Serotonin-Induced Vasodilatation in the Human Forearm Is Mediated by the “Nitric Oxide-Pathway”

Bruning, T. A.; Chang, P. C.; Blauw, Gerard J.; Vermeij, P.; Zwieten, P. A. van

doi:10.1097/00005344-199307000-00008

Cited by 40 publications

(27 citation statements)

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“…25 In accordance with these experimental findings, it was previously shown by our group that in the human forearm the vasodilator response to acetylcholine was not influenced by the competitive nitric oxide synthase inhibitor N G -monomethyl-L-arginine (L-NMMA), whereas serotonin-induced vasodilation was blunted by L-NMMA. 26 This finding provides evidence that serotonin is a more specific tool than acetylcholine to investigate endothelium-dependent nitric oxidemediated vasodilation in humans. On the basis of these experimental and human data, we therefore argue that in HTG, endothelium-dependent nitric oxide-mediated vasodilation is impaired, as measured by the intra-arterial infusion of serotonin.…”

Section: Discussionmentioning

confidence: 86%

“…The improvement of the acetylcholineinduced vasodilation by L-arginine in the HTG group may be explained by the fact that the acetylcholine response is only partially mediated by the nitric oxide pathway. 26 To elucidate the direct effect of triglycerides on endothelial function, a systemic infusion of an artificial triglyceride emulsion (Intralipid) was applied. Previous studies have demonstrated that these artificial lipid particles rapidly acquire apolipoproteins in the circulation and share the same catabolic pathway as endogenous triglyceride-rich lipoproteins.…”

Section: Discussionmentioning

confidence: 99%

“…Previously, a similar paradoxical augmented vasodilator response to intra-arterially infused acetylcholine was observed during the simultaneous infusion of the nitric oxide scavenger methylene blue. 26 Evidence was provided that methylene blue enhanced the acetylcholine-induced vasodilation by inactivation of the enzyme acetylcholinesterase. 30 Whether a similar mechanism could play a role in the present observation is subject to speculation.…”

Section: Discussionmentioning

confidence: 99%

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Not Acute but Chronic Hypertriglyceridemia Is Associated With Impaired Endothelium-Dependent Vasodilation

Man

Weverling-Rijnsburger

Laarse

et al. 2000

ATVB

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Abstract-There is controversy regarding the relation between hypertriglyceridemia (HTG) and endothelial function. This study was designed to investigate endothelial function in a patient group with chronic HTG, before and during lipid-lowering therapy by atorvastatin. In addition, the effects of acute HTG on endothelial function were studied in normolipidemic individuals. Eight male patients with chronic HTG were studied before and after 6 weeks of lipid-lowering treatment with 80 mg atorvastatin once daily. Ten age-matched control subjects were studied at baseline and immediately after a high-dose infusion of artificial triglycerides. The endothelium-dependent response to serotonin was attenuated in the HTG group, whereas the response to acetylcholine was comparable to the response in the control group. The response to the endothelium-independent vasodilator nitroprusside was comparable in both groups. In response to atorvastatin therapy, serum triglyceride and cholesterol levels decreased significantly by 43% (paired t test, Pϭ0.017) and 38% (paired t test, Pϭ0.012), respectively. After 6 weeks of treatment, the forearm blood flow response to serotonin improved from 63% to 106% (ANOVA, PϽ0.001). Induction of acute HTG in the control subjects did not affect the forearm blood flow responses to serotonin and nitroprusside; however, the response to acetylcholine was paradoxically increased. In conclusion, patients with chronic HTG have an impaired endothelium-dependent vasodilation to serotonin that is normalized after 6 weeks of lipid-lowering therapy by atorvastatin.

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Section: Discussionmentioning

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Not Acute but Chronic Hypertriglyceridemia Is Associated With Impaired Endothelium-Dependent Vasodilation

Man

Weverling-Rijnsburger

Laarse

et al. 2000

ATVB

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“…We show an impaired serotonin-induced vasodilation in forearm resistance arteries in patients with Type II diabetes. Serotonin responses can be completely blocked by NO-inhibition [19,20,21,23] strongly suggesting a specific defect in endothelial NO release in these diabetic patients.…”

Section: Effect Of 5-mthf Co-infusion On Serotonin-inducedmentioning

confidence: 96%

“…This protocol has previously been shown to cause a dose-dependent increase in endothelium-dependent, NO-mediated vasodilation. We and others have shown that the effect of serotonin can be completely abolished by L-NMMA, a specific inhibitor of NO [19,20,21,23]. Acetylcholine, which also can be used to investigate endothelium-dependent vasodilation is less specific as it stimulates both NO and EDHF.…”

Section: Subjectsmentioning

confidence: 99%

Impaired NO-dependent vasodilation in patients with Type II (non-insulin-dependent) diabetes mellitus is restored by acute administration of folate

et al. 2002

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Aims/hypothesis. Patients with diabetes are characterised by endothelial dysfunction and cardiovascular mortality. In particular endothelium-derived nitric oxide has emerged as a first line mechanism against atherosclerosis. Hyperglycaemia causes oxygen radical stress but has also been associated with endothelial nitric oxide synthase uncoupling, both lead to decreased nitric oxide-availability. We recently showed that folate reverses eNOS uncoupling in vitro. Therefore we hypothesise that folate improves endothelial function in Type II (non-insulin-dependent) diabetes mellitus in vivo. Methods. Using forearm plethysmography, we evaluated the effect of local, intra-arterial administration of 5-methyltetrahydrofolate (5-MTHF, the active form of folic acid, 1 µg/100 ml FAV/min) on forearm blood flow in 23 patients with Type II diabetes and 21 control subjects, matched for age, sex, blood pressure, body mass index, weight and smoking habits. Serotonin as a stimulator of nitric oxide-dependent vasodilation and sodium nitroprusside as a stimulator of endothelium-independent vasodilation were infused. Results. Serotonin-induced vasodilation was blunted (53±30 vs 102±66 M/C%, p<0.005) and nitroprussideinduced vasodilation was mildly reduced (275±146 vs 391±203 M/C%, p<0.05) in patients with Type II diabetes compared to control subjects. 5-MTHF improved nitric oxide-mediated vasodilation (from 53±30 to 88±59 M/C%, p<0.05) in patients with Type II diabetes mellitus. As expected, 5-MTHF had no effect on forearm blood flow in control subjects. Conclusion/interpretation. These data imply that folate can be used to improve nitric oxide status and to restore endothelial dysfunction in patients with Type II diabetes. Our results provide a strong rationale for the initiation of studies that investigate whether supplementation with folic acid prevents future cardiovascular events in this patient group. [Diabetologia (2002[Diabetologia ( ) 45:1004[Diabetologia ( -1010

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Acetylcholine

Irigoyen

Porto

Soares

et al. 2008

Cardiovascular Hormone Systems

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Serotonin-Induced Vasodilatation in the Human Forearm Is Mediated by the “Nitric Oxide-Pathway”

Cited by 40 publications

References 0 publications

Not Acute but Chronic Hypertriglyceridemia Is Associated With Impaired Endothelium-Dependent Vasodilation

Not Acute but Chronic Hypertriglyceridemia Is Associated With Impaired Endothelium-Dependent Vasodilation

Impaired NO-dependent vasodilation in patients with Type II (non-insulin-dependent) diabetes mellitus is restored by acute administration of folate

Acetylcholine

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