Jd. Symons et al., Regional blood flow responses to acute ANG II infusion: Effects of nitric oxide synthase inhibition, J CARDIO PH, 34(1), 1999, pp. 116-123
Citations number
27
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
We hypothesized that nitric oxide (NO) opposes regional vasoconstriction ca
used by acute angiotensin II (ANG II) infusion in conscious rats. Mean arte
rial pressure (MAP), blood flow, and vascular conductance (regional blood f
low/ MAP: ml/min/100 g/mm Hg) were measured and/or calculated before and at
2 min of ANG II infusion (0.05 or 1 mu g/kg/min, i.a.) in the absence and
presence of NO synthase (NOS) inhibition [N-G-nitro-L-arginine methyl eater
(L-NAME), 0.25 or 1 mg/kg, i.a.]. ANG II reduced stomach and hindlimb cond
uctance only after NOS inhibition. For example, whereas 0.05 mu g/kg/min AN
G II did not attenuate conductance in the stomach (i.e., 1.04 +/- 0.08 to 0
.93 +/- 0.12 ml/min/100 g/mm Hg), this variable was reduced (i.e., 0.57 +/-
0.14 to 0.34 +/- 0.05 ml/min/ 100 g/mm Hg; p < 0.05) when ANG II was infus
ed after 0.25 mg/kg L-NAME. In addition, whereas hindlimb conductance was s
imilar before and after administering 1 mu g/kg/min ANG II (i.e., 0.13 +/-
0.01 and 0.09 +/- 0.02, respectively), this variable was reduced (i.e., 0.0
7 +/- 0.01 and 0.02 +/- 0.00, respectively; p < 0.05) when ANG II was infus
ed after 1 mg/kg L-NAME. These findings indicate that NO opposes ANG II-ind
uced vasoconstriction in the stomach and hindlimb. In contrast, whereas bot
h doses of ANG II decreased (p < 0.05) vascular conductance in the kidneys
and small and large intestine regardless of whether NOS inhibition was pres
ent, absolute vascular conductance was lower (p < 0.05) after L-NAME. For e
xample, 1 mu g/kg ANG II reduced renal conductance from 3.34 +/- 0.31 to 1.
22 +/- 0.14 (p < 0.05). After 1 mg/kg L-NAME, renal conductance decreased f
rom 1.39 +/- 0.18 to 0.72 +/- 0.16 (p < 0.05) during ANG II administration.
Therefore the constrictor effects of NOS inhibition and ANG Ii are additiv
e in these circulations. Taken together, our results indicate that the abil
ity of NO to oppose ANG II-induced constriction is not homogeneous among re
gional circulations.