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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)