Role of kinins in the control of renal papillary blood flow, pressure natriuresis, and arterial pressure

The present study evaluated the effects of blocking kinins with the bradyki nin B-2 receptor antagonist Hoe140 on the relationship between renal perfus ion pressure, papillary blood flow (PBF), and sodium excretion. To determin e the relevance of renal kinins in the long-term control of arterial pressu re, the effect of a chronic intrarenal infusion of Hoe140 on arterial press ure and sodium balance was also studied. PBF was not autoregulated in volum e-expanded rats, and the administration of Hoe140 reduced PBF (-30%) and im proved PBF autoregulation. The kinin antagonist also decreased sodium excre tion (-35%) and blunted pressure natriuresis with no whole-kidney renal hem odynamic changes. These effects may be mediated through nitric oxide (NO), because in rats pretreated with N-G-nitro-L-arginine methyl ester, Hoe140 h ad no additional effects on PBF or pressure natriuresis, A role for NO in m ediating the renal response to Hoe140 is also supported by the finding that Hoe140 reduced basal urinary NO3-/NO2- excretion (-33%), and it blunted th e arterial pressure-induced increase in NO3-/NO2- excretion, which is compa tible with the idea that the pressure-natriuresis response may be mediated through kinins and NO. The importance of kinins in long-term regulation of arterial pressure is demonstrated by the severe arterial hypertension (172/-6 mm Hg) induced during the chronic intrarenal infusion of Hoe140 associa ted with sodium and volume retention. These data suggest that renal kinins and NO may be a part of the renal mechanism coupling changes in arterial pr essure with modifications in PBF and sodium excretion, therefore contributi ng to the long-term control of arterial pressure.