Abstract
It is known that perivascular application of CGRP induces cerebral vasodilatation. However, it is unclear whether intravenous alfa CGRP (αCGRP) induces changes in cerebral and systemic hemodynamics. Therefore, we studied the influence of an αCGRP intravenous infusion at a rate of 1.5 mcg/min in 20 min on mean arterial velocity in the middle cerebral artery (vm MCA) and in the posterior cerebral artery (vm PCA) in twenty healthy subjects using transcranial Doppler (TCD). We found out that αCGRP decreased vm MCA (p < 0.001), vm PCA (p < 0.001), mean arterial pressure (MAP) (p < 0.001) and end-tidal CO2 (Et-CO2) (p = 0.030). The heart rate (HR) increased during αCGRP infusion (p < 0.001). In addition, we found a positive relationship between Et-CO2 and vm MCA (p = 0.001) as well as vm PCA (p = 0.043). In our view, αCGRP induces changes in cerebral and systemic circulation in healthy volunteers. It might cause vasodilatation of MCA and PCA and a compensatory decrease of Et-CO2 to αCGRP related hemodynamic changes.
Highlights
Calcitonin gene-related peptide (CGRP) has been proven to play an important role in migraine and it has become a target molecule in headache migraine research and treatment [1,2,3,4,5]
It has been shown that patients with an excellent response to erenumab are highly susceptible to αCGRP provocation [6]
The velocity in the middle cerebral artery (vm middle cerebral artery (MCA)) showed a significant decrease in all points except between points 1–3 and 2–3 because of a slight increase of the signal at the recovery phase, after the end of the αCGRP infusion
Summary
Calcitonin gene-related peptide (CGRP) has been proven to play an important role in migraine and it has become a target molecule in headache migraine research and treatment [1,2,3,4,5]. It has been shown that patients with an excellent response to erenumab are highly susceptible to αCGRP provocation [6]. An αCGRP response should be regarded as an important predictive factor for selecting patients who are responders to anti-CGRP preventive treatment. Current evidence suggests that CGRP is a potent dilatator of cerebral arteries [7,8,9]. It is still unclear whether vasodilatation caused by αCGRP through intravascular interaction with an endogenous CGRP system, utilizes vascular endothelium
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