Spectral analysis measured in cooling‐evoked hemodynamic perturbations of rats indicates endogenous nitric oxide facilitating sympathomyogenic oscillations

Rapid cooling stress (CS) elicits hemodynamic perturbations (CEHP). We previously reported that CEHP is highly relevant to the sympathetic activation and nitric oxide (NO) production. This study identifies the role of NO in CEHP. Conscious rats were pretreated with the NO‐synthase inhibitor (L‐NAME) alone or superimposition of sympatholytic interventions using hexamethonium (HEX) or guanethidine (GUA), and then subjected to a CS trial. Cardiovascular indices were monitored via an implanted telemetric device throughout experimental protocol. The analyses included measurements of blood pressure (BP); heart rate (HR); the variability of BP and HR (BPV, HRV); spectral powers and coherence linkage at very‐low, low, and high frequency regions (VLF: 0.02–0.2 Hz, LF: 0.2–0.6 Hz, and HF: 0.6–3.0 Hz); and dicrotic notch (Dn). When compared with control vehicle under CS, the L‐NAME alone (a) increased BP, Dn, VLF BPV , VLF HRV , LF HRV , and HF HRV but decreased HR, HF BPV , and LF/HF ratio; (b) converted negative correlation into positive correlation for LF pair (LF HRV /LF BPV ) and VLF pair (VLF HRV /VLF BPV ); and (c) enhanced the coherence linkage between BPV and HRV at the LF region but weakened them at the HF region. We also noted divergent patterns of spectra responsiveness to HEX or GUA superimposed on L‐NAME. The effects of HEX+L‐NAME versus GUA+L‐NAME, particularly on LF and VLF between BPV and HRV, indicated an essential role for a functional adrenal medulla to release epinephrine under CS. Our results indicate that endogenous NO play an inhibitory role on the sympathovascular activation and subsequently the myogenic vascular oscillations in CEHP. Support or Funding Information Grant in aid: the Ministry of Science and Technology (MOST 102 &103‐2320‐B‐350‐001) and the National Defense Medical Center (MAB101‐40; MAB‐102‐81), Taiwan, R.O.C.