Chronic angiotensin II infusion decreases renal norepinephrine overflow in conscious dogs.

Carroll, Robert G.; Lohmeier, Thomas E.; Brown, Andrew J.

doi:10.1161/01.hyp.6.5.675

Cited by 64 publications

(55 citation statements)

References 31 publications

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“…Cessation of the angiotensin II caused blood pressure and SNA to return to control levels. The observation of sympathoinhibition during angiotensin II infusions is supported by Carroll et al (17), who measured renal norepinephrine overflow as an indirect index of RSNA. Six days of angiotensin II hypertension was associated with marked reductions (not increases) in renal norepinephrine spillover.…”

Section: The Role Of Angiotensin In Regulating Long-term Levels Of Snamentioning

confidence: 84%

“…However, this is not without debate, as measurements of peripheral plasma catecholamine levels during angiotensin II suggest sympathetic activity does not change (17,51), whereas renal norepinephrine spillover levels suggest sympathetic activity is decreased during angiotensin II hypertension (17). In part, this may reflect a differential nature of sympathetic activation with activation of RSNA and no change to other organs.…”

Section: The Role Of Angiotensin In Regulating Long-term Levels Of Snamentioning

confidence: 99%

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What sets the long-term level of sympathetic nerve activity: is there a role for arterial baroreceptors?

Malpas

2004

American Journal of Physiology-Regulatory, Integrative and Comp

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Malpas, Simon C. What sets the long-term level of sympathetic nerve activity: is there a role for arterial baroreceptors? Am J Physiol Regul Integr Comp Physiol 286: R1-R12, 2004; 10.1152/ajpregu.00496.2003.-Much of our knowledge of the influence of the sympathetic nervous system on the control of blood pressure is built on experimental approaches that focus very much on time scales Ͻ24 h. Although direct recordings of sympathetic nerve activity (SNA) over short time scales provide important information, it is difficult to place their relevance over the longer term where the development of chronic changes in blood pressure are likely to be a mixture of hormonal, renal, and neural influences. Recently new experimental approaches are now revealing a possible role for arterial baroreceptors in the chronic regulation of SNA. These studies reveal that chronic increases in blood pressure are associated with chronic changes in SNA that may be due to nonresetting of the blood pressure-SNA baroreflex relationship. This review discusses the implications of such information, highlighting new technologies for long-term recording of SNA that appear to hold much promise for revealing the role of SNA to the kidney for the long-term control of blood pressure. blood pressure; baroreflex; renal THE CONTROL OF ARTERIAL PRESSURE is a complex mixture of the long-and short-term influences of hormones, local vascular factors, and neural mechanisms. With regard to neural influences, much progress has been made in recent years on the central nervous system pathways involved in regulating sympathetic nerve activity (SNA) and the effect of that activity on vascular resistance. However, our knowledge of this control is mostly confined to short time scales of seconds and minutes, with a paucity of studies extending their focus to the longer term aspects (Ͼ24 h). Yet such information is liable to be critical in understanding the pathogenesis of hypertension where the onset of the disease is most likely to be a combination of slowly developing factors. As new tools for assessing sympathetic activity over longer time scales emerge, there is a growing desire and ability to understand longer term aspects of the regulation of SNA. It is recognized that pathways involved in regulating blood volume, osmolarity, and oxygen levels, as well as chronic changes in central nervous system function, are all likely to be important factors in understanding how SNA is controlled. However, given the revival in the hypothesis that arterial baroreflexes play a role in regulating the long-term levels of blood pressure, this review concentrates on the recent research supporting this concept. HISTORY

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Section: The Role Of Angiotensin In Regulating Long-term Levels Of Snamentioning

confidence: 84%

Section: The Role Of Angiotensin In Regulating Long-term Levels Of Snamentioning

confidence: 99%

What sets the long-term level of sympathetic nerve activity: is there a role for arterial baroreceptors?

Malpas

2004

American Journal of Physiology-Regulatory, Integrative and Comp

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“…26 Moreover, norepinephrine overflow in the kidney, an index of renal sympathetic nerve activity, was not increased in Ang II-infused dogs. 27 Finally, the present finding that there was no significant difference in postsaralasin blood pressure levels between control rats (108±4 mm Hg) and Ang II-infused rats (115±6 mm Hg) but that the difference was still significantly higher in sodium chloride-supplemented Ang II rats (136±6 versus 108±4 mm Hg, /?<0.01) suggested that other factors than the direct vascular action of Ang II are less important in the maintenance of blood pressure in Ang II-treated rats as compared with sodium chloride-supplemented Ang II rats. This is compatible with the present data, which indicate that either ECFV measured by isotope dilution method or SNS activity measured by plasma norepinephrine concentration and vasodepressor response to hexamethonium were normal in Ang II-treated rats, but both indexes were significantly increased in Ang 11+NaCI rats.…”

Section: Discussionmentioning

confidence: 99%

Role of chloride in angiotensin II-induced salt-sensitive hypertension.

1991

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The present study investigated the effect of the anion accompanying sodium on the development of angiotensin II-induced hypertension in rats and the role of the sympathetic nervous system and extracellular fluid volume in its mechanism. Hypertension was induced by intraperitoneal infusion of angiotensin II (125 ng/min) for 12 days via miniosmotic pump. High dietary intake of sodium chloride significantly augmented the angiotensin II-induced hypertension (mean blood pressure on day 13,165±6 versus 142±6 mm Hg,/?<0.05), but equimolar sodium loading provided as sodium citrate failed to enhance angiotensin II hypertension (140±6 mm Hg). Plasma norepinephrine concentration in the conscious, resting state increased with sodium chloride loading in angiotensin II-infused rats (594±42 versus 312±37 pg/ml,p<0.01), but it remained unchanged with sodium citrate loading (324±23 pg/ml). Correspondingly, maximum response to hexamethonium bromide, a ganglion blocker, was greater in sodium chlorideloaded angiotensin II rats (77.7±4.6 mm Hg) than that in angiotensin U (59.7±5.1 mm Hg) or in sodium citrate-loaded angiotensin II (57.7±4.2 mm Hg) rats. Moreover, extracellular fluid volume, measured as Na 2 35 SO 4 space, increased in sodium chloride-loaded angiotensin II rats (427±18 ml/kg body wt) as compared with that in angiotensin U rats (375±15 ml/kg body wt) but not when compared with volume in sodium citrate-loaded angiotensin II (389±7 ml/kg body wt) rats. These results suggest that the full expression of salt (sodium chloride) sensitivity in angiotensin U hypertension depends on high dietary intake of both sodium and chloride and that the increased sympathetic nervous system activity might be involved in the increased salt sensitivity of blood pressure in angiotensin II hypertension, possibly through decreased renal function for sodium excretion. {Hypertension 1991;18:622-629)

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“…Suppression of renal SNA has also been directly measured during ANG II-induced hypertension in rabbits (2) and indirectly in dogs (4), suggesting that this suppression is not a salt-dependent effect, per se, but rather a baroreceptor-mediated phenomenon. Indeed, the chronic ANG II-induced decrease in renal SNA is not observed in sinoaortic-denervated animals (17,1).…”

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confidence: 97%

Time-dependent changes in autonomic control of splanchnic vascular resistance and heart rate in ANG II-salt hypertension

Kuroki

Guzmán

Fink

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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Kuroki MT, Guzman PA, Fink GD, Osborn JW. Time-dependent changes in autonomic control of splanchnic vascular resistance and heart rate in ANG II-salt hypertension. Am J Physiol Heart Circ Physiol 302: H763-H769, 2012. First published November 23, 2011 doi:10.1152/ajpheart.00930.2011.-Previous studies suggest that ANG II-induced hypertension in rats fed a high-salt (HS) diet (ANG II-salt hypertension) has a neurogenic component dependent on an enhanced sympathetic tone to the splanchnic veins and independent from changes in sympathetic nerve activity to the kidney or hind limb. The purpose of this study was to extend these findings and test whether altered autonomic control of splanchnic resistance arteries and the heart also contributes to the neurogenic component. Mean arterial pressure (MAP), heart rate (HR), superior mesenteric artery blood flow, and mesenteric vascular resistance (MVR) were measured during 4 control days, 14 days of ANG II delivered subcutaneously (150 ng · kg Ϫ1 · min Ϫ1 ), and 4 days of recovery in conscious rats fed a HS (2% NaCl) or low-salt (LS; 0.1% NaCl) diet. Autonomic effects on MAP, HR, and MVR were assessed by acute ganglionic blockade with hexamethonium (20 mg/kg iv) on day 3 of control, days 1,3,5,7,10, and 13 of ANG II, and day 4 of recovery. MVR increased during ANG II infusion in HS and LS rats but remained elevated only in HS rats. Additionally, the MVR response to hexamethonium was enhanced on days 10 and 13 of ANG II selectively in HS rats. Compared with LS rats, HR in HS rats was higher during the 2nd wk of ANG II, and its response to hexamethonium was greater on days 7, 10, and 13 of ANG II. These results suggest that ANG II-salt hypertension is associated with delayed changes in autonomic control of splanchnic resistance arteries and the heart. salt-sensitive hypertension; differential regulation of sympathetic outflow; splanchnic nerve activity; ganglionic blockade; hemodynamic measurement in conscious rats; angiotensin II UNDER CERTAIN CONDITIONS, hypertension resulting from systemic administration of angiotensin II (ANG II-induced hypertension) is exacerbated by activation of the sympathetic nervous system (SNS). Our group and others have shown that salt intake is one such condition (19,21). In rats fed a relatively high salt diet (2% NaCl), the level of blood pressure achieved in ANG II-induced hypertension is significantly higher than in rats fed a normal salt diet (0.4% NaCl); this is associated with an increase in whole body norepinephrine (NE) spillover (14) and enhanced mean arterial pressure (MAP) responses to ganglionic blockade (13,15). In contrast, these measures of whole body sympathetic tone in rats fed a normal salt diet remain near control levels.Despite increased "whole body" sympathetic tone in ANG II-salt (i.e., those fed a high-salt diet) hypertensive rats, we recently reported that sympathetic nerve activity (SNA) to the kidney and hind limb were reduced or unchanged, respectively (28). Suppression of renal SNA has also been directly measured duri...

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Chronic angiotensin II infusion decreases renal norepinephrine overflow in conscious dogs.

Cited by 64 publications

References 31 publications

What sets the long-term level of sympathetic nerve activity: is there a role for arterial baroreceptors?

What sets the long-term level of sympathetic nerve activity: is there a role for arterial baroreceptors?

Role of chloride in angiotensin II-induced salt-sensitive hypertension.

Time-dependent changes in autonomic control of splanchnic vascular resistance and heart rate in ANG II-salt hypertension

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