Effect of isosorbide-5-mononitrate on sympathetic purinergic vasoconstriction of the rabbit saphenous artery.
- Author:
Wen-Xiu SI
1
;
Hai-Gang LU
;
Lei-Ming REN
Author Information
1. School of Pharmacy, Hebei Medical University, Shijiazhuang 050017, China.
- Publication Type:Journal Article
- MeSH:
Adenosine Triphosphate;
analogs & derivatives;
pharmacology;
Adrenergic alpha-Antagonists;
pharmacology;
Animals;
Arteries;
drug effects;
Delayed-Action Preparations;
Electric Stimulation;
Isosorbide Dinitrate;
administration & dosage;
analogs & derivatives;
pharmacology;
Male;
Norepinephrine;
pharmacology;
Prazosin;
pharmacology;
Purinergic P2 Receptor Agonists;
Rabbits;
Receptors, Purinergic P2X;
Vasoconstriction;
drug effects
- From:
Acta Pharmaceutica Sinica
2007;42(8):833-837
- CountryChina
- Language:Chinese
-
Abstract:
The aim of this study is to investigate the effect of isosorbide-5-mononitrate (ISMN) on the electric field stimulation induced sympathetic purinergic vasoconstriction of the rabbit saphenous arterial rings. Isometric vasoconstrictive responses to electric field stimulation and to exogenous noradrenaline and adenosine triphosphate were recorded. We found that the vasoconstrictive responses to electric field stimulation (15 V, 1 ms pulse duration, 2 - 16 Hz) were frequency-dependant in the rabbit saphenous arterial rings, and abolished by tetrodotoxin (0.1 micromol x L(-1)). The alpha1-adrenoceptor antagonist prazosin (1 micromol x L(-1)) did not affect the vascular responses to the electric field stimulation (2 -8 Hz). After a combination treatment with both alpha,beta-meATP (3 micromol x L(-1), desensitizing P2X1 receptors) and prazosin (1 micromol x L(-1)), the vasoconstrictive responses to electric field stimulation were abolished. When the arterial preparation was treated with ISMN (one preparation was exposed to only one concentration of ISMN), ISMN at 0.1 mmol x L(-1) significantly inhibited the vasoconstriction induced by electric stimulation at 8 Hz, 0.3 and 1.0 mmol x L(-1) significantly inhibited the vasoconstrictive responses to electric stimulation at 2 - 16 Hz. The highest concentration of ISMN (1.0 mmol x L(-1)) reduced the vasoconstrictive responses by 46% (2 Hz), 47% (4 Hz), 34% (8 Hz) and 22% (16 Hz), separately. ISMN (0.3 and 1.0 mmol x L(-1)) did not affect the vascular responses to exogenous noradrenaline (0.01-100 micromol x L(-1)) and adenosine triphosphate (1 mmol x L(-1)). It is reasonable to suggest that ISMN inhibits the purinergic vasoconstriction induced by sympathetic nerve stimulation via a prejunctional mechanism.
