The primary brain sites responsible for angiotensin-induced pressor action and dipsogenicity in the laboratory rat appear to be located in forebrain circumventricular organs (CVO). Because CVOs have a reduced blood-brain barrier, intracarotid infusion of angiotensin via a brachial arterial catheter results in direct stimulation of these sites. This investigation determined that brachial arterial infusion of angiotensin II (ANG II) into alert free-moving rats resulted in pressor and dipsogenic responses greater than those observed with equivalent doses of angiotensin III (ANG III). However, intracerebroventricular (ICV) injections of ANG II and ANG III yielded equivalent pressor and drinking responses. ICV pretreatment with the specific angiotensin receptor antagonist [Sar1, Ile8]-ANG II significantly reduced ANG II- and ANG III-induced pressor and drinking responses. This inhibition lasted approximately 20 min with recovery at 60-70 min. The results indicate that ICV-administered ANG III is a much more potent ligand than previously determined if the stickiness due to electrical charge of this compound is prevented by appropriate treatment of glassware. The receptor antagonist results encourage the possibility that ANG II and ANG III activate a common central receptor site.

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Significant plasma elevations of the powerful vasoconstrictor angiotensin II (AII) were measured in rats following exposure to either 100-dB or 20-dB SPL white noise in three environmental temperatures (5 degrees 21 degrees, and 38 degrees C). Loud noise exposure in the normal temperature condition (21 degrees C) and both temperature extremes with soft noise exposure resulted in plasma AII elevations. The two extreme temperatures combined with loud noise exposure resulted in plasma AII concentrations not different from the levels observed following 20-dB noise at normal temperature. These results indicate that separately administered noise and temperature extremes stimulate the production of AII and thus vasoconstriction. Simultaneous exposure to multiple stressors including noise and temperature extremes may result in severely elevated plasma catecholamines and reduce renal responsiveness to beta-adrenergic stimulation thus reducing plasma AII levels.

Thalidomide had no adverse effects on mating and fertility in male and female rabbits dosed up to 500 and 100 mg/kg/day, respectively, for 14 days prior to mating. After 56 day of dosing, histopathologic changes with no associated sperm abnormalities were observed in the testicles. Embryonic development NOAEL for treated females mated to untreated males was <10 mg/kg. Corresponding fertility NOAEL for treated males mated to untreated females was 500 mg/kg.