Exhaustive swimming differentially inhibits P2X1 receptor- and α1-adrenoceptor-mediated vasoconstriction in isolated rat arteries

Abstract

Aim: To investigate the effects of exhaustive swimming exercise on P2X1 receptor- and α1-adrenoceptor-mediated vasoconstriction of different types of arteries in rats.

Methods: Male Wistar rats were divided into 2 groups: the sedentary control group (SCG) and the exhaustive swimming exercise group (ESEG). The rats in the ESEG were subjected to a swim to exhaustion once a day for 2 weeks. Internal carotid, caudal, pulmonary, mesenteric arteries and aorta were dissected out. Isometric vasoconstrictive responses of the arteries to α,β-methylene ATP (α,β-MeATP) or noradrenaline (NA) were recorded using a polygraph.

Results: The exhaustive swimming exercise did not produce significant change in the EC(50) values of α,β-MeATP or NA in vasoconstrictive response of most of the arteries studied. The exhaustive swimming exercise inhibited the vasoconstrictive responses to P2X1 receptor activation in the internal carotid artery, whereas it reduced the maximal vasoconstrictive responses to α1-adrenoceptor stimulation in the caudal, pulmonary, mesenteric arteries and aorta. The rank order of the reduction of the maximal vasoconstriction was as follows: mesenteric, pulmonary, caudal, aorta.

Conclusion: Exhaustive swimming exercise differentially affects the P2X1 receptor- and α1-adrenoceptor-regulated vasoconstriction in internal carotid artery and peripheral arteries. The ability to preserve purinergic vasoconstriction in the peripheral arteries would be useful to help in maintenance of the basal vascular tone during exhaustive swimming exercise.

Figure 1

Tissue wet weight (A) and vasoconstriction to 120 mmol/L KCl (B) in the rat mesenteric (Mes), caudal (Cau), pulmonary (Pul), internal carotid (Int) arteries and aorta (Aor) from the sedentary control group (SCG, n=29−34) and the exhaustive swimming exercise group (ESEG, n=28−35). Data were expressed as mean±SEM. ^cP<0.01 vs SCG.

Figure 2

A comparison of the vasoconstrictive responses to noradrenaline between the preparations exposing to the second administration of noradrenaline (treatment with NA; n=10, left; n=9, right) and those exposing to α,β-methylene ATP (treatment with α,β-MeATP; n=24, left; n=24, right) in the rat pulmonary arteries from the sedentary control group (A) and the exhaustive swimming exercise group (B). Data were expressed as mean±SEM.

Figure 3

A comparison of the vasoconstrictive responses to noradrenaline between the preparations exposing to the second administration of noradrenaline (treatment with NA; n=11, left; n=15, right) and those exposing to α,β-methylene ATP (treatment with α,β-MeATP; n=20, left; n=20, right) in the rat caudal arteries from the sedentary control group (A) and the exhaustive swimming exercise group (B). Mean±SEM.

Figure 4

A comparison of the vasoconstrictive responses to noradrenaline between the preparations exposing to the second administration of noradrenaline (treatment with NA; n=11, left; n=9, right) and those exposing to α,β-methylene ATP (treatment with α,β-MeATP; n=22, left; n=22, right) in the rat mesenteric arteries from the sedentary control group (A) and the exhaustive swimming exercise group (B). Data were expressed as mean±SEM.

Figure 5

A comparison of the vasoconstrictive responses to noradrenaline between the preparations exposing to the second administration of noradrenaline (treatment with NA; n=11, left; n=8, right) and those exposing to α,β-methylene ATP (treatment with α,β-MeATP; n=23, left; n=22, right) in the rat thoracic aorta from the sedentary control group (A) and the exhaustive swimming exercise group (B). Data were expressed as mean±SEM.

Figure 6

A comparison of the vasoconstrictive responses to noradrenaline between the preparations exposing to the second administration of noradrenaline (treatment with NA; n=9, left; n=8, right) and those exposing to α,β-methylene ATP (treatment with α,β-MeATP; n=20, left; n=20 right) in the rat internal carotid arteries from the sedentary control group (A) and the exhaustive swimming exercise group (B). Data were expressed as mean±SEM.

Figure 7

A comparison of the vasoconstrictive responses to the second administration of noradrenaline (A) or to α,β-methylene ATP (B) in the rat pulmonary arteries between the sedentary control group (SCG; n=10, A; n=5−7, B) and the exhaustive swimming exercise group (ESEG; n=9, A; n=5−7, B). Mean±SEM. Statistical significance was analyzed by two-way ANOVA in A: ^cP<0.01 vs SCG.

Figure 8

A comparison of the vasoconstrictive responses to the second administration of noradrenaline (A) or to α,β-methylene ATP (B) in the rat caudal arteries between the sedentary control group (SCG; n=11, A; n=5, B) and the exhaustive swimming exercise group (ESEG; n=15, A; n=5, B). Data were expressed as mean±SEM. Statistical significance was analyzed by two-way ANOVA in A: ^cP<0.01 vs SCG.

Figure 9

A comparison of the vasoconstrictive responses to the second administration of noradrenaline (A) or to α,β-methylene ATP (B) in the rat mesenteric arteries between the sedentary control group (SCG; n=11, A; n=5−6, B) and the exhaustive swimming exercise group (ESEG; n=9, A; n=5−6, B). Data were expressed as mean±SEM. ^cP<0.01 vs SCG.

Figure 10

A comparison of the vasoconstrictive responses to the second administration of noradrenaline (A) or to α,β-methylene ATP (B) in the rat thoracic aorta between the sedentary control group (SCG; n=11, A; n=5−6, B) and the exhaustive swimming exercise group (ESEG; n=8, A; n=5−6, B). Data were expressed as mean±SEM. ^cP<0.01 vs SCG.

Figure 11

A comparison of the vasoconstrictive responses to the second administration of noradrenaline (A) or to α,β-methylene ATP (B) in the rat internal carotid arteries between the sedentary control group (SCG; n=9, A; n=5, B) and the exhaustive swimming exercise group (ESEG; n=8, A; n=5, B). Data were expressed as mean±SEM. ^cP<0.01 vs SCG.