Alteration of Contractile Properties to Serotonin in Gastric Fundus Smooth Muscle Isolated from Streptozotocin (STZ)-Induced Diabetic Rats.

Zhu, Banghao; Sakata, Yasushi

doi:10.1540/jsmr.32.165

Cited by 8 publications

(5 citation statements)

References 22 publications

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“…3A, 3B). This suppressive effect of PDBu on the 5-HT-induced contraction in rat stomach fundus is consistent with a previous finding (Zhu and Sakai, 1996). On the other hand, the carbachol-and ET-1-induced contractions were only partially inhibited by PDBu (Fig.…”

Section: Discussionsupporting

confidence: 93%

“…In other smooth muscles, however, such activation of PKC either has no effect on tension or it induces relaxation. For example, phorbol esters reportedly inhibit the contractions induced by histamine (Baraban et al, 1985;Holzer and Lippe, 1989), serotonin (5-HT) (Zhu and Sakai, 1996), carbachol (Menkes et al, 1986;Sasaguri and Watson, 1989) and substance P (Holzer and Lippe, 1989), and these effects are possibly induced by activation of Na + -K + -ATPase (Sasaguri and Watson, 1990) or via a negative feed-back mechanism (Baraban et al, 1985;Menkes et al, 1986). Moreover, phorbol 12,13-dibutyrate (PDBu) has been found to cause a concentration-dependent decrease in basal tone in the smooth muscle of the internal anal sphincter (Chakder et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

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Effect of phorbol 12,13-dibutyrate on smooth muscle tone in rat stomach fundus

Matsumoto

Nishiyama

Kobayashi

et al. 2005

J. Smooth Muscle Res.

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We investigated the effects of phorbol 12,13-dibutyrate (PDBu), a typical protein kinase C (PKC) activator, on smooth muscle tone in the rat stomach fundus. In 5-hydroxytriptamine (5-HT)-precontracted stomach fundus strips, PDBu induced dosedependent relaxation, but 4α-phorbol 12,13-didecanoate, a phorbol ester that does not activate PKC, did not induce relaxation. A PDBu-induced dose-dependent relaxation was also observed in strips precontracted with platelet-activating factor (PAF), carbachol, or 60 mM K + . In stomach fundus strips pretreated with PDBu, the contractile responses to 5-HT and PAF were completely blocked, but those induced by carbachol and endothelin-1 (ET-1) were only partially inhibited. In stomach fundus strips preincubated with carbachol in Ca 2+ -free medium, the Ca 2+ -induced contraction was decreased by preincubation with PDBu. In strips preincubated with 5-HT, PAF, or ET-1 in Ca 2+ -free medium, Ca 2+ -induced contractions were greatly inhibited by pretreatment with PDBu.These results suggest that in rat stomach fundus strips, PDBu-induced relaxation is mediated by activation of PKC. We speculate that a major factor mediating the relaxant action of PDBu in rat stomach fundus smooth muscle is represented by a reduction in Ca 2+ influx via an inhibition of Ca 2+ channels.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Effect of phorbol 12,13-dibutyrate on smooth muscle tone in rat stomach fundus

Matsumoto

Nishiyama

Kobayashi

et al. 2005

J. Smooth Muscle Res.

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“…Interestingly, in contrast to the bethanechol contractions, the serotonin-induced contractions were similar in the two groups. A prior study (39) has shown alterations of contractile responses to serotonin in gastric fundic smooth muscle from streptozotocin-induced diabetic rat.…”

Section: Discussionmentioning

confidence: 90%

Regional gastric contractility alterations in a diabetic gastroparesis mouse model: effects of cholinergic and serotoninergic stimulation

James¹,

Ryan²,

Crowell³

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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. Regional gastric contractility alterations in a diabetic gastroparesis mouse model: effects of cholinergic and serotoninergic stimulation. Am J Physiol Gastrointest Liver Physiol 287: G612-G619, 2004. First published April 23, 2004 10.1152/ ajpgi.00431.2003.-The C57BLKS/J db/db mouse develops hyperglycemia and has delayed gastric emptying that is improved with tegaserod, a partial 5-HT4 agonist. Our aims here were to determine regional gastric contractility alterations in C57BLKS/J db/db mice and to determine the effects of serotonin and tegaserod. The contractile effects of bethanechol, serotonin, and tegaserod in fundic, antral, and pyloric circular muscle were compared in C57BLKS/J db/db mice and normal littermates. The effects of tetrodotoxin, atropine, and 5-HT receptor antagonists were studied. Contractions in response to bethanechol were decreased in the fundus, similar in the antrum, but increased in the pylorus in diabetic mice compared with controls. Serotonin and, to a lesser extent, tegaserod caused contractions that were more pronounced in the fundus than in the antrum and pylorus in both diabetic and normal mice. Serotonin-induced contractions were partially inhibited by atropine, the 5-HT4 antagonist GR113808, and the 5-HT2 antagonist cinanseron but not tetrodotoxin. Regional gastric contractility alterations are present in this diabetic gastroparesis mouse model. Fundic contractility was decreased, but pyloric contractility was increased in the pylorus to cholinergic stimulation in diabetic mice. Serotonin's contractile effect is mediated, in part, through muscarinic, 5-HT2, and 5-HT4 receptors. This study suggests that fundic hypomotility and pyloric hypercontractility, rather than antral hypomotility, play important roles for the gastric dysmotility that occurs in diabetes.serotonin; tegaserod GASTROPARESIS (delayed gastric emptying) is frequent in diabetic patients. It is a well-recognized complication of longstanding diabetes. Although classically, gastroparesis occurs in insulin-dependent diabetic patients, it also develops in type 2 (T2DM) or non-insulin-dependent diabetes mellitus (15). Gastroparesis is associated with antral hypomotility and perhaps pyloric dysfunction (2, 23).Treatment of gastroparesis is with prokinetic agents, which accelerate gastric emptying. Tegaserod, an aminoguanidine indole compound, is a recently developed 5-HT 4 partial agonist (1). Activation of 5-HT 4 receptors triggers the release of neurotransmitters from the enteric nerves resulting in increased contractility and stimulation of the peristaltic reflex (10). Tegaserod has been shown to accelerate gastric emptying in some (6) but not all studies (28).Strains of rats and mice with spontaneously developing hyperglycemia have been recognized as useful models to study the effects of diabetes. The Jackson Laboratory C57BLKS/J db/db mouse spontaneously develops hyperglycemia (12) and is a model for non-insulin-dependent diabetes mellitus (24). Prior studies in this mouse strain (22) have shown delayed gastric em...

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“…Generally, an increased reactivity to vasoconstrictor agents, attributed to a deficiency in the vasorelaxant capacity of the endothelium, was described in streptozotocin‐injected rats (7, 8). In some cases, vascular tissue from diabetic rats showed a decrease in maximal response to serotonin or methoxamine (9–12) together with an unmodified reactivity to norepinephrine (13). As far as the endothelium‐dependent relaxation, e.g.…”

Section: Introductionmentioning

confidence: 99%

Vascular reactivity in diabetic rats: effect of melatonin

Reyes-Toso¹,

Rosón²,

Albornoz³

et al. 2002

Journal of Pineal Research

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The aim of the present study was to evaluate the in vitro contractile response of rat aorta in mild and severe type I diabetes and the effect of melatonin on it. Aortic rings were obtained from male Wistar rats injected with streptozotocin 8-12 wks earlier. Rats were divided into three groups: non-diabetic rats (NDR), mildly diabetic rats (MDR) and severely diabetic rats (SDR). Dose-response curves for acetylcholine-induced, endothelium-related relaxation of aortic rings (after previous exposure to phenylephrine) and for serotonin-induced vasoconstriction were conducted in the presence or absence of 10-5 mol/L melatonin. This protocol was repeated with rings preincubated in a high glucose solution (44 mmol/L). The contractile response to phenylephrine decreased in SDR, an effect counteracted by preincubation with high glucose. Melatonin decreased phenylephrine-induced vasoconstriction in MDR and counteracted the effect of high glucose in SDR. Acetylcholine-evoked relaxation decreased significantly after exposure to a high glucose in SDR, this effect being counteracted by melatonin. Serotonin-induced vasoconstriction decreased in SDR and augmented in MDR, but only after exposure to high glucose. Melatonin reduced the maximal tension of aortic contraction after serotonin in MDR, both under basal conditions and after preincubation in a high glucose solution. The results support the existence of differences in vasomotor responses as a function of the diabetes state and of an improvement of contractile performance in diabetic rats after exposure to melatonin at a pharmacological concentration (in terms of circulating melatonin levels but not necessarily for some other fluids or tissues).

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Alteration of Contractile Properties to Serotonin in Gastric Fundus Smooth Muscle Isolated from Streptozotocin (STZ)-Induced Diabetic Rats.

Cited by 8 publications

References 22 publications

Effect of phorbol 12,13-dibutyrate on smooth muscle tone in rat stomach fundus

Effect of phorbol 12,13-dibutyrate on smooth muscle tone in rat stomach fundus

Regional gastric contractility alterations in a diabetic gastroparesis mouse model: effects of cholinergic and serotoninergic stimulation

Vascular reactivity in diabetic rats: effect of melatonin

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