• The Korean Journal of Physiology and Pharmacology
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• 제22권4호
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• pp.437-445
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• 2018

${\alpha}$-Iso-cubebene (ICB) is a dibenzocyclooctadiene lignin contained in Schisandra chinensis (SC), a well-known medicinal herb that ameliorates cardiovascular symptoms, but the mechanism responsible for this activity has not been determined. To determine the role played by ICB on the regulation of vascular tone, we investigated the inhibitory effects of ICB on vascular contractile responses by adrenergic ${\alpha}$-receptor agonists. In addition, we investigated the role on myosin light chain (MLC) phosphorylation and cytosolic calcium concentration in vascular smooth muscle cells (VSMC). In aortic rings isolated from C57BL/6J mice, ICB significantly attenuated the contraction induced by phenylephrine (PE) and norepinephrine (NE), whereas ICB had no effects on KCl (60 mM)-induced contraction. In vasculatures precontracted with PE, ICB caused marked relaxation of aortic rings with or without endothelium, suggesting a direct effect on VSMC. In cultured rat VSMC, PE or NE increased MLC phosphorylation and increased cytosolic calcium levels. Both of these effects were significantly suppressed by ICB. In conclusion, our results showed that ICB regulated vascular tone by inhibiting MLC phosphorylation and calcium flux into VSMC, and suggest that ICB has anti-hypertensive properties and therapeutic potential for cardiovascular disorders related to vascular hypertension.

• 한국전자파학회:학술대회논문집
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• 한국전자파학회 1999년도 제3회 전자장의 생체영향에 관한 워크숍
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• pp.117-129
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• 1999

Acute effects of locally applied of static magnetic field (SMF) and extremely low frequency electromagnetic field(ELF-EMF) to the cutaneous tissue within a rabbit ear chamber (REC)were evaluated under conscious conditions. Rabbits with the REC were subjected to intravital microscopical investigation by use of microphotoelectric plethysmography(MPPG). There was no dose-response relationship between the extent of vasomotion changes and frequencies(0,20,50, 100Hz)or power levels (1, 5, 10, 25, 50, 100, 200 mT). Under low vascular tone the both fields induce vasodilatation. The effects of SMF (1 mT) on the cutaneous microcirculatory system induced the vasodilatation with enhanced vasomotion under nor-adrenaline-induced high vascular tone as well as the vasoconstriction with reduced vasomotion under acetylcholine-induced low vascular tone. This suggests that the SMF can modulate vascular tone due to the modification of vasomotion biphasically in the cutaneous tissue.

• The Journal of Korean Physical Therapy
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• 제20권4호
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• pp.35-42
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• 2008

Purpose: Alterations in the structure and function of vascular smooth muscle cells (VSMCs) are important in cardiovascular disease and maintaining chronic hypertension. Chronic hypertension is associated with changes in vascular smooth muscle tone. The spontaneous or myogenic tone of a blood vessel reflects the ability to adapt smooth muscle tone to changes in transmural pressure. However, the intracellular signaling mechanisms involved in myogenic tone are not fully understood. Methods: Here, we investigated the relationship between mitogen-activated protein kinases (MAPKs) and phosphatidylinositol-3 kinase (PI3K) in isometric contraction and enzymatic activity using muscle strips from rats made hypertensive with aldosterone-analogue deoxycorticosterone acetate (DOCA) salts. Results: Changes in myogenic tone and intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) were different after physiological salt solution (PSS) in normotensive and hypertensive rats. The myogenic tone and quiescent phosphorylation induced by the PSS treatment were inhibited by 10 ${\mu}$M PD098059, an extracellular-regulated protein kinase 1/2 (ERK1/2) inhibitor, and 10 ${\mu}$M wortmannin, an inhibitor of PI3K, in hypertensive rats. Conclusion: The development of DOCA-induced hypertension is associated with altered isometric contractions and $[Ca^{2+}]_i$ via changes in activation of ERK1/2 and PI3K after DOCA-salt treatment. Therefore, ERK1/2 and PI3K activity affect hypertension and may be suitable targets for physical therapy in cardiovascular disease.

• The Korean Journal of Physiology
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• 제28권2호
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• pp.169-179
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• 1994

The effect of extracellular and intracellular pH on vascular tone and $^{45}Ca$ uptake were investigated in aortic strips and dispersed single aortic smooth muscle cells of spontaneously hypertensive rats (SHR) and aged-matched Wistar-Kyoto rats (WKY). The contraction produced by a change of extracellular pH (pHo) in the range of $6.5{\sim}8.3$ was estimated by comparison with the level of vascular tone at pH 7.4. Contraction was induced below pHo 6.5 in WKY, pHo 7.1 in SHR, and over pHo 8.0 on both strains. The amplitude of contraction induced by high pHo (over pHo 7.7) was similar in SHR and WKY, but that induced by low pHo (below pHo 7.1) in SHR was greater than that in WKY. Either high pHo- or low pHo-induced contractions in WKY and SHR were not induced in the Ca-free Tyrode's solution and were induced by the addition of Ca. $^{45}Ca$ uptake increased progressively as pHo was increased from 6.8 to 8.1 in the single aortic smooth muscle cells of WKY and SHR. $NH_4Cl$ induced a gradually developing contraction in a dose-dependent manner $(5\;mM{\sim}30\;mM)$ and the removal of $NH_4Cl$ induced transient contraction was followed by profound relaxation in the aortic rings of both strains. The contractions induced by $NH_4Cl$ or by the removal of $NH_4Cl$ in SHR were significantly greater than that in WKY. These contractions were not induced in Ca-free Tyrode's solution. $^{45}Ca$ uptake was increased by $NH_4Cl$ (20 mM) and was not changed by the removal of $NH_4Cl$ (20 mM) in the aortic strips of WKY and SHR. As a summary of above results, the vascular tone of SHR was more sensitive to the change pHi and pHo than that of WKY. The contractions induced by change of extracellular or intracellular pH depended on extracellular Ca in the aorta of SHR nnd WKY. However, the Ca uptake was in accord with the changes of contraction but increase in contraction by low pH was not accompanied by an increase in Ca uptake in both strains.

• The Korean Journal of Physiology
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• 제30권2호
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• pp.187-195
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• 1996

• 순환기질환의공학회:학술대회논문집
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• 순환기질환의공학회 2003년도 제3회 학술대회
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• pp.2-3
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• 2003

• 대한약침학회지
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• 제23권2호
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• pp.88-89
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• 2020

• The Korean Journal of Physiology and Pharmacology
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• 제21권1호
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• pp.99-106
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• 2017

Obesity is a critical risk factor for the hypertension. Although angiotensin II (Ang II) in obese individuals is known to be upregulated in obesity-induced hypertension, direct evidence that explains the underlying mechanism for increased vascular tone and consequent increase in blood pressure (BP) is largely unknown. The purpose of this study is to investigate the novel mechanism underlying Ang II-induced hyper-contractility and hypertension in obese rats. Eight-week old male Sprague-Dawley rats were fed with 60% fat diet or normal diet for 4 months. Body weight, plasma lipid profile, plasma Ang II level, BP, Ang II-induced vascular contraction, and expression of regulatory proteins modulating vascular contraction with/without Ang II stimulation were measured. As a result, high fat diet (HFD) accelerated age-dependent body weight gaining along with increased plasma Ang II concentration. It also increased BP and Ang II-induced aortic contraction. Basal expression of p-CPI-17 and myosin light chain (MLC) kinase was increased by HFD along with increased phosphorylation of MLC. Ang II-induced phosphorylation of CPI-17 and MLC were also higher in HFD group than control group. In conclusion HFD-induced hypertension is through at least in part by increased vascular contractility via increased expression and activation of contractile proteins and subsequent MLC phosphorylation induced by increased Ang II.

• 한국어류학회지
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• 제12권1호
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• pp.38-45
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• 2000

어종에 따라 혈관의 긴장도 조절은 다양한 신경전달물질에 의하여 조절되고 있다. 그러나 아직 대부분의 어종에서 자율신경계 신경전달물질 및 혈관긴장도 조절인자들의 기능에 대하여 명확하게 규명되어 있지 않다. 본 연구는 아직 연구되지 않은 분야인 이스라엘잉어에서의 자율신경계 신경전달물질들의 혈관긴장도 조절에서의 역할을 규명하고자 적출복대동맥을 이용하여 시험하였다. 이 적출혈관에서 아세틸콜린 (ACh)은 정상혈관과 미리 일정수준 수축시킨 혈관 모두에서 수축을 유발하였으며 수축작용은 무스카린성 길항제인 아트로핀에 의해 거의 완벽하게 차단되었다. 여러 가지 아드레날린성 수용체를 동시에 흥분시키는 내인성 물질인 에피네프린 (Epi)은 혈관의 조건에 상관없이 이완반응을 유발하였다. 그러나 유사한 내인성물질인 노르에피네프린 (NE)은 정상혈관에서는 미약한 수축율, 미리수축된 혈관에서는 이완작용을 유발하였다. 한편 ${\alpha}_1$ 아드레날린성 수용체 흥분제인 페닐에프린은 수축을, $\beta$수용체 홍분제인 이소프로테레놀은 이완을 각각 유발하였으며 ${\alpha}_2$수용체 흥분제인 클로니딘은 아무런 반응을 유발하지 않았다. Epi, NE 및 이소프로테레놀에 의해 유발된 혈관이완 반응은 $\beta$ 아드레날린성 수용체 길항제인 프로프라놀롤에 의해 유의하게 억제되었다. 따라서 살아있는 상태의 이스라엘 잉어에서는 ACh는 주로 무스카린성 수용체 활성화에 의한 혈관을 수축하는 기능을, Epi과 NE는 $\beta$수용체 흥분에 의한 이완작용을 각각 발휘하는 것으로 판단된다.

• Toxicological Research
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• 제12권2호
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• pp.195-201
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• 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.