# Cold pressor‐induced sympathetic activation blunts the femoral but not carotid artery vascular responsiveness

**Authors:** Guilherme F. Speretta, Gaia Giuriato, Gianluigi Dorelli, Chiara Barbi, Anna Pedrinolla, Massimo Venturelli

PMC · DOI: 10.14814/phy2.70281 · Physiological Reports · 2025-03-20

## TL;DR

Cold-induced sympathetic activation reduces blood flow responsiveness in the femoral artery but not in the carotid artery during leg movement.

## Contribution

This study reveals differential vascular responses to sympathetic activation in femoral versus carotid arteries during passive leg movement.

## Key findings

- Cold pressor test blunts femoral artery vascular responsiveness during passive leg movement.
- Contralateral carotid artery shows increased blood flow during passive leg movement regardless of cold pressor test.
- Sympathetic modulation, as indicated by SAP low-frequency power, is enhanced during cold pressor test.

## Abstract

Vascular responsiveness due to passive leg movement (PLM) on the brain remains unknown. This study aimed to evaluate the effects of cold‐induced sympathetic activation (CPT) on femoral and ipsilateral and contralateral carotid arteries' vascular responsiveness evoked by PLM. Thirteen participants (seven males and six females; age: 27.0 ± 2.3 years) undertook a randomized session in which PLM was performed on the right leg at rest and during CPT. Right femoral (fBF) and right (ipsilateral) and left (contralateral) carotid (cBF) blood flows were measured by ultrasounds, and heart hemodynamics were assessed via photoplethysmography and impedance cardiograph. Systolic arterial pressure (SAP) time series were used to infer sympathetic modulation to the vessels. Femoral (fVC) and carotid (cVC) vascular conductance (BF/MAP) were calculated. CPT evoked changes in PLM on cBF, fBF, and fVC (interaction and time effect). cBF peak and cBF and cVC area under the curve were higher in the contralateral carotid in the two interventions. Low‐frequency power of SAP was higher in PLM‐CPT than in PLM; all p < 0.05. These results suggest that the CPT‐induced increases in sympathetic modulation attenuate the vascular responsiveness in the femoral, but not the carotid, arteries. Also, the contralateral carotid increased blood flow during PLM, regardless of the CPT.

## Full-text entities

- **Genes:** CHPT1 (choline phosphotransferase 1) [NCBI Gene 56994] {aka CPT, CPT1}, SH2D1A (SH2 domain containing 1A) [NCBI Gene 4068] {aka DSHP, EBVS, IMD5, LYP, MTCP1, SAP}
- **Diseases:** hyperemia (MESH:D006940), PLM (MESH:D014202), hypercapnia (MESH:D006935), CPT-PLM (MESH:C536214), diseases (MESH:D004194), carotid dilation (MESH:D002311), Stroke (MESH:D020521), cardiovascular, metabolic, or infectious diseases (MESH:D003141)
- **Chemicals:** PLM (-), caffeine (MESH:D002110), oxygen (MESH:D010100), water (MESH:D014867), NO (MESH:D009569)
- **Species:** Homo sapiens (human, species) [taxon 9606], Rattus norvegicus (brown rat, species) [taxon 10116]
- **Mutations:** C) for 4, C - +300 C

## Full text

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## Figures

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## References

46 references — full list in the complete paper: https://tomesphere.com/paper/PMC11923985/full.md

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Source: https://tomesphere.com/paper/PMC11923985