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. 2020 Sep 22:2020:8125805.
doi: 10.1155/2020/8125805. eCollection 2020.

Endothelium-Independent Vasodilatory Effect of Sailuotong (SLT) on Rat Isolated Tail Artery

Affiliations

Endothelium-Independent Vasodilatory Effect of Sailuotong (SLT) on Rat Isolated Tail Artery

S Y Yeon et al. Evid Based Complement Alternat Med. .

Abstract

Background: Sailuotong (SLT) is a standardized three-herb formulation consisting of extracts of Panax ginseng, Ginkgo biloba, and Crocus sativus for the treatment of vascular dementia (VaD). Although SLT has been shown to increase cerebral blood flow, the direct effects of SLT on vascular reactivity have not been explored. This study aims to examine the vasodilatory effects of SLT and the underlying mechanisms in rat isolated tail artery.

Methods: Male (250-300 g) Wistar Kyoto (WKY) rat tail artery was isolated for isometric tension measurement. The effects of SLT on the influx of calcium through the cell membrane calcium channels were determined in Ca2+-free solution experiments.

Results: SLT (0.1-5,000 μg/ml) caused a concentration-dependent relaxation in rat isolated tail artery precontracted by phenylephrine. In the contraction experiments, SLT (500, 1,000, and 5,000 μg/mL) significantly inhibited phenylephrine (0.001 to 10 μM)- and KCl (10-80 mM)-induced contraction, in a concentration-dependent manner. In Ca2+-free solution, SLT (500, 1,000, and 5,000 μg/mL) markedly suppressed Ca2+-induced (0.001-3 mM) vasoconstriction in a concentration-dependent manner in both phenylephrine (10 μM) or KCl (80 mM) stimulated tail arteries. L-type calcium channel blocker nifedipine (10 μM) inhibited PE-induced contraction. Furthermore, SLT significantly reduced phenylephrine-induced transient vasoconstriction in the rat isolated tail artery.

Conclusion: SLT induces relaxation of rat isolated tail artery through endothelium-independent mechanisms. The SLT-induced vasodilatation appeared to be jointly meditated by blockages of extracellular Ca2+ influx via receptor-gated and voltage-gated Ca2+ channels and inhibition of the release of Ca2+ from the sarcoplasmic reticulum.

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Conflict of interest statement

As a medical research institute, NICM Health Research Institute receives research grants and donations from foundations, universities, government agencies, individuals, and industry. Sponsors and donors also provide untied funding for work to advance the vision and mission of the institute. The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
HPLC chromatograms of the SLT extract. The chromatogram (a) at 203 nm (pink) shows the ginsenosides Rg1, ginsenosides Re, and ginsenosides. The chromatogram (b) at 440 nm (blue) shows crocin. The chromatogram (c) at 370 nm (maroon) shows quercetin and isorhamnetin.
Figure 2
Figure 2
Cumulative concentration-response of the SLT extract (0.1–5,000 μg/ml) on phenylephrine (1 μM)-preconstricted rat isolated tail artery with (●) or without (○) the presence of L-NAME (20 μM). Values are expressed as mean ± SEM (n = 6).
Figure 3
Figure 3
Effects of potassium channel blockers on SLT extract-induced relaxation on phenylephrine (1 μM)-preconstricted rat isolated tail artery. Tail arteries were preincubated with either vehicle control (○), tetrethyl-ammonium (TEA, a nonselective potassium channel blocker) (1 mM) (●), glibenclaminde (Glib, an ATP-sensitive potassium channel blocker) (3 μM) (■), or clotrimazole (KCa, a calcium-activated potassium channel blocker) (5 μM) (▲) for 30 minutes before construction of the concentration-response curve. Values are expressed as mean ± SEM (n = 5-6).
Figure 4
Figure 4
(a) Effect of the vehicle control (○), SLT extract (500 (●), 1000 (■), or 5000 (▲) μg/ml), or nifedipine (10 μM) (♦) on Ca2+-induced vasoconstriction in phenylephrine (PE) (10 μM)-stimulated rat isolated tail arteries. Values are expressed as mean ± SEM (∗∗∗P < 0.001 vs Control) (n = 5). (b) Effect of the vehicle control (○) and SLT extract (500 (●), 1,000 (■), or 5,000 (▲) μg/ml) on Ca2+-induced vasoconstriction in potassium chloride (KCl) (80 mM)-stimulated rat isolated tail arteries. Values are expressed as mean ± SEM (∗∗P < 0.01 vs. control ∗∗∗P < 0.001 vs. control) (n = 5–8).
Figure 5
Figure 5
(a) Effect of the vehicle control (○), SLT extract (500 (●), 1000 (■), or 5000 (▲) μg/ml), or nifedipine (10 μM) (♦) on phenylephrine-induced vasoconstriction in rat isolated tail arteries. Values are expressed as mean ± SEM (∗∗∗P < 0.001 vs. control) (n = 5). (b) Isometric tension change of phenylephrine (10 μM)-induced vasoconstriction in rat isolated tail arteries with (closed bar) or without (open bar) the presence of the SLT extract (5000 μg/ml). Values are expressed as mean ± SEM (∗∗P < 0.01) (n = 8). (c) Effect of the vehicle control (○) or SLT extract (500 (●), 1,000 (■), or 5,000 (▲) μg/ml) on potassium chloride (KCl) (80 mM)-induced vasoconstriction in rat isolated tail arteries. Values are expressed as mean ± SEM (P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001 vs. control) (n = 3). (d) Isometric tension change of KCl (80 mM)-induced vasoconstriction in rat isolated tail arteries with (closed bar) or without (open bar) the presence of the SLT extract (5,000 μg/ml). Values are expressed as mean ± SEM (∗∗P < 0.01) (n = 3).
Figure 6
Figure 6
Effect of the SLT extract (500, 1,000, and 5,000 μg/ml) on phenylephrine (10 μM)-induced transient vasoconstriction in rat isolated tail arteries. Con2/Con1 (%) refers to the ratio of the second contraction to the first contraction. Values are expressed as mean ± SEM (P < 0.05 vs control) (n = 6).

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References

    1. Gorelick P. B., Scuteri A., Black S. E., et al. Vascular contributions to cognitive impairment and dementia. Stroke. 2011;42(9):2672–2713. doi: 10.1161/str.0b013e3182299496. - DOI - PMC - PubMed
    1. Santos C. Y., Snyder P. J., Wu W. C., Zhang M., Echeverria A., Alber J. Pathophysiologic relationship between alzheimer’s disease, cerebrovascular disease, and cardiovascular risk: a review and synthesis. Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring. 2017;7(1):69–87. doi: 10.1016/j.dadm.2017.01.005. - DOI - PMC - PubMed
    1. Seto S. W., Krishna S. M., Yu H., Liu D., Khosla S., Golledge J. Impaired acetylcholine-induced endothelium-dependent aortic relaxation by caveolin-1 in angiotensin II-infused apolipoprotein-E (ApoE−/−) knockout mice. PLoS One. 2013;8(3) doi: 10.1371/journal.pone.0058481.e58481 - DOI - PMC - PubMed
    1. Lam T. Y., Seto S. W., Lau Y. M., et al. Impairment of the vascular relaxation and differential expression of caveolin-1 of the aorta of diabetic +db/+db mice. European Journal of Pharmacology. 2006;546(1–3):134–141. doi: 10.1016/j.ejphar.2006.07.003. - DOI - PubMed
    1. Seto S. W., Bexis S., Aiden McCormick P., Docherty J. R. Actions of thalidomide in producing vascular relaxations. European Journal of Pharmacology. 2010;644(1–3):113–119. doi: 10.1016/j.ejphar.2010.06.035. - DOI - PubMed

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