Skin sympathetic nerve activity component synchronized with cardiac cycle is involved in hyperosmotic suppression of cutaneous vasodilation in hyperthermia

Abstract

Recently, we have reported that a component of the SSNA spike synchronized with the cardiac cycle increased with an increase in esophageal temperature (Tes) and the increase was suppressed by hypovolemia with suppressed cutaneous vasodilation, suggesting that the component was an active vasodilator signal for skin vessels. Since cutaneous vasodilation in hyperthermia is also suppressed by hyperosmolality, in the present study, we hypothesized that this component was suppressed by hyperosmolality. Accordingly, skin sympathetic nerve activity (SSNA; microneurography) from the peroneal nerve, laser‐Doppler blood flow (LDF) on the ipsilateral dorsal foot, mean arterial pressure (MAP; sonometry), and Tes were measured before and during 45‐min of passive warming in 17 healthy males in isosmolality (IG, n=10) and hyperosmolality (HG, n=7) groups. In HG, hyperosmolality by ~7mOsm·kgH2O−1 was attained by hypertonic saline infusion after an administration of diuretic to adjust blood volume similar to that in IG. Although the SSNA component increased with an increase in Tes by ~0.5°C by the end of warming in both groups, the increase was significantly lower in HG than IG (P<0.0001), accompanied by a less increase in cutaneous vascular conductance (CVC=LDF/MAP) in HG than IG (P<0.0001). These results support our idea that the component might be an active cutaneous vasodilator signal.