Morgaienko O. Regulatory mechanisms of rat gastric smooth muscle contractile apparatus functioning under stress

Українська версія

Thesis for the degree of Candidate of Sciences (CSc)

State registration number

0413U007415

Applicant for

Specialization

  • 03.00.04 - Біохімія

16-12-2013

Specialized Academic Board

Д 26.001.24

Taras Shevchenko National University of Kyiv

Essay

Alteration of gastric motility was shown to accompany mucosa lesions formation under ulcerogenesis. But the mechanisms of ulcer origination and development have not been dissolved yet completely. In the study, smooth muscle actomyosin was isolated from rat stomachs. Actomyosin functional properties' values were shown to increase under stress-induced lesions of rat gastric mucosa. Meanwhile augmentation of [Ca2+]i level and oppositely directed changes of cAMP, cGMP content were observed in smooth muscle cells under the same conditions, and the ratio cAMP/cGMP was significantly changed. The investigation with phosphorylation and dephosphorylation of actomyosin isolated revealed ATPase activity changes that demonstrate that alteration of regulatory light chain dephosphorylation is involved in violation of actin-myosin interaction regulation under stress-induced lesions of rat gastric mucosa. Notably, mentioned changes in contractile apparatus had occurred at the background of ATP level decrease and adenylate energy charge (by Atkinson) decline in rat gastric smooth muscle tissue as well, as in blood plasma, and were accompanied by adenosine level increase. It indicates switching from high-energy to low-energy state of metabolism under stress. Activation of lipid peroxidation with decreasing of catalase activity was shown in rat blood plasma under stress that was followed by lipid-protein composition alteration. Obtained results demonstrate that changes determined in contractile apparatus under experimental stress-induced lesions of gastric mucosa lead to stimulation of gastric motility. Obtained results reveal some regulatory chains of general and specific mechanisms involved into smooth muscle contractile dysfunction under stress-induced ulceration.

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