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.
View Article and Find Full Text PDFImmersion 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.
View Article and Find Full Text PDFWe 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.
View Article and Find Full Text PDFTo 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.
View Article and Find Full Text PDFComp Biochem Physiol C Toxicol Pharmacol
March 2004
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.
View Article and Find Full Text PDFComp Biochem Physiol C Toxicol Pharmacol
August 2002
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.
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