Publications by authors named "Harrison D Broadley"
Article Synopsis
- Trace amines can cause blood vessel constriction without involving noradrenaline, and the exact mechanism behind this is still unclear.
- The study tested the effects of β-phenylethylamine (β-PEA) and a TAAR1-selective agonist on blood vessel constriction in rat aortic rings and mesenteric arteries.
- Results showed that vasoconstriction in aortic rings was not affected by common biogenic amine antagonists, suggesting TAAR1 is likely responsible for the response to trace amines.
Acetylcholine (Ach) causes vasodilatation by nitric oxide (NO) release from the vascular endothelium. Vasoconstrictors such as α-adrenoceptor agonists (phenylephrine) or thromboxane TxA mimetics (U46619) also release endothelial NO. Inhibition of nitric oxide synthase (NOS) with N-nitro-L-arginine (L-NAME) potentiates vasoconstriction by phenylephrine and the trace amine, β-phenylethylamine (PEA), indicating underlying opposing vasodilatation.
View Article and Find Full Text PDFSympathomimetic and trace amines, including β-phenylethylamine (PEA) and amphetamine, increase blood pressure and constrict isolated blood vessels. By convention this is regarded as a sympathomimetic response, however, recent studies suggest trace amine-associated receptor (TAAR) involvement. There is also uncertainty whether these amines also release nitric oxide (NO) causing opposing vasodilatation.
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