Activation of afferent renal nerves by intrarenal bradykinin in conscious rats
Smits, J.F.; Brody, M.J.
American Journal of Physiology 247(6 Pt 2): R1003-R1008
1984
ISSN/ISBN: 0002-9513 PMID: 6150645 Document Number: 227426
Bradykinin was infused i.v. and into the right renal artery of conscious rats that were chronically instrumented with catheters and miniaturized pulsed-Doppler flow probes. The effects on regional hemodynamics were compared with those in animals in which the infused kidney was denervated as well as in animals anesthetized with pentobarbital sodium. In intact rats bradykinin (1 .mu.g/min) caused an immediate increase in mean arterial blood pressure (MAP, 27 .+-. 4 mmHg), heart rate (HR, 67 .+-. 11 beats/min), mesenteric resistance (MR, 32 .+-. 10%) and both right (RRR, 42 .+-. 14%) and left renal resistance (LRR 21 .+-. 8%). These effects were significantly different from those during i.v. infusion of the same dose of bradykinin (MAP, 6 .+-. 3 mmHg; HR, 31 .+-. 7 beats/min; MR, -21 .+-. 5%; RRR, 8 .+-. 4%; LRR, 6 .+-. 3%). Pentobarbital greatly attenuated the responses to intrarenal bradykinin. In conscious animals denervation of the infused kidney completely abolished the cardiovascular effects of intrarenal bradykinin. In a separate group of animals, chlorisondamine (7.5 mg/kg i.v.) completely blocked the increases in MAP and HR during intrarenal bradykinin (1 .mu.g/min). Selective renal administration of bradykinin evidently alters afferent renal nerve activity. This results in hemodynamic changes consistent with efferent sympathetic activation. [The role of renal chemoreceptors and mechanoreceptors in cardiovascular control was described.].