Evidence of differential control of renal and lumbar sympathetic nerve activity in conscious rabbits

Ramchandra, Rohit; Barrett, Carolyn J.; Guild, Sarah-Jane; Malpas, Simon C.

doi:10.1152/ajpregu.00504.2005

Cited by 48 publications

(45 citation statements)

References 36 publications

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“…Regionalized sympathetic activation has been convincingly demonstrated by direct nerve recordings in rabbits, 40 and Esler's group [41][42][43][44][45] has elucidated the importance of regionalized sympathetic activation in human cardiovascular disease by using NE spillover techniques. The finding in this study that CGx markedly attenuated enhanced depressor responses to ganglion blockade during Ang II salt hypertension implies that the majority of the sympathetic activation in this model is directed toward the splanchnic bed and supports the possibility of regionalized sympathetic activation.…”

Section: Discussionmentioning

confidence: 99%

Splanchnic Circulation Is a Critical Neural Target in Angiotensin II Salt Hypertension in Rats

2007

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Abstract-Chronic angiotensin II (Ang II) infusion, in rats fed high salt, engages the sympathetic nervous system to increase venomotor tone. The splanchnic sympathetic nervous system is the most important regulator of venous tone, indicating that splanchnic sympathetic nervous system activity may be increased in Ang II salt hypertension. We hypothesized that celiac ganglionectomy (CGx), to selectively disrupt sympathetic innervation to the splanchnic circulation, would attenuate arterial pressure (AP), and venous tone increases in Ang II salt hypertension. Rats fed 2% or 0.4% NaCl were instrumented to allow AP measurement by radiotelemetry at the same time as surgical CGx or sham operation. Ang II was delivered by minipump (150 ng/kg per minute) for 14 days. CGx reduced AP independent of salt diet during control. CGx markedly attenuated Ang II hypertension in rats on 2% NaCl but had little effect in rats fed 0.4% NaCl. To test the possibility that CGx exerted its effects via renal denervation, rats were subjected to the same protocol but received selective bilateral renal denervation. Renal denervation decreased AP during control but had no protective effect on Ang II hypertension and actually tended to exacerbate the pressor response. Finally, separate groups of rats underwent CGx or sham operation and were instrumented to allow repeated measures of mean circulatory filling pressure, an index of venous tone. In addition to attenuating Ang II salt hypertension, CGx completely prevented Ang II salt-induced increases in mean circulatory filling pressure and substantially attenuated depressor responses to acute ganglion blockade. We conclude that, in the presence of high salt, Ang II activates the splanchnic sympathetic nervous system to increase venomotor tone and AP. Key Words: angiotensin II Ⅲ sympathetic nervous system Ⅲ splanchnic circulation Ⅲ venomotor tone Ⅲ renal denervation W e have shown recently, using repeated measures of mean circulatory filling pressure (MCFP) in conscious undisturbed rats, that chronic infusion of angiotensin II (Ang II), only when administered in combination with a high-salt diet, activates the sympathetic nervous system (SNS) to increase venomotor tone. 1 This increase in venomotor tone may contribute to the pathogenesis of Ang II salt hypertension by increasing central blood volume, resulting in a translocation of blood from the highly compliant venous system to the less compliant arterial circulation. 1 This redistribution of blood volume and the well-documented impairment of renal excretory function caused by Ang II 2 would be major factors in increasing arterial pressure (AP) in this model. [3][4][5] Splanchnic veins and venules account for most of the active capacitance responses in the circulation and are richly innervated by the SNS. 6 -8 In fact, it has been estimated that innervation to the nonhepatic splanchnic organs accounts for half of the total norepinephrine (NE) released in the entire body. 9 Therefore, our recent observations in Ang II salt hypertension of neurog...

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Section: Discussionmentioning

confidence: 99%

Splanchnic Circulation Is a Critical Neural Target in Angiotensin II Salt Hypertension in Rats

2007

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“…Our finding that the resting burst incidences of the cardiac and renal nerves are significantly different from each other in normal animals suggests that the generation of cardiac and renal bursts may be regulated by separate central circuits in the brainstem. Previous studies have suggested that there is a topographical organization of the presympathetic neurons in the rostral ventral lateral medulla (RVLM) (18,19) with respect to vasomotor control in different organs, which could lead to differentiated responses to specific stimuli (20,21). In addition to tonic drive to CSNA from the RVLM (19,20,22), recent studies have indicated that disinhibition of neurons in the rostral medullary raphé leads to increased CSNA with little accompanying vasomotor response, by a mechanism independent of the RVLM (22).…”

Section: Discussionmentioning

confidence: 99%

Basis for the preferential activation of cardiac sympathetic nerve activity in heart failure

Ramchandra

Hood

Denton

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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In heart failure (HF) , sympathetic nerve activity is increased. Measurements in HF patients of cardiac norepinephrine spillover, reflecting cardiac sympathetic nerve activity (CSNA), indicate that it is increased earlier and to a greater extent than sympathetic activity to other organs. This has important consequences because it worsens prognosis, provoking arrhythmias and sudden death. To elucidate the mechanisms responsible for the activation of CSNA in HF, we made simultaneous direct neural recordings of CSNA and renal SNA (RSNA) in two groups of conscious sheep: normal animals and animals in HF induced by chronic, rapid ventricular pacing. In normal animals, the level of activity, measured as burst incidence (bursts of pulse related activity/100 heart beats), was significantly lower for CSNA (30 ؎ 5%) than for RSNA (94 ؎ 2%). Furthermore, the resting level of CSNA, relative to its maximum achieved while baroreceptors were unloaded by reducing arterial pressure, was set at a much lower percentage than RSNA. In HF, burst incidence of CSNA increased from 30 to 91%, whereas burst incidence of RSNA remained unaltered at 95%. The sensitivity of the control of both CSNA and RSNA by the arterial baroreflex remained unchanged in HF. These data show that, in the normal state, the resting level of CSNA is set at a lower level than RSNA, but in HF, the resting levels of SNA to both organs are close to their maxima. This finding provides an explanation for the preferential increase in cardiac norepinephrine spillover observed in HF.arterial baroreflex ͉ renal sympathetic nerve activity ͉ sheep H eart failure (HF) is associated with an increase in sympathetic nerve activity (SNA) that shows a large regional heterogeneity in the extent to which activity increases. The level of SNA to different organs may be estimated by measurements of regional norepinephrine (NE) spillover, and it has been observed that in HF there is a greater increase in NE spillover from the heart than the kidney, and no change from the gut (1, 2). This increase in cardiac NE spillover occurs at an earlier stage of HF than it does to other organs (3, 4), again suggesting a preferential stimulation of cardiac SNA (CSNA) in HF. The increase in CSNA in HF is detrimental as it can promote the progression of the disease and leads to development of arrhythmias and sudden death (5). The mechanisms accounting for the increase in CSNA in HF are poorly understood.One explanation for the preferential increase in cardiac NE spillover in HF is that, in the normal state, the resting levels of CSNA and renal SNA (RSNA) are similar, but in HF, sympathetic activity increases more to the heart than to the kidney. An alternative explanation is that the resting level of CSNA is set at a lower level compared with that to other organs, such the kidney, and in HF, both CSNA and RSNA increase to near maximum levels. Both explanations seem plausible, but the resting levels of CSNA and RSNA have not been simultaneously recorded in the normal state and compared with activities ...

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“…Under these conditions, any spontaneous or evoked change reflected a variation around the mean. In a recent study performed on conscious rabbits (27), baroreflex function curves for lumbar and RSNA were compared, and the conclusion drawn was that BRS did not differ between the two SNAs. In this study, the background noise level was taken as the minimum SNA level observed during phenylephrine infusion, and data were normalized by the maximum value reached during sodium nitroprusside infusion.…”

Section: Discussionmentioning

confidence: 99%

Baroreflex control of lumbar and renal sympathetic nerve activity in conscious rats

Kanbar

Chapuis²,

Oréa³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Kanbar R, Chapuis B, Oréa V, Barrès C, Julien C. Baroreflex control of lumbar and renal sympathetic nerve activity in conscious rats. Am J Physiol Regul Integr Comp Physiol 295: R8 -R14, 2008. First published April 30, 2008 doi:10.1152/ajpregu.00147.2008This study compared the baroreflex control of lumbar and renal sympathetic nerve activity (SNA) in conscious rats. Arterial pressure (AP) and lumbar and renal SNA were simultaneously recorded in six freely behaving rats. Pharmacological estimates of lumbar and renal sympathetic baroreflex sensitivity (BRS) were obtained by means of the sequential intravenous administration of sodium nitroprusside and phenylephrine. Sympathetic BRS was significantly (P Ͻ 0.05) lower for lumbar [3.0 Ϯ 0.4 normalized units (NU)/mmHg] than for renal (7.6 Ϯ 0.6 NU/mmHg) SNA. During a 219-min baseline period, spontaneous lumbar and renal BRS were continuously assessed by computing the gain of the transfer function relating AP and SNA at heart rate frequency over consecutive 61.4-s periods. The transfer gain was considered only when coherence between AP and SNA significantly differed from zero, which was verified in 99 Ϯ 1 and 96 Ϯ 3% of cases for lumbar and renal SNA, respectively. When averaged over the entire baseline period, spontaneous BRS was significantly (P Ͻ 0.05) lower for lumbar (1.3 Ϯ 0.2 NU/mmHg) than for renal (2.3 Ϯ 0.3 NU/mmHg) SNA. For both SNAs, spontaneous BRS showed marked fluctuations (variation coefficients were 26 Ϯ 2 and 28 Ϯ 2% for lumbar and renal SNA, respectively). These fluctuations were positively correlated in five of six rats (R ϭ 0.44 Ϯ 0.06; n ϭ 204 Ϯ 8; P Ͻ 0.0001). We conclude that in conscious rats, the baroreflex control of lumbar and renal SNA shows quantitative differences but is modulated in a mostly coordinated way. arterial pressure; baroreceptor reflex; sympathetic nervous system; transfer function THE ARTERIAL BARORECEPTOR reflex plays a major role in the short-term control of arterial pressure (AP) mainly through the modulation of efferent sympathetic nerve activity (SNA) to regional circulations (12). In rats, studies aimed at characterizing the baroreflex control of SNA under physiological conditions, i.e., in the conscious state, have been based mostly on recordings of renal SNA (RSNA;3,5,7,10,13,16,20,23,25), mainly because of the purely postganglionic nature of this activity. Most often, authors implicitly assumed that RSNA provided a reliable reflection of other regional SNAs. In the meantime, evidence has accumulated suggesting a differential baroreflex control of regional SNAs in several animal species (22). In the rat, the comparison of the baroreflex control of regional SNAs has been carried out in urethane-chloralose anesthetized animals by using the vasoactive drug injection technique, i.e., the so-called pharmacological method (29,30). In these studies, it was reported that the characteristics of the baroreflex function curves differed between RSNA, lumbar SNA (LSNA), and adrenal SNA. In conscious rats, this information has not...

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Evidence of differential control of renal and lumbar sympathetic nerve activity in conscious rabbits

Cited by 48 publications

References 36 publications

Splanchnic Circulation Is a Critical Neural Target in Angiotensin II Salt Hypertension in Rats

Splanchnic Circulation Is a Critical Neural Target in Angiotensin II Salt Hypertension in Rats

Basis for the preferential activation of cardiac sympathetic nerve activity in heart failure

Baroreflex control of lumbar and renal sympathetic nerve activity in conscious rats

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