Dong Yoon Lim

Comparison of green tea extract and epigallocatechin gallate on blood pressure and contractile responses of vascular smooth muscle of Rats

The present study was conducted to investigate the effects of green tea extract (GTE) on arte-rial blood pressure and contractile responses of isolated aortic strips of the normotensive rats and to establish the mechanism of action. The phenylephrine (10~p6~10~p5M)-induced contrac-tile responses were greatly inhibited in the presence of GTE (0.3–1.2 mg/mL) in a dose-depen-dent fashion. Also, high potassium (3.5x10-p2~5.6x1CTp2 M)-induced contractile responses were depressed in the presence of 0.6–1.2 mg/mL of GTE, but not affected in low concentration of GTE (0.3 mg/mL). However, epigallocatechin gallate (EGCG, 4–12 ug/mL) did not affect the contractile responses evoked by phenylephrine and high Kp+. GTE (5–20 mg/kg) given into a femoral vein of the normotensive rat produced a dose-dependent depressor response, which is transient. Interestingly, the infusion of a moderate dose of GTE (10 mg/kg/30 min) made a significant reduction in pressor responses induced by intravenous norepinephrine. However, EGCG (1 mg/kg/30 min) did not affect them. Collectively, these results obtained from the present study demonstrate that intravenous GTE causes a dose-dependent depressor action in the anesthetized rat at least partly through the blockade of adrenergic α1-receptors. GTE also causes the relaxation in the isolated aortic strips of the rat via the blockade of adrenergic α1-receptors, in addition to the unknown direct mechanism. It seems that there is a big differ-ence in the vascular effect between GTE and EGCG.

Influence of berberine on the blood pressure of rabbits

Berberine, when administered into a ear-vein of the rabbit anesthetized with urethane, produced a long-lasting, dose-related fall in blood pressure, but intraventricular berberine did not elicit the hypotensive response. This hypotensive activity of berberine was not influenced by pretreatment of vagotomization and atropine. Depressor responses induced by berberine were not impaired by diphenhydramine, chlorisondamine, guanethidine and propranolol, but reduced significantly by phentolamine pretreatment. Berberine attenuated markedly pressor responses of norepinephrine and epinephrine. These results suggest that berberine causes the hypotensive activity that is attributable to alpha adrenoceptor blockade, but not to a direct relaxant effect upon vascular smooth muscle.

Influence of cytisine on catecholamine release in isolated perfused rat adrenal glands.

The aim of the present study was to determine the characteristics of cytisine on the secretion of catecholamines (CA) in isolated perfused rat adrenal glands, and to clarify its mechanism of action. The release of CA evoked by the continuous infusion of cytisine (1.5× 10-5 M) was time-dependently reduced from 15 min following the initiation of cytisine infusion. Furthermore, upon the repeated injection of cytisine (5× 10-5 M), at 30 min intervals into an adrenal vein, the secretion of CA was rapidly decreased following the second injection. Tachyphylaxis to the release of CA was observed by the repeated administration of cytisine. The cytisine-induced secretion of CA was markedly inhibited by pretreatment with chlorisondamine, nicardipine, TMB-8, and the perfusion of Ca2+-free Krebs solution, while it was not affected by pirenzepine or diphenhydramine. Moreover, the secretion of CA evoked by ACh was time-dependently inhibited by the prior perfusion of cytisine (5× 10-6 M). Taken together, these experimental data suggest that cytisine causes secretion of catecholamines from the perfused rat adrenal glands in a calcium-dependent fashion through the activation of neuronal nicotinic ACh receptors located in adrenomedullary chromaffin cells. It also seems that the cytisine-evoked release of catecholamine is not relevant to the activation of cholinergic M1-muscarinic or histaminergic receptors.