Neurovascular Coupling is Not Attenuated During Reflex‐Mediated Sympathetic Activation via Lower Body Negative Pressure in Humans

Abstract

IntroductionCerebral blood flow is tightly coupled with local neuronal activation and metabolism (i.e., neurovascular coupling; NVC). Attenuated NVC has been identified in several chronic diseases, including hypertension, but the underlying mechanism(s) remains unknown. Raised peripheral sympathetic vasoconstrictor activity can play a malevolent role in the pathology of hypertension and might also contribute to the blunted NVC as cerebral arteries are autonomic innervated. However, the role of sympathetic nervous system in the regulation of cerebral blood flow remains controversial. Given this, the purpose of the current study was to test the hypothesis that reflex‐mediated sympathetic activation via lower body negative pressure (LBNP) blunts NVC in humans.MethodsNVC was assessed using a visual stimulation protocol (5 cycles of 30 s eyes closed and 30 s of reading) in 10 young and healthy participants (3 women; aged 25 ± 3 years). In a randomized and counterbalanced order, NVC assessments were made under control conditions and during graded sympathetic activation via LBNP at −20 mmHg and −40 mmHg. Posterior (PCA) and middle cerebral artery (MCA) mean blood velocity (vmean) were determined (transcranial Doppler ultrasound). Vertebral artery blood flow (VAflow) was measured using duplex Doppler ultrasound and vessel wall tracking software. Mean arterial pressure (finger photoplethysmography), stroke volume (Modelflow), heart rate (electrocardiogram) and the partial pressure of end‐tidal carbon dioxide (PetCO2; capnograph) were obtained. Data are presented as mean ± SD.ResultsLBNP to −20 mmHg and −40 mmHg evoked an anticipated reduction in stroke volume and increase in heart rate, while mean arterial pressure was unchanged. Prior to visual stimulation, PCAvmean and MCAvmean were not different between control, −20 LBNP and −40 LBNP conditions (P>0.05), while VAflow was reduced at −40 mmHg (P=0.02 vs. control). Under control conditions, the NVC test evoked a robust increase in PCAvmean (Δ22 ± 4%), a modest increase in MCAvmean (Δ10 ± 3%), and a moderate rise in VAflow (Δ14 ± 5%). The magnitude of these responses was unaffected by LBNP at both −20 mmHg and −40mmHg (PCAvmean Δ23 ± 4% and Δ23 ± 4%; MCAvmean Δ10 ± 1% and Δ11 ± 4%; VAflow Δ15 ± 3% and Δ16 ± 6%; P>0.05). PetCO2 decreased at −20 mmHg (37.0 ± 3.1 mmHg) and −40 mmHg (36.3 ± 3.1 mmHg) LBNP trials compared to control (40.2 ± 3.7mmHg; P=0.004).ConclusionIn summary, these findings indicate that reflex‐mediated sympathetic activation via LBNP does not blunt the NVC response in healthy humans.Support or Funding InformationFunding received from Coordination for the Improvement of Higher Education Personnel (Finance Code 001) (MS), the University of Auckland (JPF, JFRP) and the Health Research Council of New Zealand (JPF, JFRP).