• Journal of the East Asian Society of Dietary Life
• /
• v.9 no.3
• /
• pp.378-385
• /
• 1999

A reduced NaCl intake for the general population of the world has been recommended to reduce the overall blood pressure level and hence to reduce the overall incidence of cardiovascular disease. A high NaCl diet convincingly contributes to elevated arterial pressure in humans and animal models of hypertension. Among individuals there is considerable variability of blood pressure responsiveness to NaCl intake. In normotensive as well as hypertensive subjects, blood pressure can be judged to be salt sensitivity (SS) when observed to vary directly and substantially with the net intake of NaCl. The prevalence of SS in normotensive adults in the U.S. ranges from 15% to 42% and in hypertensive adults from 28% to 74%. SS is a risk factor for hypertension and may be an important marker in the identification of children for hypertension prevention programs. High NaCl intakes produce expansion of the extracellular fluid volume and thus increase blood pressure. Nonchloride salts of sodium does not expand the extracellular fluid volume and does not alter blood pressure. Blood pressure response to NaCl may be modified by other components of the diet. Low dietary intakes of potassium or calcium augment NaCl-induced increases of blood pressure. Conversely, high dietary intakes of potassium or calcium attenuate NaCl-induced hypertension. A greater intakes of potassium or calcium may prevent or delay the occurrence of hypertension. SS occurs when dietary potassium is even marginally deficient but is dose-dependently suppressed when dietary potassium is increased within its normal range. Orally administered KHCO$_3$, abundant in fruits and vegetates, but not KCl has a calcium-retaining effect which may contributed to its reversal of pressor effect of dietary NaCl. Since nutrients other than NaCl also affect blood pressure levels, a reduced NaCl intake should be only one component of a nutritional strategy to lower blood pressure.

• Natural Product Sciences
• /
• v.10 no.5
• /
• pp.228-236
• /
• 2004

The aim of the present study was to examine whether green tea extract (CUMC6335) affects the blood pressure and the isolated aortic contractility of the rabbit in comparison with one of the most powerful active catechins, epigallocatechin gallate (EGCG). The phenylephrine $(1-10\;{\mu}M)-induced$ contractile responses were greatly inhibited in the presence of CUMC6335 (0.3-1.2 mg/ml). Also, high potassium (56 mM)-induced contractile responses were depressed in high concentration (0.6-1.2 mg/ml), but not affected in low concentration CUMC6335 (0.3 mg/ml). However, epigallocatechin gallate $(EGCG,\;4-12\;{\mu}g/ml)$ did not affect the contractile responses evoked by phenylephrine and high $K^+$. The infusion of CUMC6335 with a rate of 20 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 suggest that intravenous CUMC6335 causes depressor action in the anesthetized rat at least partly through the blockade of adrenergic ${\alpha}_1-receptors$. CUMC6335 also causes the relaxation in the isolated aortic strips of the rabbit partly via the blockade of adrenergic ${\alpha}_1-receptors$, in addition to the unknown direct mechanism. It seems that there is no species difference in the vascular effect between the rat and the rabbit.

• The Korean Journal of Physiology
• /
• v.4 no.2
• /
• pp.83-89
• /
• 1970

전기적 자극법은 심맥관계기능의 신경성조절을 이해하기위해 널리 이용되는 방법이며, 일반적으로 중추신경에는 고빈도, 말초신경에서는 저빈도 자극에 의해 최대반응이 유발된다고 알려지고 있으며, 이는 흥분파의 민도가 말초로 내려오며 감소되기 때물이라 해석되고 있다. 또한편 신경계의 어떤 단위위에서건 자극민도가 어느 한계를 넘으면 유발된 반응은 유지되지를 못하고 감쇠소실되는 것으로 이는 주로 시납스간 흥분파전달능 부전에 기인될 것이라고 믿어지고있다. 그러나 고위주추계와 말초를 연결하고 있는 척수에 있어서는 아직 최적전기적 자극조건도 분명히 알려져 있지 않을 뿐 아니라 이 부위에서도 고빈도자극시에 반응이 어느 정도 감쇠하는지에 대한 보고가 없기에 이를 추구코자 저자는 고양이의 상부경수를 면수와 연결부에서 완전 절단하기 전후 여러가지 자극조건으로 자극하여 몇 가지 결론을 얻었기에 보고하는 바이다. 1) 연수와 연결부에서 완전절단을 하기 전에는 경수$(C_1{\sim}C_2)$의 백질, 회백질의 여러부위에서 심맥관반응이 유발되었으나 절단후에는 백질중의 만두부위(좌 $2{\sim}3\;mm$, 배면으로 부터 $0.3{\sim}1.0\;mm$및 $2.5{\sim}3.5\;mm$)에만 반응이 유발되었으며, 이 두 부위는 심맥관계기능을 지배조절하는 원심성 섬유의 통로라고 사료되었다. 2) 최대반응은 자극조건(빈도 자극파지속시간 강도) 100/sec-1 mesc-3V 및 20/sec-3 msec-3V에서. 최장지속반응은 20/sec-3msec에서 유발되었으므로, 후자가 척수부에 있어 심맥관계반응을 유발키 위한 최적자극조건으로 생각된다. 3) 자극면도 20/sec 이하에서 반응유지가 잘된다는 결과는 생리적 조건하에서 척수를 통과하는 흥분파의 빈도가 20/sec를 넘지 않을 것이란 것을 시사한다. 4) 반응지속정도는 최초의 최대반응의 반으로 감쇠되기까지 소요되는시간 즉 50% 반응감쇠시간으로 표시하였으며, 척수에서는 대뇌피질 및 간뇌에서보다 심맥관계반응의 50%반응감쇠시간이 현저히 긴 것을 알 수 있었다.

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

• Toxicological Research
• /
• v.12 no.2
• /
• pp.195-201
• /
• 1996

Endotoxic shock causes death in humans and animals via extreme hypoperfusion of peripheral organs. A massive production of nitric oxide (NO) both from the endothelical cells and smooth muscle cells has been proposed as a possible mechanism in this process. Since NO attenuated the contractility to vasoconstricting agents such as norepinephrine (NE) by directly acting on the smooth muscle cells, this mechanism was considered mainly as a postsynaptic mechanism. In this research it was investigated whether NO, thus released, also participates in the presynaptic events for the regulation of vascular tone in endotoxic shock. The role of NO was studied by adding NO donors or NO synthase inhibitor $N^\omega $methyl-L-arginine (NMA) in stimulated sympathetic nerves of the mesenteric vascular bed and the Langendorff heart of rats. Sodium nitroprusside (SNP), an NO donor, reduced the pressor responses of isolated mesenteric artery either to electrical stimulation or exogenously administered phenylephrine (PE). In this mesentery, although neither agent influenced NE release, in the presence of the adrenergic $\alpha_2$-receptor antagonist yohimbine, elecrical stimulation-evoked NE release was augumented by SNP. In the heart SNP facilitated the NE release induced by electrical stimulation, while NMA had no effect. From these results it is proposed that there exists a local reflex phenomenon in the junction between the sympathetic nerve terminals and the smooth muscle of resistance blood vessels; by which sympathetic responses are reduced by NO at the postjunctional level while NO facilitates NE release contributing to augumentation of sympathetic tone. All these facts suggest that NO produced during endotoxic shock has dual effects: whereas NO blunts the vasoconstrictive activity of NE at the postsynaptic level, NO presynaptically facilitates the release of NE from sympathetic nerve terminals.

• Journal of Dental Anesthesia and Pain Medicine
• /
• v.23 no.5
• /
• pp.273-280
• /
• 2023

Background: Intraoral local anesthesia is essential for delivering dental care; however, injection of this local anesthetic is perceived as the most painful and distressing agent for children, parents, and healthcare providers. Reducing pain as much as possible is essential to ensure smooth subsequent treatment procedures, especially in pediatric dentistry. In clinical practice, oral sucrose administration has been reported to decrease the pain during heel lance and cold pressor tests in neonates and children. This study aimed to determine whether the prior administration of a 30% sucrose solution reduced the pain related to inferior alveolar nerve block in children. Methods: A total of 42 healthy children aged 7-10 years requiring dental treatment of mandibular molars involving inferior alveolar nerve block were recruited. The participants' demographic details were recorded, height and weight were measured, and the anesthetic injection was delivered after receiving the respective intraoral sucrose solution and distilled water by the intervention (group 1) and control (group 2) group participants for 2 min. The subjective pain perceived during injection was measured using an animated emoji scale. The pain scores between the groups were compared using the Mann-Whitney U test. Results: The median pain score and range for the intervention and control groups were 4 (2 - 6) and 6 (4 - 8), respectively, and statistically significant differences (P < 0.001) were observed in the intervention group. Age, sex, height, and weight did not influence the analgesic effect of the sucrose solution. Conclusion: Oral administration of sucrose may relieve pain associated with inferior alveolar nerve block in children.

• Journal of Pharmaceutical Investigation
• /
• v.8 no.3
• /
• pp.16-23
• /
• 1978

This study was carried out for the purpose of observing the effect of Korean Acanthopanax Radicis Cortex on renal hypertension and to clarify the mechanism of this effect, making use of its ethanol extract. Adult male or female rats, weighing 180-250g, were divided into 3 groups; the first for normotensive control, the second for hypertensive control and the third for hypertensive Acantopanax-treatment. Rats in the normotensive and hypertensive control group were administered 0.9% saline subcutaneously only, whereas those in the Acanthopanax-treated hypertensive group were administered 50mg/kg Acanthopanax ethanol extract subcutanously once a day. Changes of original blood pressure, and responses of blood pressure to various 4gents(norepinephrine, angiotensin, acetylcholine, serotonin and histamine) were recorded for each group on the initial, 18th, 32nd and 46th days of the experiment. The results obtained in this experiment are as follows: 1) The initial blood pressure was $102.6{\pm}7.6mmHg$ on the average. The blood pressures of the normotensive control group were not observed to alter significantly at any period in the course of the experiment. 2) The mean blood pressures in the hypertensive control group were recorded at $120.3{\pm}10.4mmHg$ on the 18th day, at $134.5{\pm}9.2$ on the 32nd day and at $138.8{\pm}8.3$ on the 46th day, thus revealing significant elevation in comparison with the corresponding normotensive control group blood pressures. On the other hand, the mean blood pressures in Acanthopanax-treated hypertensive group on the 18th, 32nd and 46th days were $118.3{\pm}9.7,\;129.9{\pm}8.3\;and\;120.2{\pm}8.3mmHg$ respectively. The blood pressures of the hypertensive-Acanthopanax group recorded. on the 46th day revealed a significant difference as compared with those of the corresponding hypertensive control group. 3) On the 46th day of this experiment, the responses of blood pressure to acetylcholine in the hypertensive-Acanthopanax group were suppressed significantly as compared with those of the hypertensive control group, and in the latter group, angiotensin was decreased markedly as compared with the corresponding normotensive control group. In contrast, pressor action of norepinephrine and depressor action of serotonin and histamine did not differ significantly among the three groups. These results suggest that Acanthopanax ethanol extract suppresses the induction of renal hypertension by means of a cholinergic action such as that caused by acetylcholine.

• Journal of Hospice and Palliative Care
• /
• v.22 no.4
• /
• pp.198-206
• /
• 2019

Purpose: The Act on Hospice and Palliative Care and Decisions on Life-sustaining Treatment for Patients at the End of Life was enacted in 2016 and has taken effect since 2018 February. The content of this act was based on Physician Orders for Life-Sustaining Treatment (POLST) in the United States and we modified it for terminal cancer patients registering hospice. The object of this study is to investigate preference and implementation rate for modified Korean POLST (MMK-POLST) items in hospice ward. Methods: From February 1, 2017 to April 30, 2019, medical records regarding MMK-POLST were retrospectively analyzed for all patients hospitalized in the hospice ward of Gyeongsang National University Hospital. Results: Of the eligible 387 total cohorts, 295 patients filled out MK-POLST. MK-POLST has been completed in 133 cases (44.1%) by the patient themselves, 84 cases (28.5%) by the spouse, and 75 cases (25.4%) by their children, respectively. While only 13 (4.4%) out of 295 MK-POLST completed patients refused the parenteral nutrition and 5 patients (1.7%) for palliative sedation, the absolute majority of 288 (97.6%) patients did not want cardiopulmonary resuscitation (CPR) and ventilators and 226 people (76.9%) for pressor medications. Kappa values for the matched strength of MK-POLST implementation were poor for all items except CPR, ventilators and palliative sedation. Conclusion: Hospice patients refused to conduct cardiopulmonary resuscitation, ventilators and pressor agents. In contrast, antibiotics, parenteral nutrition and palliative sedation were favored in the majority of patients.

• The Korean Journal of Physiology
• /
• v.27 no.1
• /
• pp.57-66
• /
• 1993

Effects of a voltage dependent calcium channel antagonist, nifedipine, on the responses of blood pressure, and secretion of atrial natriuretic peptide (ANP) and aldosterone to angiotensin II (Ang II) were compared in male Wistar and spontaneously hypertensive rats (SHR). A low, control or high sodium diet (2, 10 or 25 mmol Na/100 g diet) was fed for 6 weeks from the age of 6 weeks. On the morning of the experiment catheters were inserted under ether anesthesia in the femoral artery for pressure recording and blood sampling, and in the femoral vein for drug infusion. Ang II was infused at a rate of 250 ng/kg/min for 20 min. Nifedipine mixed with Ang II was infused at a rate of $16{\mu}g/kg/min$ for 20 min. Arterial blood samples were collected before and after infusion of Ang II with or without nifedipine. The control plasma level of aldosterone was inversely related to the amount of salt intake, whereas the plasma ANP level was not different between the salt groups. SHR showed a higher basal plasma ANP but a lower aldosterone concentration than Wistar rats. Infusion of Ang II produced a significant increase in blood pressure and plasma levels of aldosterone and ANP: The % increase was not significantly different either between the salt groups or between SHR and Wistar rats. SHR showed a greater pressor response to Ang II but a remarkably smaller decrease in heart rate after Ang II infusion than Wistar rats, With increasing sodium intake, the effect of Ang II on aldosterone secretion was decreased, whereas that on ANP secretion or blood pressure was not changed. Nifedipine decreased the responses of blood pressure and heart rate to Ang II in all groups. Nifedipine caused almost a complete inhibition of Ang II induced ANP secretion, but only a partial inhibition of Ang II induced aldosterone secretion or vasoconstriction. These results indicate that calcium dependent processes were involved in Ang II induced vasoconstriction, and secretions of aldosterone and ANP. However, the calcium dependent process far ANP secretion was considerably different from that for aldosterone secretion or vasoconstriction evoked by ang II. The ang II induced increase in ANP secretion appeared to be caused primarily by activating voltage-dependent calcium channels, whereas Ang II induced aldosterone secretion and vasoconstriction was not.

• The Korean Journal of Pharmacology
• /
• v.28 no.1
• /
• pp.49-60
• /
• 1992

This study was designed to evaluate the responses of cardiovascular system to endothelin (ET) and neuropeptide Y (NPY) in 12 week-old SHR treated with or without enalapril (ENP) for 6 weeks. The diastolic blood pressure and heart rate were lower in ENP-treated SHR than in control. The pressor response to intravenous, but not intracerebroventricular, ET or NPY was attenuated by ENP treatment. The chronotropic action induced by electrical stimulation was attenuated by ENP or ET. The negative chronotropic action of ET was blocked by yohimbine. The increase in aortic tension induced by electrical field stimulation (EFS) was depressed in ENP-treated group as compared with non-treated group, and enhanced by ET, but not NPY, in the non-treated group. The ET-induced increase in tension was enhanced by removal of endothelium in the control group but not in ENP-treated group. The plasma concentration of norepinephrine and ET-induced increase in concentration of norepinephrine and epinephrine in plasma were decreased in ENP-treated group. These results suggest that preventive effect of enalapril on the development of hypertension may result from depressing vasoactive action of endothelin and neuropeptide Y, and sympathetic neurotransmission at peripheral nervous system.