S. Adler et al., Modulation of renal oxygen consumption by nitric oxide is impaired after development of congestive heart failure in dogs, J CARDIO PH, 37(3), 2001, pp. 301-309
Citations number
21
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
We investigated the role of nitric oxide (NO) in the modulation of renal O-
2 consumption in dogs with pacing-induced congestive heart failure (CHF). O
-2 consumption in the: renal cortex (C) and medulla (M) of normal dogs and
dogs with CHF was measured under control conditions and in the presence of
increasing concentrations of three stimulators of NO production, bradykinin
, ramiprilat, and amlodipine, or the NO donor S-nitroso-N-acetylpenicillami
ne (SNAP). Baseline O-2 consumption (nmol O-2/min per gram) was similar in
the CHF group (C: 637 +/- 65; M: 618 +/- 83) and the control group (C: 601
+/- 58, M: 534 +/- 55). In normal dogs, bradykinin (10(-4) M), ramiprilat (
10(-4) M), amlodipine (10(-5) M) and SNAP (10(-4) M) all significantly redu
ced O-2 consumption in the cortex (-31.5 +/- 3.5%, -33 +/- 2.5%, -28.4 +/-
4.9%, -49.3 +/- 3.1%) and medulla (-26.9 +/- 2.2%, -31.4 +/- 2.2%, -23.1 +/
- 1.3%, -48.3 +/- 4%). respectively. The responses to bradykinin, ramiprila
t and amlodipine were significantly attenuated in dogs with CHF (C: -22.2 /- 1.8%, -20.1 +/- 2.6%, -14.2 +/- 2.5%; M: -20.8 +/- 1.7%, -17.8 +/- 1.9%,
-15.6 +/- 2.6%, respectively: p < 0.05). The responses in dogs with CHF we
re not altered by NO synthase blockade with L-NAME (10(-4) M). In contrast,
in normal kidneys treatment with L-NAME significantly attenuated the respo
nse to all three stimuli of NO production. Responses to SNAP were not affec
ted either by CHF or L-NAME. These data indicate that the role of NO produc
tion in the modulation of tissue O-2 consumption in the kidney is impaired
after the development of pacing-induced heart failure in dogs.