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General Health & Fitness
Nutrition and Supplements
The Effects of Oral l-Arginine and l-Citrulline Supplementation on Blood Pressure
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<blockquote data-quote="madman" data-source="post: 154791" data-attributes="member: 13851"><p>[ATTACH=full]7942[/ATTACH]</p><p><strong><span style="color: rgb(184, 49, 47)">Figure 1.</span></strong> <strong>Mechanisms of nitric oxide-mediated vasodilation. Plasma Arg provides the substrate for the synthesis of nitric oxide (NO) via the enzyme endothelial nitric oxide synthase (eNOS) located in the vascular endothelium. The enzymatic reaction requires the co-substrates O2 and nicotinamide adenine dinucleotide phosphate (NADPH) and the cofactors BH4, flavin adenine dinucleotide (FAD), and flavin mononucleotide (FMN). NO diffuses from the endothelial cell to the smooth muscle cell and activates soluble guanylyl cyclase (sGC), resulting in increased cyclic guanosine monophosphate (cGMP) production. cGMP subsequently activates protein kinase G (PKG), resulting in decreased [Ca2+]i via at least four mechanisms: 1. Inhibition of voltage-dependent calcium channels (VDCC), reducing calcium influx. 2. Activation of plasma membrane calcium ATPases (PMCA), increasing ATP-dependent calcium efflux. 3. Inhibition of inositol triphosphate receptors (IP3R), reducing calcium release from the sarcoplasmic reticulum (SR) to the cytoplasm. 4. Activation of sarcoplasmic calcium ATPases (SERCA), increasing the ATP-dependent sequestration of calcium from the cytoplasm to the SR. Decreased [Ca2+]i mediates smooth muscle relaxation via the activation of myosin light chain kinase and the inhibition of myosin light chain phosphatase (not shown in figure), resulting in vasodilation.</strong></p></blockquote><p></p>
[QUOTE="madman, post: 154791, member: 13851"] [ATTACH=full]7942[/ATTACH] [B][COLOR=rgb(184, 49, 47)]Figure 1.[/COLOR][/B] [B]Mechanisms of nitric oxide-mediated vasodilation. Plasma Arg provides the substrate for the synthesis of nitric oxide (NO) via the enzyme endothelial nitric oxide synthase (eNOS) located in the vascular endothelium. The enzymatic reaction requires the co-substrates O2 and nicotinamide adenine dinucleotide phosphate (NADPH) and the cofactors BH4, flavin adenine dinucleotide (FAD), and flavin mononucleotide (FMN). NO diffuses from the endothelial cell to the smooth muscle cell and activates soluble guanylyl cyclase (sGC), resulting in increased cyclic guanosine monophosphate (cGMP) production. cGMP subsequently activates protein kinase G (PKG), resulting in decreased [Ca2+]i via at least four mechanisms: 1. Inhibition of voltage-dependent calcium channels (VDCC), reducing calcium influx. 2. Activation of plasma membrane calcium ATPases (PMCA), increasing ATP-dependent calcium efflux. 3. Inhibition of inositol triphosphate receptors (IP3R), reducing calcium release from the sarcoplasmic reticulum (SR) to the cytoplasm. 4. Activation of sarcoplasmic calcium ATPases (SERCA), increasing the ATP-dependent sequestration of calcium from the cytoplasm to the SR. Decreased [Ca2+]i mediates smooth muscle relaxation via the activation of myosin light chain kinase and the inhibition of myosin light chain phosphatase (not shown in figure), resulting in vasodilation.[/B] [/QUOTE]
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General Health & Fitness
Nutrition and Supplements
The Effects of Oral l-Arginine and l-Citrulline Supplementation on Blood Pressure
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