l(−)(1)). PACAP 27 and PACAP 38 (10(−)(7)mol l(−)(1)) reduced the amplitude of the contractions but did not usually affect the resting tension. In the circular preparations, the mean active force developed (above resting level; +/− s.e.m.) was reduced from 0. 62+/−0.18 mN to 0.03+/−0.03 mN (N=10) by PACAP 27 and from 0.53+/−0. 20 mN to 0.31+/−0.13 mN (N=7) by PACAP 38, while neither cod nor mammalian VIP (10(−)(10)-10(−)(6)mol l(−)(1)) had any effect. In the longitudinal preparations, PACAP 27 reduced the force developed from 1.58+/−0.22 mN to 0.44+/−0.25 mN (N=8) and PACAP 38 reduced it from 1.61+/−0.47 mN to 0.75+/−0.28 mN (N=5). The nitric oxide donor sodium nitroprusside (NaNP) almost abolished the contractions in the circular preparations, reducing the mean force developed from 0. 47+/−0.05 mN to 0.02+/−0.06 mN (10(−)(6)mol l(−)(1); N=9) and 0+/−0. 07 mN (10(−)(5)mol l(−)(1); N=8). In the longitudinal preparations, NaNP reduced the force developed from 2.03+/−0.36 mN to 0.33+/−0.22 mN (10(−)(6)mol l(−)(1); N=8) and 0.19+/−0.30 mN (10(−)(5)mol l(−)(1); N=8). The L-arginine analogue N(G)-nitro-L-arginine methyl ester (L-NAME; 3×10(−)(4)mol l(−)(1)) enhanced the contractions in both circular and longitudinal preparations, increasing the mean force developed from 0.51+/−0.12 mN to 0.94+/−0.21 mN (N=8) and from 1.49+/−0.36 mN to 3.34+/−0.67 mN (N=7), respectively. However, preincubation with L-NAME before a second addition of PACAP 27 (10(−)(7)mol l(−)(1)) did not affect the response to PACAP, neither did preincubation with the guanylate cyclase inhibitor 6-anilinoquinoline-5,8-quinone (LY83583; 10(−)(5)mol l(−)(1)), while the inhibitory response to NaNP (3×10(−)(7)mol l(−)(1)) was abolished by LY83583. The PACAP analogue PACAP 6–27 (3×10(−)(7)mol l(−)(1)) had no effect on the response to either NaNP (3×10(−)(7)mol l(−)(1)) or PACAP 27 (10(−)(8)mol l(−)(1)) in the circular preparations. These findings indicate the presence of both a cholinergic and a nitrergic tonus in the smooth muscle preparations of the cod. Although PACAP and NaNP both inhibit contractions, there is no evidence of any interactions between the two substances. In addition, NaNP, but not PACAP, probably acts via stimulating the production of cyclic GMP. In conclusion, both PACAP and nitric oxide may act as inhibitory transmitters, using distinct signalling pathways, in the control of intestinal motility in the Atlantic cod.

scholarly journals Enteric reflexes and nitric oxide in the fish intestine

1995 ◽  
Vol 198 (11) ◽  
pp. 2405-2412 ◽  
Author(s):  
P Karila ◽  
S Holmgren
Keyword(s):  
Nitric Oxide ◽  
Electrical Stimulation ◽  
Gadus Morhua ◽  
Atlantic Cod ◽  
Circular Muscle ◽  
Synthesis Inhibitor ◽  
Fish Intestine ◽  
Balloon Distension ◽  
Spontaneous Contractions ◽  
High Degree

The aim of the present study was to elucidate the possible regulation of peristalsis in the intestine of the Atlantic cod Gadus morhua. For this purpose, the mid intestine was dissected out and placed in a partitioned bath. Balloon distension (0.1­0.4 ml) and intramural field stimulation (8 Hz, 10 V) were carried out and the responses of the circular muscle were recorded 1.5 cm orally and anally to the stimulus using force transducers. The preparations developed spontaneous contractions propagating in the anal direction with a frequency of about one contraction per 2 min. Distension of the muscle wall with a balloon did not evoke any recordable peristaltic reflexes. Intramural stimulation caused a contraction oral to the stimulation and a relaxation anal to the stimulation in most cases. Tetrodotoxin abolished the responses to electrical stimulation in both directions. Atropine reduced and methysergide abolished the oral contractions caused by electrical stimulation. Administration of the nitric oxide synthesis inhibitor l-NG-nitro-arginine methyl ester (l-NAME) abolished the anal relaxation caused by electrical stimulation and augmented the oral contractions. The results indicate the presence in teleost fish intestine of an ascending excitatory peristaltic reflex which involves a cholinergic­serotonergic pathway and a descending inhibitory reflex involving a nitrergic pathway. These observations suggest a high degree of conservation of peristaltic mechanisms during vertebrate evolution.

Neuropeptide Y effects on vasorelaxation and intestinal contraction in the Atlantic cod Gadus morhua

2002 ◽  
Vol 282 (5) ◽  
pp. R1414-R1421 ◽  
Author(s):  
Fatemeh Shahbazi ◽  
Susanne Holmgren ◽  
Dan Larhammar ◽  
Jörgen Jensen
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Neuropeptide Y ◽  
Indirect Effect ◽  
Gadus Morhua ◽  
Atlantic Cod ◽  
Direct Action ◽  
Physiological Role ◽  
Cardiovascular Effects ◽  
Nerve Fibers

Neuropeptide Y (NPY) has prominent cardiovascular effects in mammals and sharks, but no such effect has previously been demonstrated in any teleost fish. In the Atlantic cod, we found that cod NPY (10−10–10−6 M) relaxed celiac arteries precontracted with epinephrine, and weak contractions were elicited in intestinal ring preparations. A few NPY-immunoreactive nerve fibers were present along small gut arteries. The results suggest that cod NPY produces vasorelaxation both by a direct action on smooth muscle and by release of prostaglandins, but with no involvement of nitric oxide, leukotrienes, or endothelium-derived relaxing factors. An additional indirect effect involving another neurotransmitter may occur. Cod NPY (10−7 M) and human NPY (10−7 M) had identical effects on the vessels. Small differences only in the effects of porcine [Leu31,Pro34]NPY, NPY-(13–36), and cod NPY suggest the presence of a Y1 subfamily receptor, similar to the zebrafish Ya receptor. A physiological role for NPY in teleost vasculature is concluded, but surprisingly the effect, a vasodilation, is opposite to that in mammals and is mediated by prostaglandins.

Some ectoparasitic trichodinids from Atlantic cod, Gadus morhua L., with a description of Trichodina cooperi n.sp.

1989 ◽  
Vol 67 (7) ◽  
pp. 1793-1800 ◽  
Author(s):  
S. L. Poynton ◽  
J. Lom
Keyword(s):  
Nova Scotia ◽  
Body Surface ◽  
Gadus Morhua ◽  
Atlantic Cod ◽  
Geographic Range ◽  
The Body ◽  
Wild Fish ◽  
Eastern Canada ◽  
Mean Diameter ◽  
The Mean

Trichodina murmanica Polyanskiy, 1955 (= Trichodina domerguei subsp. saintjohnsi Lom and Laird, 1969) and Trichodina cooperi n.sp. were commonly encountered on skin and fins of Atlantic cod, Gadus morhua L., near Halifax, Nova Scotia, Canada. A third species of Trichodina, probably new, was recorded from the skin of one fish. This is believed to be the first report of the genus Trichodina from the body surface of gadoid fish from eastern Canada, and the known geographic range of T. murmanica is extended. Trichodina cooperi n.sp. has an adoral ciliary spiral of 370–380° and is relatively large, the mean diameter of the body is 110 μm, of the adhesive disc (with dark center), 95 μm, and of the denticulate ring, 59 μm. The denticulate ring consists of 24–29 denticles (usually 27), with 7–9 radial pins per denticle. Each denticle has a broad blade, a large central part, and a slightly curved thorn of moderate to broad width, with a central rib when mature. The thorn is approximately twice the length of the blade. The horseshoe-shaped macronucleus has a diameter of 80.0 μm and the micronucleus is in the +y position. Trichodina spp. infected 26% of 39 wild fish 20 to < 60 cm long. Most wild fish yielded less than five ciliates per 24 × 50 mm smear.

scholarly journals Diminished nitroprusside-induced relaxation of inflamed colonic smooth muscle in mice

1998 ◽  
Vol 7 (4) ◽  
pp. 283-287 ◽  
Author(s):  
J. D. van Bergeijk ◽  
H. van Westreenen ◽  
P. Adhien ◽  
F. J. Zijlstra
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Muscle Contraction ◽  
Regional Differences ◽  
Distal Colon ◽  
Smooth Muscle Contraction ◽  
Sodium Sulphate ◽  
Nitric Oxide Donor ◽  
Colonic Tissue ◽  
Dextran Sodium Sulphate

The dextran sodium sulphate (DSS) induced colitis in mice was used as a experimental model to study the contractility of murine longitudinal colonic smooth muscle during inflammation. Smooth muscle segments of proximal, middle and distal colon were mounted in organ baths . Smooth muscle contraction was induced by carbachol, showing an aboral increase in activity, where as in the inflamed middle colonics egment a marked decr ease in activity was observed. The dilatative effect of sodium-nitroprus -side (SNP) as a nitric oxide donor was investigated after precontraction by carbachol. Both in normal and DSS segments administration of SNP to isolated mouse colonic smooth muscle preparations caused regional differences in relaxation, the highest relaxation seen in normal proximal colonic tissue. However, this relaxation was markedly reduced in inflamed proximal preparations , associated with a diminished cGMP contents .

Role of K+Channels in Augmented Relaxations to Sodium Nitroprusside Induced by Mexiletine in Rat Aortas

2000 ◽  
Vol 92 (3) ◽  
pp. 813-820 ◽  
Author(s):  
Hiroyuki Kinoshita ◽  
Toshizo Ishikawa ◽  
Yoshio Hatano
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Sodium Nitroprusside ◽  
Guanylate Cyclase ◽  
Nitric Oxide Donor ◽  
Nitric Oxide Donors ◽  
K Channels ◽  
Vasodilator Effect ◽  
Isolated Rat

Background A class Ib antiarrhythmic drug, mexiletine, augments relaxations produced by adenosine triphosphate (ATP) sensitive K+ channel openers in isolated rat aortas, suggesting that it produces changes in the vasodilation mediated by ATP-sensitive K+ channels. Nitric oxide can induce its vasodilator effect via K+ channels, including ATP-sensitive K+ channels, in smooth muscle cells. Effects of mexiletine on arterial relaxations to nitric oxide donors, have not been studied. Therefore, the current study in isolated rat aortas was designed to (1) evaluate whether mexiletine augments relaxation in response to nitric oxide donors, including sodium nitroprusside, and (2) determine the role of K+ channels in mediating effects of mexiletine on such nitric oxide-mediated relaxation. Methods Rings of rat aortas without endothelia were suspended for isometric force recording. Concentration-response curves of sodium nitroprusside (10(-10) to 10(-5) M) and 1-hydroxy-2-oxo-3-(N-methyl-3-aminopropyl)-3-methyl-1-triazene (NOC-7; 10(-9) to 10(-5) M) were obtained in the absence and in the presence of mexiletine, in combination with a soluble guanylate cyclase inhibitor, 1H-[1,2,4]oxadiazolo [4,3,-a]quinoxaline-1-one (ODQ), or inhibitors for ATP-sensitive K+ channels (glibenclamide), inward rectifier K+ channels (BaCl2), delayed rectifier K+ channels (4-aminopyridine), large conductance Ca2+-dependent K+ channels (iberiotoxin), or small conductance Ca2+-dependent K+ channels (apamin). Results Mexiletine (10(-5) or 3 x 10(-5) M) augmented relaxations to sodium nitroprusside and NOC-7. In arteries treated with glibenclamide (10(-5) M), mexiletine (3 x 10(-5) M) did not affect relaxations to nitric oxide donors, whereas mexiletine augmented relaxations to sodium nitroprusside despite the presence of BaCl2 (10(-5) M), 4-aminopyridine (10(-3) M), iberiotoxin (5 x 10(-8) M) and apamin (5 x 10(-8) M). Relaxations to sodium nitroprusside were abolished by ODQ (5 x 10(-6) M), whereas these relaxations were augmented by mexiletine (3 x 10(-5) M) in arteries treated with ODQ (5 x 10(-6) M). Conclusions These results suggest that ATP-sensitive K+ channels in vascular smooth muscle, contribute to the augmented vasodilator effect of a nitric oxide donor, sodium nitroprusside induced by mexiletine, and that the vasodilator effect is produced, at least in part, via the guanylate cyclase-independent mechanism.

scholarly journals Endothelium-Independent Relaxation of Vascular Smooth Muscle Induced by Persimmon-Derived Polyphenol Phytocomplex in Rats

Nutrients ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 89
Author(s):  
Risa Kudo ◽  
Katsuya Yuui ◽  
Shogo Kasuda
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Mesenteric Arteries ◽  
Inositol Triphosphate ◽  
Sprague Dawley ◽  
Vasorelaxant Effect ◽  
Sprague Dawley Rats ◽  
The Mean ◽  
Artery Disease ◽  
Nitric Oxide Pathway

The vasorelaxant effect of polyphenols is well known, and the mortality rate due to coronary artery disease is low in people who consume polyphenol-containing foods. We aimed to elucidate the mechanism by which polyphenols derived from persimmon juice (PJ) and persimmon leaves (PLs) induce vasorelaxation and suppress vasocontraction in the superior mesenteric arteries isolated from male Sprague Dawley rats. Vasocontraction was induced with 1 µM phenylephrine, and polyphenol-induced vasorelaxation was expressed as a percentage of the previous tone induced by phenylephrine. PJ powder (100 mg/L) induced higher levels of vasorelaxation (mean ± standard error of the mean, 88.6% ± 4.4%) than PLs powder (1 g/L; 72.0% ± 10.8%). Nitric oxide pathway inhibitors (NG-nitro-L-arginine methyl ester + carboxy-PTIO) did not affect persimmon-derived polyphenol-induced vasorelaxation, whereas potassium chloride, tetraethylammonium, and potassium-channel inhibitors did. Vasorelaxation was endothelium independent with both extracts. Phenylephrine-induced vasocontraction was suppressed by pretreatment with PJ and PLs powder, even when inositol triphosphate-mediated Ca2+ release and extracellular Ca2+ influx were inhibited. These results suggest that persimmon-derived polyphenol phytocomplex cause vasorelaxation and inhibit vasocontraction through hyperpolarization of smooth muscle cells. Persimmon-derived polyphenols may be able to prevent cardiovascular diseases caused by abnormal contraction of blood vessels.

Mechanisms underlying the nitric oxide inhibitory effects in mouse ileal longitudinal muscle

2005 ◽  
Vol 83 (8-9) ◽  
pp. 805-810 ◽  
Author(s):  
Maria Grazia Zizzo ◽  
Flavia Mulè ◽  
Rosa Serio
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Mechanical Activity ◽  
Calcium Stores ◽  
Organ Bath ◽  
Inhibitory Effects ◽  
Longitudinal Smooth Muscle ◽  
Sarcoplasmatic Reticulum ◽  
Spontaneous Contractions ◽  
Mouse Ileum

We investigated the mechanisms involved in the nitric oxide (NO)-induced inhibitory effects on longitudinal smooth muscle of mouse ileum, using organ bath technique. Exogenously applied NO, delivered as sodium nitroprusside (SNP; 0.1–100 µmol/L) induced a concentration-dependent reduction of the ileal spontaneous contractions. 1H-[1,2,4]oxadiazolol[4,3,a]quinoxalin-1-one (ODQ; 1 µmol/L), a guanilyl cyclase inhibitor, reduced the SNP-induced effects. Tetraethylammonium chloride (20 mmol/L), a non-selective K+ channel blocker, and charybdotoxin (0.1 µmol/L), blocker of large conductance Ca2+-dependent K+ channels, significantly reduced SNP-induced inhibitory effects. In contrast, apamin (0.1 µmol/L), blocker of small conductance Ca2+-dependent K+ channels, was not able to affect the response to SNP. Ciclopiazonic acid (10 µmol/L) or thapsigargin (0.1 µmol/L), sarcoplasmatic reticulum Ca2+-ATPase inhibitors, decreased the SNP-inhibitory effects. Ryanodine (10 µmol/L), inhibitor of Ca2+ release from ryanodine-sensitive intracellular stores, significantly reduced the SNP inhibitory effects. The membrane permeable analogue of cGMP, 8-bromoguanosine 3′,5′-cyclic monophosphate (100 µmol/L), also reduced spontaneous mechanical activity, and its effect was antagonized by ryanodine. The present study suggests that NO causes inhibitory effects on longitudinal smooth muscle of mouse ileum through cGMP which in turn would activate the large conductance Ca2+-dependent K+ channels, via localized ryanodine-sensitive Ca2+ release.Key words: nitric oxide, mouse ileum, potassium channels, calcium stores.

scholarly journals Quality of Nephrops as food for Atlantic cod (Gadus morhua L.) with possible implications for fisheries management

2004 ◽  
Vol 61 (6) ◽  
pp. 983-991 ◽  
Author(s):  
Björn Björnsson ◽  
Maria Álvaro Dongala Dombaxe
Keyword(s):  
Growth Rate ◽  
Gadus Morhua ◽  
Specific Growth ◽  
Condition Factor ◽  
Atlantic Cod ◽  
Gonadosomatic Index ◽  
Conversion Ratio ◽  
Food Conversion ◽  
The Mean

Abstract Nephrops was found to be of low quality as food for cod. In a laboratory experiment the mean specific growth rate of 1 kg cod was 0.184 and 0.415% d−1 when fed to satiation on Nephrops and capelin, respectively. This large difference in growth rate resulted not only from less intake of Nephrops (1.19 kg cod−1) than capelin (1.55 kg cod−1) but also because more Nephrops (4.6 kg) than capelin (2.2 kg) were required to produce each kilogramme of cod. Higher food conversion ratio was consistent with lower fat content of Nephrops (1.3%) than capelin (9.2%) but the exoskeleton also reduced the digestion rate of Nephrops. In the groups where Nephrops and capelin of equal mean weight were offered simultaneously, 40% of the diet consisted of Nephrops during the first week and 10% during the final seven weeks of the experiment. At the end of the experiment, condition factor, liver index, and gonadosomatic index were significantly lower for cod fed on Nephrops (0.967, 5.7, 7.1, respectively) than for those fed on capelin (1.086, 15.8, 11.2, respectively). These results suggests that predation by cod on Nephrops might be reduced by regular release of capelin or other similar food in the distributional areas of Nephrops.

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