Tasks performed
Ngoc-Trang Thi Huynh works as a staff engineer in the following research group:
Ngoc-Trang Thi Huynh teaches practical courses in Physiology.
Publications
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Skogestad, Jonas; Albert, Ingrid; Hougen, Karina; Lothe, Gustav B; Lunde, Marianne & Eken, Olav Søvik
[Show all 25 contributors for this article]
(2023).
Disruption of Phosphodiesterase 3A Binding to SERCA2 Increases SERCA2 Activity and Reduces Mortality in Mice with Chronic Heart Failure.
Circulation.
ISSN 0009-7322.
147(16),
p. 1221–1236.
doi:
10.1161/CIRCULATIONAHA.121.054168.
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Berg, Torill; Walaas, S. Ivar; Roberg, Bjørg Åse; Ngoc-Trang, Thi Huynh & Jensen, Jørgen
(2012).
Plasma norepinephrine in hypertensive rats reflects alpha2-adrenoceptor release control only when re-uptake is inhibited.
Frontiers in Neurology.
ISSN 1664-2295.
3.
doi:
10.3389/fneur.2012.00160.
Full text in Research Archive
Show summary
α2-adrenoceptors (AR) lower central sympathetic output and peripheral catecholamine release, thereby protecting against sympathetic hyperactivity and hypertension. Norepinephrine re-uptake–transporter effectively (NET) removes norepinephrine from the synapse. Overflow to plasma will therefore not reflect release. Here we tested if inhibition of re-uptake allowed presynaptic α2AR release control to be reflected as differences in norepinephrine overflow in anesthetized hypertensive spontaneously hypertensive rats (SHR) and normotensive rats (WKY). We also tested if α2AR modulated the experiment-induced epinephrine secretion, and a phenylephrine-induced, α1-adrenergic vasoconstriction. Blood pressure was recorded through a femoral artery catheter, and cardiac output by ascending aorta flow. After pre-treatment with NET inhibitor (desipramine), and/or α2AR antagonist (yohimbine, L-659,066) or agonist (clonidine, ST-91), we injected phenylephrine. Arterial blood was sampled 15 min later. Plasma catecholamine concentrations were not influenced by phenylephrine, and therefore reflected effects of pre-treatment. Desipramine and α2AR antagonist separately had little effect on norepinephrine overflow. Combined, they increased norepinephrine overflow, particularly in SHR. Clonidine, but not ST-91, reduced, and pertussis toxin increased norepinephrine overflow in SHR and epinephrine secretion in both strains. L-659,066 + clonidine (central α2AR-stimulation) normalized the high blood pressure, heart rate, and vascular tension in SHR. α2AR antagonists reduced phenylephrine-induced vasoconstriction equally in WKY and SHR. Conclusions: α2AAR inhibition increased norepinephrine overflow only when re-uptake was blocked, and then with particular efficacy in SHR, possibly due to their high sympathetic tone. α2AAR inhibited epinephrine secretion, particularly in SHR. α2AAR supported α1AR-induced vasoconstriction equally in the two strains. α2AR malfunctions were therefore not detected in SHR under this basal condition.
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Utheim, Tor Paaske; Raeder, Sten; Olstad, Ok; Utheim, Øa; De la paz, Maria & Cheng, Richard
[Show all 10 contributors for this article]
(2009).
Comparison of the histology, gene expression profile, and phenotype of cultured human limbal epithelial cells from different limbal regions.
Investigative Ophthalmology and Visual Science.
ISSN 0146-0404.
50(11),
p. 5165–5172.
doi:
10.1167/iovs.08-2884.
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Published
Apr. 13, 2011 10:59 AM
- Last modified
May 30, 2023 7:19 AM