No abstract

Pulsed emissive probe techniques have been used to determine the plasma potential distribution of high power impulse magnetron sputtering (HiPIMS) discharges. An unbalanced magnetron with a niobium target in argon was investigated for pulse length of 100 µs at a pulse repetition rate of 100 Hz, giving a peak current of 170 A. The probe data were taken with a time resolution of 20 ns and a spatial resolution of 1 mm. It is shown that the local plasma potential varies greatly in space and time. The lowest potential was found over the target's racetrack, gradually reaching anode potential (ground) several centimeters away from the target. The magnetic pre-sheath exhibits a funnel-shaped plasma potential resulting in an electric field which accelerates ions toward the racetrack. In certain regions and times, the potential exhibits weak local maxima which allow for ion acceleration to the substrate. Knowledge of the local E and static B fields lets us derive the electrons' E × B drift velocity, which is about 10 5 m/s and shows structures in space and time.

A chymase (also referred to as angiotensin I-convertase) specific for the conversion of angiotensin (Ang) I to Ang II has been identified in human heart. This serine protease is also present in dog and marmoset vasculature. We examined the vasoconstrictor effects of Ang II putatively generated from an angiotensin-converting enzyme (ACE)-resistant convertase synthetic substrate (SUB) in vivo and in vitro. In marmosets, SUB (7 to 700 /ig/kg IV) or Ang I (0.1 to 30 /ig/kg) caused similar dose-dependent increases in mean arterial pressure (10 to 100 mm Hg) and decreases in heart rate. Pressor effects of SUB were slightly attenuated at low (but not high) doses by captopril (CAP, 1 mg/kg IV) and blocked by losartan (5 mg/kg IV); in contrast Ang I pressor effects were substantially blocked by both. In isolated canine superior mesenteric artery, Ang I-induced contraction was

The anterior ventral region of the third ventricle (AV3V) is a major central site in the regulation of cardiovascular and renal function. To examine the role of the central nervous system in the regulation of atrial natriuretic peptide (ANP) secretion, the effect of lesions in this region on basal, volume-stimulated, and osmotic-stimulated plasma ANP was determined. Basal levels of plasma ANP were not different in sham- and AV3V-lesioned rats. Volume expansion with a continuous infusion of saline or with a bolus administration of saline increased plasma ANP in sham-lesioned rats. In AV3V-lesioned rats, continuous infusion of saline had no effect on plasma ANP, and a bolus administration of saline decreased plasma ANP. Osmotic stimulation with hypertonic saline increased plasma ANP in sham-lesioned rats but had no effect on plasma ANP in AV3V-lesioned rats. These results suggest that the central nervous system is involved in the regulation of ANP secretion and that altered ANP regulation may contribute to the cardiovascular and renal deficiencies in AV3V-lesioned rats.