The investigators will test the null hypothesis that there will be no changes in the insulin-mediated suppression of endogenous glucose production (EGP) in response to autonomic blockade. To test this hypothesis, the investigators propose to determine the role of the autonomic nervous system in hepatic insulin resistance.

Start Date17 Apr 2017

Sponsor / Collaborator

Vanderbilt University Medical Center

NCT01137253

/ CompletedPhase 1IIT

The Autonomic Nervous System, Nitric Oxide and TPA Interactions

The investigators are interested in the role of the autonomic nervous system in the regulation of endothelial function among obese hypertensive subjects. In particular, the investigators will study how endothelial function (response to intra-arterial acetylcholine) changes during autonomic withdrawal.

Start Date01 Jun 2010

Sponsor / Collaborator

Vanderbilt University

NCT01122407

/ CompletedPhase 1IIT

Obesity, Hypertension in African American Women, Neuro-metabolic Mechanism

The overall goal of this proposal is to determine the autonomic and nitric oxide contribution in the pathogenesis of hypertension and insulin resistance in obese African American women. For this purpose we will use two non-FDA approved drugs:
Trimethaphan IND# 63826 Approval date 12/20/2001 L-NMMA IND# 41735 Approval date 09/1993

Start Date01 Jan 2010

Sponsor / Collaborator

Vanderbilt University Medical Center

[+1]

100 Clinical Results associated with Trimethaphan Camsylate

100 Translational Medicine associated with Trimethaphan Camsylate

100 Patents (Medical) associated with Trimethaphan Camsylate

893

Literatures (Medical) associated with Trimethaphan Camsylate

01 Apr 2025·Plant Biotechnology Journal

Multi‐omics analysis identified the GmUGT88A1 gene, which coordinately regulates soybean resistance to cyst nematode and isoflavone content

Article

Author: Jiang, Haipeng ; Li, Yongguang ; Zhan, Yuhang ; Zhao, Xue ; Liu, Fang ; Li, Haiyan ; Qu, Shuo ; Teng, Weili ; Han, Yingpeng ; Sun, Haowen

SummarySoybean cyst nematode (SCN, Heterodera glycines) is a major pathogen harmful to soybean all over the world, causing huge yield loss every year. Soybean resistance to SCN is a complex quantitative trait controlled by a small number of major genes (rhg1 and Rhg4) and multiple micro‐effect genes. Therefore, the continuous identification of new resistant lines and genes is needed for the sustainable development of global soybean production. Here, a novel disease‐resistance quantitative trait locus Rscn‐16 was identified and fine mapped to an 8.4‐kb interval on chromosome 16 using an F2 population. According to transcriptome and metabolome analysis, a UDP‐glucosyltransferase encoding gene, GmUGT88A1, was identified as the most likely gene of Rscn‐16. Soybean lines overexpressing GmUGT88A1 exhibited increased resistance to SCN, higher isoflavone glycosides and larger seed size while the phenotype of RNA‐interference and knockout soybean lines showed sensitivity to SCN and decreased in seed size compared to wild‐type plants. GmMYB29 gene could bind to the promoter of GmUGT88A1 and coordinate with GmUGT88A1 to regulate soybean resistance to SCN and isoflavone accumulation. Under SCN infection, GmUGT88A1 participated in the reorientation of isoflavone biosynthetic metabolic flow and the accumulation of isoflavone glycosides, thus protecting soybean from SCN stress. GmUGT88A1 was found to control soybean seed size by affecting transcription abundance of GmSWEET10b and GmFAD3C, which are known to control soybean seed weight. Our findings provide insights into the regulation of SCN resistance, isoflavone content and seed size through metabolic flux redirection, and offer a potential means for soybean improvement.

01 Nov 2024·Journal of Computational Biophysics and Chemistry

Molecular Docking, Quantum Mechanics and Molecular Dynamics Simulation of Anti-CAD Drugs Against High-Risk Xanthine Dehydrogenase Variants Associated with Oxidative Stress Pathways

Author: Ahmed, Shiek S. S. J. ; Ahmad, Sheikh F. ; Emran, Talha Bin ; Janakiraman, V. ; Attia, Sabry M. ; Sudhan, M.

Xanthine dehydrogenase (XDH) contributes significantly to generating reactive oxygen species in coronary artery disease (CAD). XDH has been proposed as a therapeutic target, but its genetic variants could affect protein structure and drug response. We aimed to assess protein structure modification occur due to genetic variants and to screen 215 CAD drugs for their utility in personalized CAD treatment against the XDH variants. A series of computational methods were implemented to identify pathogenic variants that cause XDH structure instability localized at the con served regions contributing to functional significance. Then, the XDH structures with the pathogenic variants were modeled using two different approaches to select the best models for docking with the CAD drugs. Finally, the stability of the docked complexes and their ability to transfer electrons were evaluated using molecular dynamics (MD) simulations and quantum mechanics/molecular mechanics (QM/MM) calculation. Among 751 variants examined; R149C and Q919R showed high pathogenicity, localized in conserved regions could alter protein structure and function. Further, docking of CAD drugs against XDH (native, R149C and Q919R) showed vericiguat with higher affinity, ranging from −7.95 kcal/mol to −10.41 kcal/mol, than the well-known XDH inhibitor (febuxostat, −5.73 kcal/mol to −8.35 kcal/mol). This indicates that vericiguat will be effective in CAD treatment, regardless of the XDH variants. Additionally, MD simulation and QM/MM confirmed vericiguat stability and electron transfer ability to form hydrogen bonds with the XDH protein. In conclusion, vericiguat will be beneficial for the personalized treatment of CAD by inhibiting XDH variants. Additional clinical studies are necessary to confirm our findings.

01 Aug 2024·Clinical Autonomic Research

Complete autonomic blockade reveals nitric oxide contribution to blood pressure regulation in obese Black women

Article

Author: Kulapatana, Surat ; Rahman, Sharla ; Kirabo, Annet ; Biaggioni, Italo ; Saleem, Mohammad ; Diedrich, André ; Shibao, Cyndya A ; Gamboa, Alfredo

AbstractPurposeHypertension is one of the major causes of cardiovascular morbidity and mortality in the USA and disproportionately affects Black women. Endothelial-derived nitric oxide (eNO) substantially regulates blood pressure in humans, and impaired NO-mediated vasodilation has been reported in the Black population. Previous studies using an NO synthase inhibitor, NG-monomethyl-L-arginine (L-NMMA) did not fully determine the NO contribution to blood pressure because of baroreflex buffering. Therefore, in the present study we used trimethaphan, a ganglionic blocker, to inhibit baroreflex buffering and study NO modulation of blood pressure in Black women during L-NMMA infusion.MethodsL-NMMA at doses of 250 μg/kg per minute was infused in combination with trimethaphan at doses of 4 mg/min to eliminate baroreflex mechanisms. Heart rate (HR) was obtained with continuous electrocardiogram monitoring, and continuous blood pressure was measured with the volume clamp method. The increase in systolic blood pressure (SBP) during both infusions was used to estimate the contribution of NO to blood pressure.ResultsTen Black (age range 30–50 years, body mass index [BMI] 30–45 kg/m2), and nine White women (age range 30–50 years, body mass index 30–45 kg/m2) were enrolled in this study. During autonomic blockade, there was no difference in the decrease in SBP between Black and White women (− 20 ± 16.45 vs. − 24 ± 15.49 mm Hg, respectively; P = 0.659). When autonomic blockade was combined with L-NMMA, Black women had a significant increase in SBP compared to White women (54 ± 13.62 vs. 39 ± 09.64 mm Hg, respectively; P = 0.022, respectively).ConclusionAutonomic blood pressure regulation was similar between Black and White women. However, NO contribution to blood pressure was significantly greater in Black women compared to White women.RegistrationClinicalTrials.gov: NCT01122407.

100 Deals associated with Trimethaphan Camsylate

External Link

KEGG	Wiki	ATC	Drug Bank
-	Trimethaphan Camsylate	C02BA01	DB01116

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