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

Abstract

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 degrees C (heat stress; HT) or 34.5 degrees 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 approximately 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 degrees C) than in HT-NOSM (0.30 +/- 0.07 degrees 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.

The effect of plasma osmolality and baroreceptor loading status on postexercise heat loss responses

“…However, it is well established that recovery from exercise is associated with a state of hyperosmolality (and therefore, activation of osmoreceptors) (4) and that hyperosmolality negatively influences sweating during passive heat stress (2,16,24,31,36) and exercise (8). A novel extension in the current study is that an increase in plasma osmolality of ϳ12 mmol/kg of solvent above baseline levels attenuated upper back sweat rate by ϳ25% by end-exercise relative to natural recovery (a plasma osmolality increase of only ϳ6 mmol/kg of solvent), and this suppression persisted into the 60-min recovery despite core temperature elevations of Ն0.9°C above baseline.…”

“…Moreover, hypovolemia simulated with lower body negative pressure (LBNP) application during passive heat stress can independently delay the onset threshold for cutaneous vasodilation, with no effect on sweating (24). Hypovolemia that is induced via reductions in blood volume during exercise (i.e., through profuse sweating) can reduce the thermosensitivity of sweating (7), as well as peak forearm blood flow (8, 28).To our knowledge, only two studies have assessed the combined effects of hyperosmolality and hypovolemia on the heat loss responses, and these have been limited to passive heat stress (16,24). Examining solely the skin blood flow response, Ito et al (16) demonstrated greater reductions in forearm vascular conductance when graded levels of LBNP were applied in a hyperosmotic state compared with an isosmotic state.…”

“…To our knowledge, only two studies have assessed the combined effects of hyperosmolality and hypovolemia on the heat loss responses, and these have been limited to passive heat stress (16,24). Examining solely the skin blood flow response, Ito et al (16) demonstrated greater reductions in forearm vascular conductance when graded levels of LBNP were applied in a hyperosmotic state compared with an isosmotic state.…”

Osmotic Stress-induced Phosphorylation of H2AX by Polo-like Kinase 3 Affects Cell Cycle Progression in Human Corneal Epithelial Cells

“…Changes of the extracellular osmotic pressure are often found in some pathologic conditions, such as diabetes mellitus, uremia, dehydration after exercise, heat shock, fatal burns, and inflammation sites in various tissues including the cornea (1)(2)(3)(4). It has been shown that persistent hyperosmotic stress can induce DNA damage, cell cycle arrest, and apoptosis (5,6).…”

Non-thermal modification of heat-loss responses during exercise in humans

“…Recently, it is reported that the elevation of core temperature threshold for cutaneous vasodilation with plasma hyperosmolality is due primarily to elevation of the threshold for onset of active vasodilation (Shibasaki et al 2009a, b). In addition, it seems that the reduction of peripheral vascular conductance in response to lower body negative pressure, which induces baroreceptors unloading, was enhanced by plasma hyperosmolality during heat stress (Ito et al 2005), suggesting that this interactive effect could contribute effectively to maintenance of arterial pressure during heat stress in thermal dehydration.…”