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GLP-1 receptor activation is documented to increase resting heart rate through two mechanisms that likely operate in parallel: direct sympathetic nervous system stimulation — evidenced by concurrent increases in muscle sympathetic nerve activity measured by microneurography in healthy subjects given exenatide, arguing against reflex tachycardia alone as the explanation — and vasodilation of peripheral resistance vessels via cAMP/PKA and nitric oxide pathways, which reduces total peripheral resistance and may recruit baroreflex-driven chronotropy as a secondary effect (Vianna et al., 2012)
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