Our results suggest that during the first trimester of normal pregnancy, active renin concentration in the plasma is increased and that renin is not the factor that limits angiotensin II synthesis. These results also confirm decreased activity of the renin-angiotensin-aldosterone system in preeclampsia. This could contribute to the diminished hemodynamic control observed in pregnant women developing preeclampsia.

Unlike diazepam, lorazepam has repeatedly been shown to impair perceptual priming as well as explicit memory. To determine whether this deleterious effect was due to an impairment in acquisition of information, 60 healthy volunteers were randomly assigned to five treatment groups (placebo, lorazepam 0.026 or 0.038 mg/kg, diazepam 0.2 or 0.3 mg/kg) and successively performed perceptual priming tasks and a free-recall task. Priming performance on information learned before or 2 h after drug administration, i.e. at the peak concentration of lorazepam, was assessed under the influence of the drugs, using a picture-fragment and a word-stem completion task. Free-recall performance was altered by both drugs. Lorazepam decreased priming performance when information was acquired after, but not before, drug administration, indicating that the drug alters the acquisition of information. Lorazepam also impaired the ability to identify fragmented pictures, but there was no evidence that this perceptual effect accounts for the priming impairment. Surprisingly, diazepam also decreased priming when information was acquired after drug administration, suggesting that, at least in certain circumstances, the two benzodiazepines may exert similar effects on priming measures.

Renin (RA) and angiotensin-converting enzyme (ACE) activities and angiotensinogen, ANG I, and ANG II levels were measured in the kidney (cortex and medulla) and plasma of Wistar-Kyoto rats on a low-sodium (LS; 0.025% NaCl; n = 8), normal-sodium (NS; 1% NaCl; n = 7), or high-sodium (HS; 8% NaCl; n = 7) diet for 21 days. RA, ANG I, and ANG II levels increased in a manner inversely related to sodium content of the diet in both plasma and renal tissues. The LS diet resulted in a 16-, 2.8-, and 1.8-fold increase in plasma RA, ANG I, and ANG II levels, respectively, compared with those in HS rats. In the renal cortex and medulla, RA, ANG I, and ANG II levels were also increased by diminution of dietary salt content but, in contrast to plasma, ANG II levels increased much more than RA or ANG I levels [5.4 (cortex)- and 4.7 (medulla)-fold compared with HS rats]. In summary, we demonstrated variations of ANG II levels in the kidney during dietary salt modifications. Our results confirm that RA and ACE activity are not the steps limiting intrarenal ANG II levels. Nevertheless, despite RA and ACE activity differences between renal cortex and medulla, ANG I and ANG II levels are equivalent in these two tissues; these results argue against a compartmentalization of RAS in these two intrarenal areas.

No abstract

This study was designed to determine the involvement of AT(1) receptors in the uptake of ANG II in the kidney of rats exposed to differing salt intake. Male Wistar-Kyoto rats were treated with a normal-salt (NS; 1% NaCl, n = 7) or a low-salt (LS; 0.025% NaCl, n = 7) diet combined with (LS+Los, n = 7; NS+Los, n = 7) or without losartan (30 mg. kg(-1). day(-1)), an AT(1) receptor antagonist. Renin (RA) and angiotensin-converting enzyme (ACE) activities and angiotensinogen, ANG I, and ANG II levels were measured in plasma, renal cortex, and medulla. In LS rats, in both plasma and renal cortex, the increase in RA was associated with an increase in ANG I and ANG II levels compared with NS rats, but intrarenal ANG II levels increased more than ANG I levels. In NS+Los rats, the increase in RA in plasma was followed by a marked increase in plasma ANG I and ANG II levels compared with NS rats whereas in the kidney the increase of renal RA was followed by a decrease of the levels of these peptides. The same pattern was observed in LS+Los rats, but the decrease in renal ANG II levels was much more pronounced in LS+Los rats than in NS+Los rats. Our results suggest that the increase in renal ANG II levels after salt restriction results mainly from an uptake of ANG II, via AT(1) receptors. Such elevated intrarenal ANG II levels could contribute to maintain sodium and fluid balance and arterial blood pressure during salt-deficiency states.