Plasma hyperosmolality augments peripheral vascular response to baroreceptor unloading during heat stress

• Published in: American journal of physiology. Regulatory, integrative and comparative physiology Vol. 289; no. 2; pp. R432 - R440
• Main Authors: Ito, Tomoyuki, Itoh, Toshiyuki, Hayano, Takashi, Yamauchi, Katsuya, Takamata, Akira
• Format: Journal Article
• Language: English
• Published: United States 01.08.2005
• Subjects: Adult; Arginine Vasopressin - blood; Blood - metabolism; Blood Vessels - physiopathology; Forearm - blood supply; Heat Stress Disorders - physiopathology; Hemodynamics; Hormones - blood; Humans; Hypovolemia - physiopathology; Lower Body Negative Pressure; Male; Osmolar Concentration; Pressoreceptors - physiopathology; Saline Solution, Hypertonic - pharmacology
• ISSN: 0363-6119; 1522-1490
• DOI: 10.1152/ajpregu.00027.2004

Departments of 1 Physiology and 2 Pediatrics, Kyoto Prefectural University of Medicine, Kamigyo-ku, Kyoto; 3 Department of Rehabilitation Medicine, Hamamatsu University School of Medicine, Hamamatsu; and 4 Department of Environmental Health, Nara Women's University, Nara, Japan Submitted 14 January 2004 ; accepted in final form 13 April 2005 The aim of this study was to elucidate the interactive effect of central hypovolemia and plasma hyperosmolality on regulation of peripheral vascular response and AVP secretion during heat stress. Seven male subjects were infused with either isotonic (0.9%; NOSM) or hypertonic (3.0%; HOSM) NaCl solution and then heated by perfusing 42°C (heat stress; HT) or 34.5°C water (normothermia; NT) through water perfusion suits. Sixty minutes later, subjects were exposed to progressive lower body negative pressure (LBNP) to –40 mmHg. Plasma osmolality (P osmol ) increased by 11 mosmol/kgH 2 O in HOSM conditions. The increase in esophageal temperature before LBNP was much larger in HT-HOSM (0.90 ± 0.09°C) than in HT-NOSM (0.30 ± 0.07°C) ( P < 0.01) because of osmotic inhibition of thermoregulation. During LBNP, mean arterial pressure was well maintained, and changes in thoracic impedance and stroke volume were similar in all conditions. Forearm vascular conductance (FVC) before application of LBNP was higher in HT than in NT conditions ( P < 0.001) and was not influenced by P osmol within the thermal conditions. The reduction in FVC at –40 mmHg in HT-HOSM (–9.99 ± 0.96 units; 58.8 ± 4.1%) was significantly larger than in HT-NOSM (–6.02 ± 1.23 units; 44.7 ± 8.1%) ( P < 0.05), whereas the FVC response was not different between NT-NOSM and NT-HOSM. Plasma AVP response to LBNP did not interact with P osmol in either NT or HT conditions. These data indicate that there apparently exists an interactive effect of P osmol and central hypovolemia on the peripheral vascular response during heat stress, or peripheral vasodilated conditions, but not in normothermia. plasma osmolality; baroreflexes; forearm vascular conductance; lower body negative pressure; arginine vasopressin Address for reprint requests and other correspondence: A. Takamata, Environmental Physiology Laboratory, Dept. of Environmental Health, Nara Women's Univ., Kitauoya Niashimachi, Nara 630-8506, Japan (E-mail: takamata{at}cc.nara-wu.ac.jp )