• Archives of Pharmacal Research
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• v.26 no.3
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• pp.214-223
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• 2003

The present study was conducted to investigate the effects of green tea extract (GTE) on arterial blood pressure and contractile responses of isolated aortic strips of the normotensive rats and to establish the mechanism of action. The phenylephrine ($10^{-6}~10^{-5}M$)-induced contractile responses were greatly inhibited in the presence of GTE (0.3~1.2 mg/mL) in a dose-dependent fashion. Also, high potassium ($3.5{\times}10^{-2}~5.6{\times}10^{-2}{\;}M$)-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, $4~12{\;}{\mu}g/mL$) did not affect the contractile responses evoked by phenylephrine and high $K^+$. 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 $\alpha_1$-receptors. GTE also causes the relaxation in the isolated aortic strips of the rat via the blockade of adrenergic $\alpha_1$-receptors, in addition to the unknown direct mechanism. It seems that there is a big difference in the vascular effect between GTE and EGCG.

• The Korean Journal of Physiology
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• v.11 no.1
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• pp.27-32
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• 1977

Diospyros Kaki Thunberg is the species of persimmon tree that grows in Korea. Although its fresh or dried fruits are often served as a desert, it has little been known if persimmon tree has any specific pharmacological action. The leaves and branches of persimmon tree has long been used as folk remedies for palsy and frostbite in the southern part of Korea and it is also in use for the treatment of hiccup and nocturnal enuresis in chinese herbal medicine. Recently it was reported that an intravenous administration of Diospyros Kaki Thunberg ethanol extract (KTEE) into the animals lowered arterial blood pressure. Lee concluded from his study on the mechanism of depressor action of KTEE that at least a part of depressor response he observed was caused by acetylcholine-like action of KTEE. On the other hand little study has been made on the effect of KTEE on the motility of isolated animal intestines. Therefore the present study was undertaken to investigate effect of KTEE and the mechanism of its action on the motility of isolated rabbit duodenum. Ethanol extract of Diospyros Kaki Thunberg was prepared by boiling 1 kg of dried branches of persimmon tree in 1 liter of ethanol and the motility of isolated rabbit duodenum was recorded on physiograph by means of force transducer connected with Magnus apparatus. Doses of KTEE used were $5{\times}10^{-4}gm/ml,\;1{\times}10^{-3}gm/ml,\;and\;2{\times}10^{-3}gm/ml$. And the isolated duodenum was separately pretreated with acetylcholine $(5{\times}10^{-7}gm/ml)$, pilocarpine $(2.5{\times}10^{-6}gm/ml)$, histamine $(5{\times}10^{-6}gm/ml)$ and barium chloride $(2.5{\times}10^{-5}gm/ml)$ in order to find out interactions of these drugs with KTEE. The results obtained are as follows: 1. At doses of $5{\times}10^{-4}gm/ml,\;1{\times}10^{-3}gm/ml$ KTEE reduced contractions of isolated duodenum, while tonus as well as contaction of duodenum were depressed with $2{\times}10^{-3}gm/ml$ of KTEE. 2. Since the inhibitory effect of KTEE on the intestinal motility was not blocked by pretreatment with acetylcholine, pilocarpine, and barium chloride, it was strongly suggested that the inhibitory action of KTEE on intestinal motility is mainly Caused by its antihistamine effect. 3. It is also concluded that the principal substance of KTEE responsible for inhibition of intestinal motility may also have a vasodilating activity and would not be an acetylcholine-like substance in case it is same substance as that cause depressor responses.

• The Korean Journal of Physiology
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• v.23 no.1
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• pp.129-138
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• 1989

In an attempt to characterize the ventral root afferent fibers, arterial blood pressure responses to stimulation of the ventral root (VR) were observed in anesthetized cats. Effects of the morphine administered either intravenously or direct spinally and of the spinal lesions on the pressor responses were compared. Followings are the results obtained. 1) Stimulation of the VR with C-strength, high frequency stimuli evoked a marked pressor response. No depressor response, which had been reported during peripheral nerve stimulation, was observed during VR stimulation with low frequency. 2) Acute cervical spinalization abolished the pressor response, indicating the involvement of supraspinal mechanism. 3) The ascending spinal pathways of the pressor response were located in the dorsolateral funiculus bilaterally. 4) Intravenously administered morphine exaggerated the pressor response to VR stimulation, while direct spinally administered morphine suppressed it. From the above results it was concluded that the ventral root afferent fibers have more similar properties to muscular C-afferent fibers than to cutaneous C-fibers.

• The Korean Journal of Pharmacology
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• v.8 no.1
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• pp.63-65
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• 1972

It is well known that pharmacological actions of bradykinin are smooth muscle dilatation, increase in capillary permeability, accumulation and migration of leucocytes and inducement of pain. The most significant action of bradykinin is the dilatation of blood vessels. The responses of bradykinin (0.5ug/kg, i. v. injection) on blood pressure were observed before and after single i. v. administration of guanethidine (2mg/kg) in the rabbits. The result of experiment was as follows: In the rabbit pretreated with guanethidine, the depressor response of bradykinin was much pronounced in comparison with that of normal rabbit.

• Journal of the Korean Home Economics Association
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• v.25 no.1
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• pp.51-58
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• 1987

This study was undertaken to investigate changes in blood pressure and heart rate in normal cats by administration of Korean native green tea. The chemical components of Korean native green tea which determined are water(2.2%), water extract(32.7%), vitamin C(480%), caffeine(2.6%), tannin(32.7%) and amino acid of water soluble content 5.8%. Effect on blood pressure in administration 100mg/kg, 300mg/kg, 500mg/kg of extract of green tea, the mean depressor response is 44.8$\pm$3.3mmHg, 60.5$\pm$3.6mmHg, and 65.0$\pm$3.3mmHg in normal cats. Effect on heart rate in administration 100mg/kg, 300mg/kg of extract of Korean native green tea, the mean decreased heart rate is 2.8$\pm$4.5 beats/min, 15.2$\pm$6.4beats/min and 19.1$\pm$4.0 beats/min.

• The Journal of Korean Medicine
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• v.17 no.1 s.31
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• pp.37-46
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• 1996

The aim of this experiments was to investigate the effect of Lycii Fructus water extracts on the blood pressure, plasma renin activity and plasma levels of atrial natriuretic peptide in two-kidney one clip Goldblatt hypertensive rats. Systolic blood pressure was decreased significantly after administration of Lycii Fructus water extracts. Plasma levels of atrial natriuretic peptide was increased significantly after adminstration of Lycii Fructus water extracts. Plasma renin activity was not changed after adminstration of Lycii Fructus water extracts. Thease results suggested that the depressor response after adminstration of Lycii Fructus water extracts were related with the changes of the plasma levels of atrial natriuretic peptide.

• The Journal of Korean Medicine
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• v.21 no.2
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• pp.37-42
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• 2000

Objectives and Methods : Unlike respiratory anaphylaxis responses, mediators responsible for cardiovascular responses are not clearly elucidated. Main characteristics of cardiovascular anaphylaxis include hypotension and cardiac failure (anhythmia and cardiac contraction failure). In this experiment, the fractionations of Sophorae Radix (SR) were tested for its preventive effects against cardiovascular anaphylaxis in pithed rats. Results : Of the SR fractionations, water fractions, at the concentration of 20 and 60mg/kg, was significantly effective on all the cardiovascular changes in pithed rats. Also, of the cardiovascular changes, depressor response was significantly attenuated by the ethyl acetate (EA) fraction, at the concentration of 60mg/kg. Conclusions : These results suggest that water and EA fractions of the SR fractionations possess anti. anaphylactic effects in pithed rats. Additional research is needed to identify active principles for the observed pharmacological effects.

• Archives of Pharmacal Research
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• v.20 no.5
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• pp.389-395
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• 1997

We investigated the interaction between nitric oxide and the renin angiotensin system in regulating isolated pulmonary arterial tension and pulmonary arterial pressure (PAP) in renal hypertensive rats (RHR) made by complete ligation of left renal artery. Losartan induced a depressor response that was smaller in RHR than in normotensive rats (NR) (3.3 and 7.0 mmHg, respectively, at 3.0 mg/kg, p<0.05), and the response was significantly reduced by $N^{G}$-nitro-Larginine methyl ester (L-NAME). Angiotensin II elevated the PAP (7.6 and 10.8 mmHg at $0.1 {\mu}g/kg$; 20.3 and 23.6 mmHg at $1.0{\mu}g/kg$, respectively) and contracted the isolated pulmonary artery ($pD_2$: 8.79 and 8.71, respectively) from both NR and RHR with similar magnitude, and these effects were significantly enhanced by L-NAME in NR, but not in RHR. Acetylcholine lowered the PAP slightly less effectively in RHR than in NR (3.8 and 6.0 mmHg at 10 .mu.g/kg, respectively) and relaxed the pulmonary artery precontracted with norepinephrine in both rats with similar magnitude ($E_max$: 60.8 and 63.6%, respectively), and the effect being completely abolished after pretreatment.with L-NAME or removal of endothelial cells. These results suggest that nitric oxide interacts with renin angiotensin system to control the pulmonary vascular tension and pulmonary arterial circulation of RHR.R.

• Korean Journal of Veterinary Research
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• v.28 no.1
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• pp.29-36
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• 1988

To examine the selectivity of verapamil, used in the cardiovascular diseases, on alpha-1 and alpha-2 adrenoceptor-induced pressor rsponses, effects of verapamil on alpha-adrenoceptor agonist-induced pressor responses were investigated in urethane-anesthetized rabbits, spinal rabbits, rats and pithed rats. To evaluate the effects of verapamil on each pressor response induced by norepinephrine, phenylephrine and clonidine, these agonists were previously injected into a ear vein, and then same procedures were performed 1~2 min after treatment with intravenous verapamil. The results are summarized as follows: 1. Intravenous verapamil produced dose-dependent depressor response in rabbits and rats. 2. Pressor responses to intravenous norepinephrine($10{\mu}g/kg$) and phenylphrine($30{\mu}g/kg$) were inhibited by pretreatment with intravenous verapamil in rabbits and no difference was noted between the degree of both inhibitions of the pressor response by verapamil. 3. Pressor responses to intravenous norepinephrine($3{\mu}g/kg$), phenylephrine($20{\mu}g/kg$) and clonidine ($300{\mu}g/kg$) were inhibited by pretreatment with intravenous verapamil in spinal rabbits. No difference was noted between the inhibition of norepinephrine-induced pressor response and that of phenylephrine-induced pressor response by verapamil. The inhibition of clonidine-induced pressor response by verapamil was more prominent than that of norepinephrine- or phenylephrine-induced pressor response. 4. Pressor responses to intravenous norepinephrine($3{\mu}g/kg$) and phenylephrine($10{\mu}g/kg$) were inhibited by pretreatment with intravenous verapairlil in rats and no difference was noted between the degree of both inhibitions of the pressor response by verapamil. 5. Pressor responses to intravenous norepinephrine ($3{\mu}g/kg$), phenylephrine($30{\mu}g/kg$) and clonidine($100{\mu}g/kg$) were inhibited by pretreatment with intravenous verapamil in pithed rats. No difference was noted between the inhibition of norepinephrine-induced pressor response and that of phenylephrine-induced pressor response by verapamil. The inhibition of clonidine-induced pressor response by verapamil was more prominent than that of norepinephrine- or phenylephrine-induced pressor response. These results suggest that verapamil significantly inhibits both pressor responses mediated by alpha-1 and alpha-2 adrenoceptors and the inhibition is greater in alpha-2 adrenoceptor-induced response than in alpha-1 adrenoceptor-induced one, and calcium channel takes part in the process of the pressor response mediated by alpha-1 adrenoceptors as well as alpha-2 adrenoceptors.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.3
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• pp.345-351
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• 1998

The role of nitric oxide (NO) in the hemorrhagic hypotension was examined using a NO synthase inhibitor, $N^{\omega}-nitro-L-arginine$ methyl ester (L-NAME), in conscious rats. The rats were bled at a constant rate (2 ml/kg/min) through a femoral arterial catheter until the mean arterial pressure (MAP) was reduced by 50 mmHg. We studied the responses to hemorrhage under normal condition (Control) and after the pretreatment with 3 doses of L-NAME (1.6, 8, 40 mg/kg i.v. of NOX1.6, NOX8, and NOX40, respectively). Intravenous bolus injection of L-NAME produced a sustained increase in MAP and decrease in heart rate (HR). During hemorrhage, the MAP fell faster in the NOX8 and NOX40-treated groups than in Control group, but the control group showed same response to NOX1.6. HR greatly increased in NOX groups. The recovery from hemorrhagic hypotension was slowed in the control group, which was not treated with L-NAME. In comparison with the control group, NOX8 and NOX1.6-treated groups registered a significant recovery in MAP during the 15 min recovery period, but NOX40 brought about only a slight increase in MAP. NO precursor, L-arginine (150 mg/kg i.v.), produced significant bradycardic responses before and after hemorrhage and significant depressor response only after hemorrhagic hypotension regardless of pretreatment with L-NAME. These data suggest that the role of NO in blood pressure regulation is greater after hemorrhagic hypotension than basal condition, but the effect of NO can be detrimental to the recovery from hemorrhagic hypotension. In addition, the bradycardic response of L-arginine provides indirect evidence that NO may inhibit sympathetic activity, especially after hemorrhagic hypotension.