Search

In contrast to other sympathetic outflow tracts, renal sympathetic nerve activity (RSNA) decreases in response to hypotensive hemorrhage. The functional significance of this 'paradox' is not known. We tested the hypothesis that RSNA modulates renal perfusion and thus erythropoietin (EPO) release after transient hypotensive hemorrhage in anesthetized rats. Plasma EPO was measured before and after 30 min of transient hypotensive hemorrhage (i.e., -40 mmHg from mean baseline blood pressure, followed by reinfusion of shed blood) and 120 min thereafter in sham-denervated rats, and after renal denervation (DNX) or bilateral cervical vagotomy (VX) to abolish/blunt the RSNA decrease mediated by a cardiopulmonary reflex. RSNA, renal Doppler flow, renal vascular resistance (RVR), resistance index, and oxygen delivery/uptake ([DO.sub.2]/[[??]O.sub.2]) were measured. RSNA decreased in intact animals (-40 [+ or -] 5% from baseline, P < 0.05). This was blunted by VX. With intact nerves, EPO level did not increase. In DNX rats, EPO was increased at minute 120 (49 [+ or -] 3 vs. 74 [+ or -] 2 mU/ml; P < 0.05), in VX rats this (47 [+ or -] 2 vs. 62 [+ or -] 4 mU/ml; P < 0.05) was less pronounced. [DO.sub.2] in DNX rats was lower compared with intact and VX rats (0.25 [+ or -] 0.04 vs. 0.51 [+ or -] 0.06 and 0.54 [+ or -] 0.05 ml [O.sub.2]/min; P < 0.05) due to lower Doppler flow and increased RVR. RVR and [DO.sub.2] were similar in intact and VX rats, but resistance index differed between all groups (0.70 [+ or -] 0.02 vs. 0.78 [+ or -] 0.02 vs. 0.85 [+ or -] 0.02; P < 0.05, intact vs. VX vs. DNX), indicating differential reactivity of renal vasculature. [[??]O.sub.2] was unaffected by VX and DNX. Renal sympathoinhibition during hypotensive hemorrhage might help to preserve sufficient oxygenation of renal tissue by modulation of hemodynamic mechanisms that act to adapt renal oxygen availability to demand. renal nerve; oxygen delivery

Left ventricular (LV) end-diastolic pressure (LVEDP) increase due to volume expansion (VExp) enhances mechanosensitive vagal cardiac afferent C-fiber activity (CNFA), thus decreasing renal sympathetic nerve activity (RSNA). Hypotensive hemorrhage (hHem) attenuates RSNA despite decreased LVEDP. We hypothesized that CNFA increases with any change in LVEDP. Coronary perfusion pressure (CPP), supposedly affected in both conditions, might also be a stimulus of CNFA. VExp and hHem were performed in anesthetized male Sprague-Dawley rats while blood pressure, heart rate, and RSNA were measured. Cervical vagotomy abolished RSNA response in both reflex responses. Single-unit CNFA was recorded while LVEDP was changed. Rapid changes ([+ or -] 4, [+ or -] 6, [+ or -] 8 mmHg) were obtained by graded occlusion of the caval vein and descending aorta. Prolonged changes were obtained by VExp and hHem. Furthermore, CNFA was recorded in a modified Langendorff heart while CPP was changed (70, 100, 40 mmHg). Rapid LVEDP changes increased CNFA [caval vein occlusion: + 16 [+ or -] 3 Hz (approximately +602%); aortic occlusion: +15 [+ or -] 3 Hz (approximately +553%); 70 units; P < 0.05]. VExp and hHem (n = 6) increased CNFA [VExp: +10 [+ or -] 4 Hz (approximately +1,033%); hHem: +10 [+ or -] 2 Hz (approximately +1,225%); P < 0.05]. An increase in CPP increased CNFA [+2 [+ or -] 1 Hz (approximately +225%); P < 0.05], whereas a decrease in CPP decreased CNFA [-0.8 [+ or -] 0.4 Hz (approximately -50%); P < 0.05]. All C fibers recorded originated from the LV. CNFA increased with any LVEDP change but changed equidirectionally with CPP. Thus neither LVEDP nor CPP fully accounts directly for afferent C-fiber and reflex sympathetic responses. The intrinsic afferent stimuli and receptive fields accounting for reflex sympathoinhibition still remain cryptic. cardiac afferent C fiber; renal sympathetic nerve activity; cardiorenal reflexes

The effects of pulmonary vagal C fibers with 5-HT3 serotonin receptors in the regulation of renal sympathetic nerve activity (RSNA) were analyzed in male Sprague-Dawley rats. Administration of phenylbiguanidine (PBG) in rats reduced blood pressure (BP), heart rate (HR) and RSNA. However, the effects of PBG on BP and HR were attenuated by intrapericardial procaine which inhibited the activity of cardiac afferents. The effects of PBG indicated the regulatory role of pulmonary serotonin on the RSNA.