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首页> 外文期刊>Life sciences >Nitrergic relaxation in rat gastric fundus: influence of mechanism of induced tone and possible role of sarcoplasmic/endoplasmic reticulum Ca2+ ATPase.
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Nitrergic relaxation in rat gastric fundus: influence of mechanism of induced tone and possible role of sarcoplasmic/endoplasmic reticulum Ca2+ ATPase.

机译：大鼠胃底的亚硝酸盐松弛：诱导的语气机制的影响以及肌浆/内质网Ca2 + ATPase的可能作用。

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The aim of this study was to investigate the influence of the mechanism of induced tone and the role of sarcoplasmic/endoplasmic reticulum Ca2+ ATPase (SERCA) in nitrergic relaxation of rat gastric fundus. Prostaglandin F(2alpha) (PGF(2alpha)), thapsigargin (TSG) and cyclopiazonic acid (CPA) were used in concentrations that induced a similar contraction (20 g force/g tissue). Nifedipine (3 x 10(-7) M) completely relaxed PGF(2alpha)-contracted tissues and relaxed tissues contracted by TSG and CPA by 20 +/- 6% and 56 +/- 12% respectively; contraction induced by the three contractile agents was fully reversed by a general Ca2+ entry blocker 1-[2-(4-methoxyphenyl)-2-[3-(4-metoxyphenyl)propoxy]ethyl-1H-imidazole HCl (SKF 96365; 10(-5) M). In the presence of nifedipine (3 x 10(-7) M) or verapamil (10(-5) M), PGF(2alpha) and CPA-induced contractions were still approximately 50% relaxed by SKF 96365. This suggests that contractions induced by PGF(2alpha) are related to Ca2+ entry through L-type voltage-operated Ca2+ channels and that contractions by TSG are mainly related to Ca2+ entry through store-operated Ca2+ channels. Relaxant responses to exogenous nitric oxide (NO), to endogenous NO released by electrical field stimulation, and to vasoactive intestinal polypeptide (VIP) were studied in tissues contracted by TSG and CPA and compared to responses in tissues contracted by PGF(2alpha). Responses to exogenous and endogenous NO were greatly attenuated in TSG-contracted tissues, but not in CPA-contracted tissues. When contraction was induced by CPA in the presence of nifedipine or verapamil, relaxations to exogenous and endogenous NO were also significantly reduced. Relaxation induced by VIP was reduced in tissues contracted by either TSG or CPA in the presence of nifedipine or verapamil. These results suggest that the ability of the nitrergic neurotransmitter to induce relaxation of rat gastric fundus is influenced by the mechanism used to induce tone and are indicative for a role for SERCA in nitrergic relaxation. However, activation of SERCA appears to not be unique for nitrergic relaxation, but might also be used by VIP, a co-transmitter of NO in this tissue.
机译：这项研究的目的是调查诱导的语调的机制和肌浆网/内质网Ca2 + ATPase（SERCA）在大鼠胃底硝化舒张中的作用。前列腺素F（2α）（PGF（2α）），毒胡萝卜素（TSG）和环吡唑酸（CPA）的使用浓度可引起类似的收缩（20 g力/ g组织）。硝苯地平（3 x 10（-7）M）使PGF（2α）收缩的组织完全放松，TSG和CPA分别使收缩的组织收缩20 +/- 6％和56 +/- 12％;一般的Ca2 +进入阻滞剂1- [2-（4-甲氧基苯基）-2- [3-（4-甲氧基苯基）丙氧基]乙基-1H-咪唑HCl（SKF 96365; 10）完全逆转了三种收缩剂引起的收缩（-5）M）。在存在硝苯地平（3 x 10（-7）M）或维拉帕米（10（-5）M）的情况下，SKF 96365仍可将PGF（2alpha）和CPA诱导的收缩保持约50％的舒张。这表明收缩可诱导PGF（2alpha）的作用与通过L型电压操作的Ca2 +通道进入Ca2 +有关，而TSG的收缩主要与通过存储操作的Ca2 +通道进入Ca2 +有关。在由TSG和CPA收缩的组织中研究了对外源性一氧化氮（NO），电场刺激释放的内源性NO和对血管活性肠多肽（VIP）的松弛反应，并将其与PGF（2alpha）收缩的组织中的反应进行了比较。在TSG收缩的组织中，对外源性和内源性NO的反应大大减弱，而在CPA收缩的组织中则没有。当在硝苯地平或维拉帕米存在下CPA引起收缩时，对外源性和内源性NO的松弛也显着降低。在硝苯地平或维拉帕米存在下，由TSG或CPA收缩的组织减少了VIP引起的放松。这些结果表明，硝化神经递质诱导大鼠胃底松弛的能力受诱导音调机制的影响，并指示SERCA在硝化松弛中的作用。但是，SERCA的激活对于硝化舒张似乎不是唯一的，但也可以由VIP（NO在该组织中的共同递质）使用。

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