Spectra of W39+^{39+}-W47+^{47+} in the 12 nm to 20 nm region observed with an EBIT light source

We observed spectra of highly ionized tungsten in the extreme ultraviolet with an electron beam ion trap (EBIT) and a grazing incidence spectrometer at the National Institute of Standards and Technology. Stages of ionization were distinguished by varying the energy of the electron beam between 2.1 keV and 4.3 keV and correlating the energies with spectral line emergence. The spectra were calibrated by reference lines of highly ionized iron produced in the EBIT. Identification of the observed lines was aided by collisional-radiative modeling of the EBIT plasma. Good quantitative agreement was obtained between the modeling results and the experimental observations. Our line identifications complement recent results for W$^{40+}$-W$^{45+}$ observed in a tokamak plasma by P\"{u}tterich {\it et al} (\jpb {\bf 38}, 3071, 2005). For most lines we agree with their assignment of ionization stage. Additionally, we present new identifications for some allowed and forbidden lines of W$^{39+}$, W$^{44+}$, W$^{46+}$, and W$^{47+}$. The uncertainties of our wavelengths range from 0.002 nm to 0.010 nm.Comment: 19 pages, 8 figure

Angiotensin AT1 receptor-mediated excitation of rat carotid body chemoreceptor afferent activity

A high density of angiotensin II receptors was observed in the rat carotid body by in vitro autoradiography employing 125I-[Sar1,Ile8]-angiotensin II as radioligand. Displacement studies demonstrated that the receptors were of the AT1 subtype.The binding pattern indicated that the AT1 receptors occurred over clumps of glomus cells, the principal chemoreceptor cell of the carotid body. Selective lesions of the sympathetic or afferent innervation of the carotid body had little effect on the density of receptor binding, demonstrating that the majority of AT1 receptors were intrinsic to the glomus cells.To determine the direct effect of angiotensin II on chemoreceptor function, without the confounding effects of the vasoconstrictor action of angiotensin II, carotid sinus nerve activity was recorded from the isolated carotid body in vitro. The carotid body was superfused with Tyrode solution saturated with carbogen (95% O2, 5% CO2), maintained at 36 °C, and multi-unit nerve activity recorded with a suction electrode.Angiotensin II elicited a dose-dependent excitation of carotid sinus nerve activity (maximum increase of 36 ± 11% with 10 nm angiotensin II) with a threshold concentration of 1 nm. The response was blocked by the addition of an AT1 receptor antagonist, losartan (1 μm), but not by the addition of an AT2 receptor antagonist, PD123319 (1 μm).In approximately 50% of experiments the excitation was preceded by an inhibition of activity (maximum decrease of 24 ± 8% with 10 nm angiotensin II). This inhibitory response was markedly attenuated by losartan but not affected by PD123319.These observations demonstrate that angiotensin II, acting through AT1 receptors located on glomus cells in the carotid body, can directly alter carotid chemoreceptor afferent activity. This provides a means whereby humoral information about fluid and electrolyte homeostasis might influence control of cardiorespiratory function