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Mechanisms underlying the cardiovascular responses to cooling
Author(s) -
Tung Che-Se,
Yang Chien-Fan,
Liu Yia-Ping,
Chang Shang-Tang,
Huang Chuen-Lin
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.891.1
Subject(s) - hexamethonium , nitric oxide , medicine , chemistry , endocrinology , blockade , heart rate , vasodilation , vasoconstriction , antagonist , blood pressure , stimulation , anesthesia , receptor
We investigated the mechanisms of hunting response, i.e. cold‐evoked vasoconstriction (CEC) and latter vasodilatation (CED) at the lowest temperatures. Rats were immersed soles in a cage containing 2 cm iced water (4±2°C) for 10 min and then the responses through cooling (C) were monitored by changes of blood pressure and heart rate with variability in frequency domain: very low (VLF), low (LF) and high (HF). Firstly, we tested the brain dopamine‐β hydroxylase (DBH) mechanisms. Rats were given lateral ventricularly (icv) DBH‐shRNA to knock‐down DBH. Secondly, we tested the origins of CED. Rats with or without given tail‐venously (iv) a ganglion blockade, Hexamethonium (H, 10 mg/kg), were then given centrally (1 mg/h, icv) or peripherally (30 mg/kg, iv) an antagonist of nitric oxide (NO) production (L‐NAME). The results indicate (1) C causes significant CEC followed by CED; CED correlates highly with the falling of VLF, (2) icv DBH‐shRNA is dominant in attenuating CEC and CED, (3) both iv and icv L‐NAME cause reversal of the CED‐VLF changes, (4) H alone attenuates CEC but not CED; H plus iv L‐NAME attenuate the effects of iv L‐NAME on CED‐VLF changes. We conclude that brain DBH may participate in mechanisms of autonomic cardiovascular responses to C, and CED is due to both central and peripheral increased NO production. Grant in aid: National Defense Medical Center (DOD‐100‐I‐17) and Cardinal Tien Hospital (CTH‐100‐1‐2A04)