Leszek Szadujkis-Szadurski, Jan Talar, Krzysztof Wiśniewski, Wiesław Tomaszewski, Małgorzata Łukowicz, Rafał Szadujkis-Szadurski

Leszek Szadujkis-Szadurski, Jan Talar, Krzysztof Wiśniewski, Wiesław Tomaszewski, Małgorzata Łukowicz, Rafał Szadujkis-Szadurski – The modulating effects of laser radiation on the extra- and intracellular Ca2+ store and vascular resistance in the perfused tail artery of the rat. Fizjoterapia Polska 2002; 2(1); 11-20

Abstract
Background. Low-level laser radiation modulates many cell functions, but the operating mechanism of its effects has not been sufficiently explained. Our research indicates that these effects are closely with impact on the cellular signaling system, where the ion receptors and channels play a central role.Material and method. The research involved perfused rat tail arteries based on two independent experimental models: model I, in which only the intracellular Ca2+ ion store is ised in the contraction reaction of arterial smooth muscle tissue, and model II, in which the extracellular poor is used. In model I only phenylephrine (an agonist of the alpha-1-adrenergic receptor) elicits contraction, whereas in model II both phenylephrine and BAY K8644 elicit contractions. These models were used to study the impact of low-power laser radiation (10-110 mV).Results. Our research indicated that phenylephrine causes an increase in perfusion pressure as a result of mobilizing the both the intracellular and extracellular stores of Ca2+ ions. The increased perfusion pressure obtained in this way is maintained for ca. 20-30 minutes. The exposure of arteries to laser radiation (10-110 mV) in a manner dependent on the radiation power reduces this reaction. BAY K8644, acting directly on the L-type Ca2+ ion channels, under these conditions does not cause an increase in perfusion pressure. After the intracellular store of Ca2+ ions is emptied, the increased perfusion pressure reactions to phenylephrine and BAY K8644 can be triggered by supplementing the missing CaCl2 in EGTA-Krebs fluid without Ca2+. The exposure of arteries to similar laser radiation reduces the reactions of arteries to phenylephrine and has no impact on the reactions triggered by BAY K8644. The L-NAME inhibitor NO – synthase effectively protects the arteries against the modulating effect of laser radiation.Conclusions. The results obtained here confirmed the association between the effect of laser radiation the contraction reaction of arteries triggered by phenylephrine and NO synthesis. A comparison to the effect of phenylephrine with BAY K8644 suggests that the effect of modulating the arteries’ reactions is conditioned by binding of G protein with the receptor. This suggestion is consistent with the fact that is no inhibiting action of laser radiation on the direct effect of BAY K8644.

Key words:
Phenylephrine, perfusion pressure, BAY K 8644, NO synthesis