Effects of ATP and adenosine on contraction amplitude of rat soleus muscle at different temperatures

Abstract

ATP is involved in both pre- and postsynaptic regulation of rat soleus muscle contractility, and these processes are significantly more pronounced at low temperatures. Muscle Nerve 55: 417-423, 2017.

The effects of ATP on the contractions of rat and mouse fast skeletal muscle

“…In this study, we have shown that in contrast to rat soleus muscle where contractility increases at low temperatures, rat and mouse EDL demonstrate a decrease in the amplitude of muscle contractions induced either by electric stimulation of the nerve or carbachol application under hyothermia. Interestingly, suramin, a non‐selective antagonist of P2 receptors, but not 8‐ p SPT, a non‐selective antagonist of adenosine receptors, fully prevented the decrease of EDL contractility at low temperatures similarly to its inhibitory action on hypothermia‐induced increase of contractility in the rat soleus muscle . We hypothesize that the hypothermia‐dependent decrease of ES‐induced contractions of the EDL muscle might be due to a negative feedback mechanism provided by endogenous ATP via presynaptic P2Y receptors since suramin completely blocks that mechanism and prevents the hypothermic decrease in contractility.…”

“…For example, in the frog sartorius muscle, agonists of P2Y receptors inhibited acetylcholine release at the presynaptic level and that effect became more prominent at hypothermic temperatures than that at physiological conditions . In the rat soleus muscle similar P2Y receptor‐mediated presynaptic inhibition of acetylcholine release was significant at physiological temperatures, but gradually diminished with a decrease of bath temperature . At the postsynaptic level, ATP at normothermia did not affect carbacholine‐induced contractions of rat soleus muscles, but under hypothermic conditions such contractions became significantly higher in the presence of ATP .…”

“…In the rat soleus muscle similar P2Y receptor‐mediated presynaptic inhibition of acetylcholine release was significant at physiological temperatures, but gradually diminished with a decrease of bath temperature . At the postsynaptic level, ATP at normothermia did not affect carbacholine‐induced contractions of rat soleus muscles, but under hypothermic conditions such contractions became significantly higher in the presence of ATP . It was hypothesized that the hypothermia‐induced potentiation of contractions caused by ATP post‐synaptically overlapped and masked an increased, but to a lesser extent, inhibitory effect of ATP on presynaptic structures.…”

“…Studies have indicated that ATP within neuromuscular synapses can also modify the action of agonists of postsynaptic nicotinic receptors and, thus, can affect contractions of skeletal muscle induced by such agonists. For example, recently we have shown that ATP at low temperature conditions potentiates the contractile responses of the rat soleus muscle (a “slow” skeletal muscle) induced by an enzymatically stable analog of acetylcholine (carbachol), while adenosine has no effect on such contractions …”

“…For example, recently we have shown that ATP at low temperature conditions potentiates the contractile responses of the rat soleus muscle (a "slow" skeletal muscle) induced by an enzymatically stable analog of acetylcholine (carbachol), while adenosine has no effect on such contractions. 9 At the neuromuscular junction, the effects of ATP are terminated by two enzymes: ectonucleoside triphosphate diphosphohydrolase1 (ecto-NTPDase1, CD39), which converts ATP (and adenosine-5'-diphosphate, ADP) to adenosine-5'-monophosphate (AMP), and ecto-5'-nucleotidase (CD73), which in turn catalyzes the degradation of AMP to adenosine. 10 Termination of adenosine's action on G-protein coupled adenosine (P1) receptors occurs by its intracellular uptake (by nucleoside transporters), or by its metabolic breakdown to inosine (by adenosine deaminase), or through conversion back to AMP (by adenosine kinase).…”