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ORIGINAL ARTICLE
Year : 2020  |  Volume : 63  |  Issue : 2  |  Page : 53-59

Portal vein innervation underlying the pressor effect of water ingestion with and without cold stress


1 Department of Emergency Medicine, National Defense Medical Center, Tri-service General Hospital, Taipei, Taiwan
2 Department of Rehabilitation, Cheng Hsin General Hospital, Taipei, Taiwan
3 Division of Medical Research and Education, Cheng Hsin General Hospital, Taipei, Taiwan
4 Department of Psychiatry, Cheng Hsin General Hospital, Taipei, Taiwan

Correspondence Address:
Dr. Che-Se Tung
Division of Medical Research and Education, Cheng Hsin General Hospital, No. 45, Cheng Hsin Street, Beitou, Taipei 11280
Taiwan
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Source of Support: This work was supported by grants from the Ministry of Science and Technology (MOST 103.2320.B.350.001) and the Cheng Hsin General Hospital.National Defense Medical Center cooperative research project (CH.NDMC.108.30 and 109.16), Taipei, Taiwan, ROC., Conflict of Interest: None


DOI: 10.4103/CJP.CJP_96_19

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Water-induced pressor response appears mediated through the activation of transient receptor potential channel TRPV4 on hepatic portal circulation in animals. We sought to elucidate the mechanism of portal vein signaling in this response. Forty-five rats were divided into four groups: control rats without water ingestion (WI), control rats with WI, portal vein denervation rats with WI (PVDWI), and TRPV4 antagonist-treated rats with WI (anti-TRPV4WI). Cardiovascular responses were monitored throughout the experiments. Data analysis was performed using descriptive methods and spectral and cross-spectral analysis of blood pressure variability (BPV) and heart rate variability (HRV). Key results showed that at baseline (PreCS) before cold stress trial (CS), WI elicited robust pressor and tachycardia responses accompanied by spectral power changes, in particular, increases of low-frequency BPV (LFBPV) and very-LFBPV (VLFBPV), but decrease of very-low-frequency HRV. PVDWI, likewise, elicited pressor and tachycardia responses accompanied by increases of high-frequency BPV, high-frequency HRV, LFBPV, low-frequency HRV, and VLFBPV. When compared with WI at PreCS, WI at CS elicited pressor and tachycardia responses accompanied by increases of high-frequency BPV, LFBPV, and VLFBPV, whereas in WI, the CS-evoked pressor response and the accompanied LFBPV and VLFBPV increases were all tended augmented by PVDWI. When compared with WI and PVDWI at both PreCS and CS, however, anti-TRPV4WI attenuated their pressor responses and attenuated their increased LFBPV, VLFBPV, and very-low-frequency HRV. The results indicate that the portal vein innervation is critical for a buffering mechanism in splanchnic sympathetic activation and water-induced pressor response.


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