Hw. Liu et al., BRAIN ANG-II AND PROSTAGLANDINS MEDIATE THE PRESSOR-RESPONSE AFTER CENTRAL BLOCKADE OF NITRIC-OXIDE SYNTHASE, Brain research, 785(2), 1998, pp. 317-328
Central inhibition of nitric oxide synthase (NOS) by intracerebroventr
icular (i.c.v.) administration of N-G-nitro-L-arginine methyl ester (L
-NAME; 150 mu g/5 mu l) to conscious rats produced a biphasic presser
response characterized by an initial transient increase within 5 min,
and a delayed response starting between 60-90 min. The effect was ster
eospecific, as D-NAME (250 mu g/5 mu l) did not modify the resting art
erial blood pressure, nor did L-arginine (323 mu g/5 mu l, i.c.v.), in
dicating the substrate for NOS is not rate-limiting. Intracerebroventr
icular pretreatment with losartan (25 mu g/5 mu l), a non-peptide anta
gonist of the angiotensin II AT(1) receptor subtype, or indomethacin (
100 mu g/5 mu l), a blocker of cyclooxygenase, however, prevented the
initial increase in blood pressure without affecting the delayed press
er response. In contrast, neither intravenous losartan (10 mg/kg b.wt)
nor prazosin, an alpha(1) adrenergic receptor antagonist, at doses of
5 mu g/5 mu l (i.c.v.) or 0.3 mg/kg b.wt (i.v.) were effective in alt
ering the presser responses. These results indicate that centrally pro
duced NO maintains the resting arterial blood pressure at least partia
lly through modulation of the brain angiotensin system and prostagland
ins. (C) 1998 Elsevier Science B.V.