Modulation of renal oxygen consumption by nitric oxide is impaired after development of congestive heart failure in dogs

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-acetylpenicillamine (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 reduced 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, ramiprilat 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 were not altered by NO synthase blockade with L-NAME (10(-4) M). In contrast, in normal kidneys treatment with L-NAME significantly attenuated the response to all three stimuli of NO production. Responses to SNAP were not affected either by CHF or L-NAME. These data indicate that the role of NO production in the modulation of tissue O-2 consumption in the kidney is impaired after the development of pacing-induced heart failure in dogs.