Leszek Szajdukis-Szadurski, Wiesław Tomaszewski, Anna Talar, Rafał Szajdukis-Szadurski, Katarzyna Szajdukis-Szadurska, Jolanta Kujawa, Iwona Pyszczek

Leszek Szajdukis-Szadurski, Wiesław Tomaszewski, Anna Talar, Rafał Szajdukis-Szadurski, Katarzyna Szajdukis-Szadurska, Jolanta Kujawa, Iwona Pyszczek – The modulating effect of laser radiation and low-power ultrasounds on the contraction reaction in perfused arteries. Fizjoterapia Polska 2003; 3(2); 120-132

Abstract
Background. In vascular smooth muscle tissue, Ca2+ signal changes in response to the occupation of G-protein-linked receptors, such as the alpha-1 adrenoceptor, is composed of two parts: the release of Ca2+ from the intracellular store, triggered by inositol 1,4,5-trisphosphate (IP3), and Ca2+ influx. Material and methods. The increase of perfusion pressure in rat tail arteries induced by norepinephrine and phenylephrine or BAY K8644 and KCl in solution with or without Ca2+ can be used as a marker of both intracellular Ca2+ release through the IP3 receptor pathway and Ca2+ influx. In order to probe the relationship between these events, we monitored the increase of perfusion pressure before and after exposition to low power laser and low dose ultrasound. The present study was also designed to investigate whether low – power laser light and low-dose ultrasound could interfere with Ca2+ influx through the Ca2+ channels and modulate intracellular Ca2+ release through different pathways in vascular smooth muscle. Phasic contractions of the rat tail artery induced by norepinephrine (NE) and phenylephrine (PHE) in Ca2+-free solution were used to mark intracellular Ca2+ release through the IP3 receptor pathway. The increases of perfusion pressure evoked by NE and PHE in Ca – solution were used as indicators of Ca2+ influx via the Ca2+ channel. BAY K 8644 in a solution containing Ca2+ was used as an indicator of indirect action on Ca2+ influx through the L-type Ca2+ channels. KCl (60mM/l) served as an indicator of activation on the Ca2+ voltage open channel. Results. NE and PHE evoked an increase in perfusion pressure of the rat tail arteries in both Ca2+-free and Ca2+ – containing solutions in a dose-dependent manner. BAY K 8644 and KCl evoked contraction of the rat tail arteries only in solution containing Ca2+. Low-dose ultrasound increased vascular responses to NE and PHE in both solutions, with or without Ca2+. Ultrasound increased perfusion pressure induced by KCL and BAY K8644 in solution with Ca2+. Low-power laser significantly attenuated the NE- and PHE-induced contractions of the rat tail arteries in solutions with or without Ca2+. Low power laser had no effect on vascular contractions induced by KCl and BAY K 8644.Conclusions. Low-intensity ultrasound significantly increased both Ca2+ influx and Ca2+ release, and increased the phasic contractions evoked by NE and PHE. Ultrasound also increased phasic contraction of the rat tail evoked by BAY K8644 and KCl in calcium solutions. Low-power laser significantly decreased vascular response to NE and PHE by inhibition of both Ca influx and IP3-dependent Ca release, but had no effect on vascular contraction induced by KCL and BAY K 8644.

Key words:
laser radiation, ultrasounds, receptors, contraction arteries