Relaxation Of Porcine Coronary Arteries Research Articles

O-218 - Inhibitory mechanism of LDL in endothelium-dependent relaxation in porcine coronary arteries. Effects of p-bromophenacyl bromide.

O-218 - Inhibitory mechanism of LDL in endothelium-dependent relaxation in porcine coronary arteries. Effects of p-bromophenacyl bromide.

LDLによる内皮依存性弛緩反応抑制のメカニズム

Thrombin and other proaggregators have been reported to induce endothelium dependent relaxation in porcine coronary arteries and LDL blocked the relaxation rapidly and reversibly (Tomita et al., Circ. Res. 1990, 66, 18-27). This inhibitory mechanism of LDL was investigated. Lysolecithin acyltransferase (LAT) activity was dose depenedently enhanced by LDL within the range of LDL concentrations in which it exerted an inhibitory effect on the relaxation. This enzyme activity was demonstrated in cultured endothelial cells from porcine aortas, and the activity in the intact cells was profoundly enhanced in the presence of thrombin and LDL in the medium. Heat-treatment (60°, 10min), or acid-treatment (pH 2, 30min at room temp) of LDL, resulted in a complete loss of the stimulatory effect on LAT activity as it caused a loss of LDL-inhibitory effects on the relaxation. In contrast, the DFP-treatment did not alter either of the effects of LDL. Thimerosal (10-8-10-4 M) induced endothelium-dependent relaxation, while the activation by LDL of LAT was blocked in the presence of thimerosal (10-4 M). Thus, the effective deactivation mechanism of LDL inhibition of the endothelium-dependent relaxation coincided well with that for the enhancement of LAT activity. These results suggest that the profound enhancing effect of LDL on LAT activity in the endothelium was possibly involved in the inhibition of endothelium-dependent relaxation by LDL.

P-147 - The Ca-tension relationship during bradykinin-induced endothelium dependent relaxation of porcine coronary artery.

P-147 - The Ca-tension relationship during bradykinin-induced endothelium dependent relaxation of porcine coronary artery.

Lack of an effect of soman on norepinephrine-induced relaxations of porcine coronary arteries

Lack of an effect of soman on norepinephrine-induced relaxations of porcine coronary arteries

O-103 - The inhibitory mechanism of low density lipoproteins in the endothelium dependent relaxation of porcine coronary arteries

O-103 - The inhibitory mechanism of low density lipoproteins in the endothelium dependent relaxation of porcine coronary arteries

Dietary omega 3 fatty acids and endothelium-dependent relaxations in porcine coronary arteries

Dietary supplementation with cod-liver oil significantly augments endothelium-dependent relaxations in porcine coronary arteries. The present study was designed to examine the effect of dietary administration of omega 3 polyunsaturated fatty acids (mainly eicosapentaenoic acid, the major component of fish oil) on endothelium-dependent relaxations in porcine coronary arteries. Male Yorkshire pigs were maintained 4 wk on a regular diet with or without supplementation with purified eicosapentaenoic acid (3.5 g/day) and docosahexaenoic acid (1.5 g/day). Endothelium-dependent relaxations were examined in vitro. In rings from the treated group, endothelium-dependent relaxations were augmented in response to bradykinin, serotonin, and ADP, but not to the calcium ionophore A23187. These augmentations were not altered by indomethacin but were significantly inhibited by methylene blue, an inhibitor of guanylate cyclase. In the treated group, endothelium-dependent relaxations to aggregating platelets also were significantly augmented; platelet-induced contractions of quiescent rings were inhibited more by the presence of the endothelium than in arteries from the control group. Bioassay experiments demonstrated that the release of endothelium-derived relaxing factor(s) by bradykinin and relaxations of the vascular smooth muscle to the factor(s) were greater in arteries from the treated group. These observations indicate that dietary omega 3 polyunsaturated fatty acids augment receptor-operated endothelium-dependent relaxations, partly due to the augmented release of endothelium-derived relaxing factor(s) and partly due to the augmented relaxation of the vascular smooth muscle to the factor(s).

Demonstration of beta 1-adrenoceptor mediating relaxation of porcine coronary artery by radioligand binding and pharmacological methods.

beta-adrenoceptors in the porcine coronary artery were characterized by a radioligand binding assay using (-)-[3H]dihydroalprenolol (DHA) and also by measuring the relaxant response of isolated coronary artery to norepinephrine. Specific (-)-[3H]DHA binding in the porcine coronary artery was saturable, reversible and of high affinity (Kd = 1.6 nM) with a maximal number of binding sites of 63 fmol/mg protein, and it showed a pharmacological specificity as well as stereoselectivity which characterized beta-adrenoceptors. The Hofstee analysis of inhibition of (-)-[3H]DHA binding by atenolol, practolol and ICI 118551 has shown that the averaged concentration of beta 1 and beta 2-adrenoceptors in this tissue was 68% and 32% respectively. The relaxant response of isolated coronary artery to norepinephrine was competitively antagonized by (-)propranolol, (+)propranolol, atenolol, practolol and ICI 118551. The pA2 values of these adrenoceptor antagonists were significantly correlated with the Ki values for beta 1 but not beta 2-adrenoceptors determined by the (-)-[3H]DHA binding assay. Thus, the present study demonstrates that the relaxant response of porcine coronary artery to norepinephrine is predominantly mediated through the stimulation of beta 1-adrenoceptors on vascular smooth muscles.