Contribution of central versus sweat gland mechanisms to the seasonal change of sweating function in young sedentary males and females.

In summer and winter, young, sedentary male (N = 5) and female (N = 7) subjects were exposed to heat in a climate chamber in which ambient temperature (Ta) was raised continuously from 30 to 42°C at a rate of 0.1°C min(-1) at a relative humidity of 40%. Sweat rates (SR) were measured continuously on forearm, chest and forehead together with tympanic temperature (Tty), mean skin temperature (⁻Ts) and mean body temperature ⁻Tb. The rate of sweat expulsions (Fsw) was obtained as an indicator of central sudomotor activity. Tty and ⁻Tb were significantly lower during summer compared with winter in males; SR was not significantly different between summer and winter in males, but was significantly higher during summer in females; SR during winter was higher in males compared with females. The regression line relating Fsw to ⁻Tb shifted significantly from winter to summer in males and females, but the magnitude of the shift was not significantly different between the two subject groups. The regression line relating SR to Fsw was steepened significantly from winter to summer in males and females, and the change in the slope was significantly greater in females than in males. Females showed a lower slope in winter and a similar slope in summer compared to males. It was concluded that sweating function was improved during summer mediated by central sudomotor and sweat gland mechanisms in males and females, and, although the change of sweat gland function from winter to summer was greater in females as compared with males, the level of increased sweat gland function during summer was similar between the two subject groups.

Effects of immersion in water containing high concentrations of CO2 (CO2-water) at thermoneutral on thermoregulation and heart rate variability in humans.

Immersion in high concentrations of CO2 dissolved in freshwater (CO2-water) might induce peripheral vasodilatation in humans. In this study, we investigated whether such immersion could affect the autonomic nervous system in humans using spectral analysis of heart rate variability. Ten healthy men participated in this study. Tympanic temperature, cutaneous blood flow and electrocardiogram (ECG) were measured continuously during 20 min of immersion in CO2-water. The ECG was analyzed by spectral analysis of R-R intervals using the maximal entropy method. The decrease in tympanic temperature was significantly greater in CO2-water immersion than in freshwater immersion. Cutaneous blood flow at the immersed site was significantly increased with CO2-water immersion compared to freshwater. The high frequency component (HF: 0.15-0.40 Hz) was significantly higher in CO2-water immersion than in freshwater immersion, but the low frequency (LF: 0.04-0.15 Hz) /high frequency ratio (LF/HF ratio) was significantly lower in CO2-water immersion than in freshwater immersion. The present study contributes evidence supporting the hypothesis that CO2-water immersion activates parasympathetic nerve activity in humans.

Inhibition of angiotensin II- and endothelin-1-stimulated proliferation by selective MEK inhibitor in cultured rabbit gingival fibroblastsdagger.

We investigated the implication of extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) in the proliferation stimulated by angiotensin II (Ang II) and endothelin-1 (ET-1) in cultured rabbit gingival fibroblasts (CRGF). Ang II stimulated activation of ERK1/2 and the activation was inhibited by CV-11974, an AT1 antagonist, and saralasin, an AT1/AT2 antagonist, but not by PD123,319, an AT2 antagonist in the CRGF. Ang II-stimulated proliferation was inhibited by PD98059 or U0126, selective MEK inhibitors. Furthermore, ET-1 stimulated proliferation via G-protein-coupled ETA receptors, which were identified by Western blot analysis of membrane protein from the CRGF. ET-1 also stimulated activation of ERK1/2 and the activation was inhibited by BQ-123, an ETA inhibitor, and TAK044, an ETA/ETB inhibitor, but not by BQ-788, an ETB inhibitor. ET-1-stimulated proliferation was inhibited by PD98059 or U0126. These findings suggest that ERK1/2 play a role in the signaling process leading to proliferation stimulated by Ang II and ET-1 via G-protein-coupled receptors, AT1 and ETA in CRGF.

Effects of body posture on local sweating and sudomotor outflow as estimated using sweat expulsion.

To estimate the effects of changes in body posture on sudomotor function, sweat rates on the forearm, chest and thigh, tympanic temperature (Tty), and skin temperatures were recorded in an upright sitting and a supine position under a hot environment of 40 degrees C Ta and 40% relative humidity for 60 min. Sweat expulsions were identified on sweat rate curves and their rates (Fsw) were calculated. Tty was higher, and its initial fall was greater, in the supine position than in the sitting position. On the forearm and the chest, the regression line relating sweat rate to mean body temperature (Tmb) had a gentler slope in the supine position, whereas on the thigh, it showed a steeper slope. The regression line relating Fsw to Tmb had a steeper slope in the supine position than in the sitting position, suggesting that the gain in the mechanisms for central integration and rhythm-generation was enhanced in the supine position. The parameter of sweat rate divided by Fsw was lower on the forearm and the chest, whereas it was higher on the thigh in the supine position than in the sitting position, suggesting that sudomotor outflow was modified at the spinal cord in association with skin pressure. It was concluded that body posture affects sudomotor functions through both brain and spinal mechanisms.

Pharmacological properties of angiotensin II receptors in cultured rabbit gingival fibroblasts.

We demonstrated that angiotensin II (Ang II, 10-1000 nM) induced proliferation of cultured rabbit gingival fibroblasts in a concentration-dependent manner. The Ang II-induced proliferation was inhibited by CV-11974 (AT1 antagonist; 1 microM) and saralasin (AT1/AT2 antagonist; 1 microM), but not by PD123,319 (AT2 antagonist; 1 microM), suggesting that Ang II-induced proliferation was mediated via AT1 receptors present in and/or on gingival fibroblasts. The results of Western blot analysis indicated the presence of AT1 and AT2 receptors in/on the fibroblasts. In a subsequent radioligand binding assay, the binding of [3H]Ang II to the fibroblasts was specific and saturable with both high- and low-affinity sites. Competition binding experiments indicated that Ang II completely displaced [3H]Ang II binding, and CV-11974 and PD123,319 maximally displaced up to approximately 63% and 37% of the total binding, respectively. Ang II and CV-11974 completely displaced the [3H]DuP753 binding but PD123,319 did not, indicating a single population of binding site. These findings demonstrate that gingival fibroblasts contain both AT1 and AT2 receptor subtypes for Ang II, and support that Ang II stimulation of AT1 receptors results in proliferation of the fibroblasts.

Proliferative effects of angiotensin II and endothelin-1 on guinea pig gingival fibroblast cells in culture.

We investigated whether phenytoin (PHT) and nifedipine (NIF) induce angiotensin II (Ang II) and endothelin-1 (ET-1) generation by cultured gingival fibroblasts derived from guinea pigs and whether Ang II and ET-1 induce proliferation of these cells. Immunohistochemical experiments showed that PHT (250 nM) and NIF (250 nM) increased the immunostaining intensities of immunoreactive Ang II and ET-1 (IRET-1) in these cells. Captopril (3 microM), an angiotensin-converting enzyme inhibitor, reduced these enhanced intensities to control levels. Ang II (100 nM) enhanced the immunostaining intensity of IRET-1. PHT (250 nM) and NIF (250 nM)-induced cell proliferation. Both PHT- and NIF-induced proliferation was inhibited by captopril (3 microM). Ang II (100 nM) and ET-1 (100 nM) also induced cell proliferation. Ang II-induced proliferation was inhibited by CV11974 (1 microM), an AT(1) receptor antagonist and saralasin (1 microM), an AT(1)/AT(2) receptor antagonist, but not by PD123,319 (1 microM), an AT(2) receptor antagonist. ET-1-induced proliferation was inhibited by BQ123 (10 microM), an ET(A) receptor antagonist, but not by BQ788 (1 microM), an ET(B) receptor antagonist. These findings suggest that PHT- and NIF-induced gingival fibroblast proliferation is mediated indirectly through the induction of Ang II and ET-1 and probably mediated through AT(1) and ET(A) receptors present in or on gingival fibroblasts.