Acupuncture modulates mechanical responses of smooth muscle produced by transmural nerve stimulation in gastric antrum of genetically hyperglycemic rats.

Department of Cell Physiology, Graduate School of Medical Sciences, Nagoya City University, Mizuho-ku, Nagoya, Japan.
Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi 08/2009; 45(4):167-85. DOI: 10.1540/jsmr.45.167
Source: PubMed

ABSTRACT Effects of acupuncture treatment on mechanical responses produced by transmural nerve stimulation (TNS) and acetylcholine (ACh) were investigated in circular smooth muscle preparations isolated from the antrum of the stomach of genetically hyperglycemic rats. While control rats had blood glucose levels of about 140 mg/dl, this was approximately tripled in the genetically hyperglycemic rats, but only doubled in the acupuncture treated genetically hyperglycemic rats. Antrum smooth muscle produced phasic contractions spontaneously, with a similar frequency and amplitude in the three groups of rats. Effects of atropine and Nomega-nitro-L-arginine (L-NA) on TNS-induced responses revealed that in the antrum smooth muscle of the control rats, cholinergic excitatory, non-adrenergic non-cholinergic excitatory (NANCE), nitrergic inhibitory and off-responses produced projections: the last projection was considered to be non-adrenergic non-cholinergic non-nitrergic (NANCNN) in nature. In genetically hyperglycemic rats, nitrergic and NANCNN projections were enhanced and NANCE projections were absent. Acupuncture treated genetically hyperglycemic rats showed a reduction of NANCNN projection and enhancement of cholinergic projection, with no alteration to nitrergic projection, but a recovery of NANCE projection. ACh elicited inhibitory responses at low concentrations (1-30 nM) and excitatory responses at high concentrations (100-300 nM), in the three groups of rats. L-NA converted the ACh-induced inhibitory responses to excitatory responses. Immunohistochemical examination indicated no significant difference in the distribution of c-Kit expressing cells in the antrum smooth muscle from the three groups of rats. The results indicated that in antral smooth muscle, hyperglycemia was associated with enhanced activity in nitrergic and NANCNN projections and attenuation of NANCE projections, and that acupuncture treatment caused both a reduced blood glucose level and attenuated NANCNN projections. In genetically hyperglycemic rats, cholinergic responses were enhanced by acupuncture, possibly due to the enhanced cholinergic projections, with no change in the sensitivity of postjunctional muscarinic receptors to ACh.

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    ABSTRACT: Background Effects of acupuncture stimulation on blood glucose concentration and body weight were investigated in the Otsuka Long-Evans Tokushima Fatty (OLETF) rat, a model for type-2 diabetes. Material and Methods Three groups of rats were used: OLETF, acupuncture-treated OLETF (AcOLETF), and Long-Evans Tokushima Otsuka (LETO) rats (as control for the OLETF rats). In AcOLETF rats, acupuncture stimulation was applied twice a week to 6 points (zhongwan, tianshu, qihai, ganshu, pishu, shenshu) and changes in blood glucose concentration and body weight were measured. Results Initially, at 6 weeks old, there was no significant difference in blood glucose levels between groups. Blood glucose levels increased with age in each group, reaching a maximum of about 430 mg/dl at 37 weeks in OLETF rats. In AcOLETF rats, blood glucose levels increased at a slower rate than in OLETF rats, reaching a maximum concentration of about 280 mg/dl at 37 weeks of age, significantly lower than that in OLETF rats. The concentration of blood glucose in LETO rats had stabilized at a maximum value of 120~140 mg/dl by 16 weeks, remaining at this level for up to 39 weeks. In each group, body weight increased with age and was not affected by acupuncture treatment. Conclusions In OLETF rats, acupuncture treatment significantly reduced blood glucose levels, but not their body weight, suggesting that acupuncture therapy was effective in preventing the development of type-2 diabetes mellitus.
    Medical science monitor basic research. 01/2014; 20:70-5.