Effects of external magnetic filter on behaviors of fast primary electrons in a volume negative ion source.
The relationship between enhancement of hydrogen negative ion H(-), volume production, and behaviors of fast primary electrons is studied theoretically. Trajectories of fast primary electrons are calculated, including collisional effects with hydrogen molecules. Active region of fast electrons depends strongly on the field intensity of the magnetic filter (MF), B(MF), and filament position. Therefore, spatial distributions of ionization and vibrational excitation collision points are also affected with changing B(MF). Although number of vibrational excitation collision points is much smaller than that of ionization collision points due to different mean free path, the relative intensity is varied by changing energy of fast electrons. According to the results and discussions including transport of produced vibrationally excited molecules, for enhancement of H(-) production, it is desired that fast electrons should approach the MF position and move into the downstream region as deep as possible without destruction of H(-) ions. To realize these conditions, good combination between filament position and the intensity of the MF should be required.
Modelling of negative ion transport in caesium-seeded volume negative ion sources
Trajectories of H− ions are calculated numerically by solving the 3D motion equation, including effects of collisional destruction, elastic collisions and charge exchange collisions. According to these trajectories, the extraction probability of H− ions produced at any location inside the source and the energy relaxation of extracted H− ions are estimated as a function of gas pressure. Effects of production zone and field intensity of the magnetic filter on extraction probability are also discussed. The extraction probability of surface produced H− ions is much higher than that of volume produced H− ions. The kinetic energy of extracted H− ions is reduced mainly by charge exchange collisions with H in higher pressure region and by elastic collisions with H+ in lower pressure region. We also briefly discuss the pressure dependence of extracted negative ion currents combining the present numerical results and the results of the model calculation with the zero-dimensional code.
The bradykinin B1 receptor and the central regulation of blood pressure in spontaneously hypertensive rats
We evaluated if the brain bradykinin (BK) B1 receptor is involved in the regulation of blood pressure (BP) in conscious rats. Basal mean BP and HR were 115±2 and 165±3 mmHg and 345±10 and 410±14 beats min−1 in Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR), respectively. Intracerebroventricular (i.c.v.) injection of 1 nmol B1 receptor agonist Lys‐desArg9‐BK significantly increased the BP of WKY and SHR by 7±1 and 19±2 mmHg, respectively. One nmol Sar[D‐Phe8]‐desArg9‐BK, a kininase‐resistant B1 agonist, increased the BP of WKY and SHR by 19±2 and 17±2 mmHg, respectively and reduced HR in both strains. I.c.v. injection of 0.01 nmol B1 antagonists, LysLeu8‐desArg9‐BK or AcLys[D‐βNal7,Ile8]‐desArg9‐BK (R715), significantly decreased mean BP in SHR (by 9±2 mmHg the former and 14±3 mmHg the latter compound), but not in WKY. In SHR, the BP response to R715 was associated to tachycardia. I.c.v. Captopril, a kininase inhibitor, increased the BP of SHR, this response being partially prevented by i.c.v. R715 and reversed into a vasodepressor effect by R715 in combination with the B2 antagonist Icatibant. I.c.v. antisense oligodeoxynucleotides (ODNs) targeted to the B1 receptor mRNA decreased BP in SHR, but not in WKY. HR was not altered in either strain. Distribution of fluorescein‐conjugated ODNs was detected in brain areas surrounding cerebral ventricles. Our results indicate that the brain B1 receptor participates in the regulation of BP. Activation of the B1 receptor by kinin metabolites could participate in the pathogenesis of hypertension in SHR.