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Title: Control of lumbar sympathetic nerve traffic by vagal cardiopulmonary baroreflexes in renal hypertension. Author: Thames MD, Yuih SN, Fortner CA, Brands DB. Journal: Circ Res; 1987 Oct; 61(4 Pt 2):I72-5. PubMed ID: 3652405. Abstract: Renal nerve traffic is inhibited during volume expansion mainly because of stimulation of vagal cardiopulmonary baroreflexes. These responses are impaired in rabbits with renal hypertension caused by impaired cardiopulmonary baroreflexes. Previous studies have suggested that there may be differences in the extent to which renal hypertension alters reflex control of lumbar as compared with renal sympathetic nerve activity. The goals of this study were to determine if the responses to volume expansion of lumbar sympathetic nerve traffic also are impaired in renal hypertension and if this abnormality, if present, is caused by abnormalities in the vagal cardiopulmonary baroreflex. Experiments were done in alpha-chloralose-anesthetized normotensive (n = 9) and renal hypertensive (n = 7; 1 kidney, 1 wrap) rabbits. Infusion of dextran in saline raised arterial and left atrial pressures in both groups and decreased lumbar nerve traffic by -4.4 +/- 0.4% mm Hg rise in arterial pressure in the normotensive group and by -1.5 +/- 0.1% mm Hg in the hypertensive group (p less than 0.01). These responses were nearly abolished by sinoaortic denervation in both groups. These data indicate that the responses of lumbar nerve traffic to volume expansion are impaired in renal hypertension; this is mainly because of impaired arterial baroreflexes since vagal cardiopulmonary baroreceptors have minimal influence on lumbar nerve traffic, even in normotensive rabbits. These findings for the lumbar nerves are strikingly different from those reported previously for reflex control of the renal nerves in both normotensive and hypertensive rabbits.[Abstract] [Full Text] [Related] [New Search]