Activation of a renin–angiotensin system in ischemic cardiac sympathetic nerve endings and its association with norepinephrine release

2002 ◽  
Vol 2 (13-14) ◽  
pp. 1965-1973 ◽  
Author(s):  
Roberto Levi ◽  
Randi B Silver ◽  
Christina J Mackins ◽  
Nahid Seyedi ◽  
Motohiro Koyama
Keyword(s):  
Sympathetic Nerve ◽  
Renin Angiotensin System ◽  
Nerve Endings ◽  
Cardiac Sympathetic Nerve ◽  
Norepinephrine Release ◽  
Angiotensin System ◽  
Renin Angiotensin

NG-nitro-l-arginine methyl ester-induced norepinephrine release from cardiac sympathetic nerve endings in anesthetized cats

2003 ◽  
Vol 353 (3) ◽  
pp. 205-208 ◽  
Author(s):  
Yuji Takauchi ◽  
Toji Yamazaki ◽  
Tsuyoshi Akiyama ◽  
Kenji Sunagawa
Keyword(s):  
Methyl Ester ◽  
Sympathetic Nerve ◽  
Nerve Endings ◽  
Cardiac Sympathetic Nerve ◽  
Norepinephrine Release

EctoNucleotidase in Cardiac Sympathetic Nerve Endings Modulates ATP-Mediated Feedback of Norepinephrine Release

2002 ◽  
Vol 300 (2) ◽  
pp. 605-611 ◽  
Author(s):  
Casilde Sesti ◽  
M. Johan Broekman ◽  
Joan H. F. Drosopoulos ◽  
Naziba Islam ◽  
Aaron J. Marcus ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Nerve Endings ◽  
Cardiac Sympathetic Nerve ◽  
Norepinephrine Release

Presynaptic effects of epinephrine on norepinephrine release from cardiac sympathetic nerves in dogs

1993 ◽  
Vol 265 (1) ◽  
pp. H205-H211 ◽  
Author(s):  
G. Boudreau ◽  
F. Peronnet ◽  
J. De Champlain ◽  
R. Nadeau
Keyword(s):  
Left Ventricle ◽  
Intravenous Administration ◽  
Sympathetic Nerve ◽  
Sympathetic Nerves ◽  
Nerve Endings ◽  
Facilitatory Effect ◽  
Cardiac Sympathetic Nerve ◽  
Norepinephrine Release ◽  
Epinephrine Infusion ◽  
Beta 2

The possible functional role of tissue epinephrine in the modulation of norepinephrine release from cardiac sympathetic nerve endings in anesthetized dog was investigated. Observations were carried out under control conditions and after a short- (10 min) and long-term (180 min) epinephrine infusion (92 ng.kg-1.min-1). An increase in the stimulation-induced release of norepinephrine after intravenous administration of a selective beta 2-agonist (fenoterol, 0.5 micrograms/kg) indicated the presence of the beta 2-facilitatory mechanism. Furthermore, the facilitatory effect of fenoterol was inhibited by intravenous administration of a selective beta 2-antagonist (ICI 118551, 1 mg/kg). Short-term epinephrine infusion did not facilitate the stimulation-induced release of norepinephrine, when tissue epinephrine content in the left ventricle was increased 1.5-fold, without, as well as with, alpha 2-blockade (yohimbine, 0.3 mg/kg). However, stimulation-induced release of norepinephrine from the myocardium was significantly potentiated in animals in which tissue epinephrine in the left ventricle was greatly increased (5.6-fold) by a prolonged infusion of epinephrine (180 min). It is concluded that a facilitatory mechanism mediated by presynaptic beta 2-adrenoceptors is present in cardiac sympathetic nerve endings of the dog. Some of our observations support the hypothesis that this mechanism may be influenced by locally released epinephrine and, thus, by tissue epinephrine content.

scholarly journals A brain leptin-renin angiotensin system interaction in the regulation of sympathetic nerve activity

2012 ◽  
Vol 303 (2) ◽  
pp. H197-H206 ◽  
Author(s):  
Aline M. Hilzendeger ◽  
Donald A. Morgan ◽  
Leonard Brooks ◽  
David Dellsperger ◽  
Xuebo Liu ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Food Intake ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Renin Angiotensin System ◽  
Melanocortin Receptor ◽  
Nerve Activity ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
The Brain

The sympathetic nervous system, leptin, and renin-angiotensin system (RAS) have been implicated in obesity-associated hypertension. There is increasing evidence for the presence of both leptin and angiotensin II receptors in several key brain cardiovascular and metabolic control regions. We tested the hypothesis that the brain RAS plays a facilitatory role in the sympathetic nerve responses to leptin. In rats, intracerebroventricular (ICV) administration of losartan (5 μg) selectively inhibited increases in renal and brown adipose tissue (BAT) sympathetic nerve activity (SNA) produced by leptin (10 μg ICV) but did not reduce the SNA responses to corticotrophin-releasing factor (CRF) or the melanocortin receptor agonist MTII. In mice with deletion of angiotensin II type-1a receptors (AT1aR−/−), increases in renal and BAT SNA induced by leptin (2 μg ICV) were impaired whereas SNA responses to MTII were preserved. Decreases in food intake and body weight with ICV leptin did not differ in AT1aR−/− vs. AT1aR+/+ mice. ICV leptin in rats increased AT1aR and angiotensin-converting enzyme (ACE) mRNA in the subfornical organ and AT1aR mRNA in the arcuate nucleus, suggesting leptin-induced upregulation of the brain RAS in specific brain regions. To evaluate the role of de novo production of brain angiotensin II in SNA responses to leptin, we treated rats with captopril (12.5 μg ICV). Captopril attenuated leptin effects on renal and BAT SNA. In conclusion, these studies provide evidence that the brain RAS selectively facilitates renal and BAT sympathetic nerve responses to leptin while sparing effects on food intake.

Forebrain renin-angiotensin system has a tonic excitatory influence on renal sympathetic nerve activity

2002 ◽  
Vol 282 (3) ◽  
pp. H890-H895 ◽  
Author(s):  
Shun-Guang Wei ◽  
Robert B. Felder
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Renin Angiotensin System ◽  
Nerve Activity ◽  
Angiotensin System ◽  
Renal Sympathetic Nerve Activity ◽  
Renin Angiotensin ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

All elements of the renin-angiotensin system (RAS) are present in the forebrain, particularly in circumventricular organs surrounding the third cerebral ventricle. We tested the hypothesis that forebrain angiotensin-converting enzyme (ACE) has a tonic excitatory influence on sympathetic drive. Neurally intact and sinoaortic-denervated pentobarbital-anesthetized rats were treated with forebrain-directed intracarotid artery (ICA) versus intravenous injections of angiotensin I (ANG I) and of the ACE inhibitor captopril. In intact rats, ICA ANG I elicited a rise in arterial pressure and a concomitant reduction in renal sympathetic nerve activity (RSNA; ICA captopril elicited the opposite responses). In barodenervated rats, ICA ANG I increased and ICA captopril decreased arterial pressure and RSNA in parallel; intravenous ANG I had no effect on RSNA. The findings suggest that the intrinsic forebrain RAS has a tonic excitatory influence on sympathetic drive that is overshadowed in normal rats by baroreflex mechanisms, but may assume a more prominent role in pathophysiological states (e.g., heart failure) in which baroreflex mechanisms are impaired and RAS activity is augmented.

Aldosterone acts centrally to increase brain renin-angiotensin system activity and oxidative stress in normal rats

2008 ◽  
Vol 294 (2) ◽  
pp. H1067-H1074 ◽  
Author(s):  
Zhi-Hua Zhang ◽  
Yang Yu ◽  
Yu-Ming Kang ◽  
Shun-Guang Wei ◽  
Robert B. Felder
Keyword(s):  
Oxidative Stress ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Renin Angiotensin System ◽  
Nerve Activity ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Ru 28318 ◽  
The Brain ◽  
And Oxidative Stress

Aldosterone acts upon mineralocorticoid receptors in the brain to increase blood pressure and sympathetic nerve activity, but the mechanisms are still poorly understood. We hypothesized that aldosterone increases sympathetic nerve activity by upregulating the renin-angiotensin system (RAS) and oxidative stress in the brain, as it does in peripheral tissues. In Sprague-Dawley rats, aldosterone (Aldo) or vehicle (Veh) was infused for 1 wk via an intracerebroventricular (ICV) cannula, while RU-28318 (selective mineralocorticoid receptor antagonist), Tempol (superoxide dismutase mimetic), losartan [angiotensin II type 1 receptor (AT1R) antagonist], or Veh was infused simultaneously via a second ICV cannula. After 1 wk of ICV Aldo, plasma norepinephrine was increased and mean arterial pressure was slightly elevated, but heart rate was unchanged. These effects were ameliorated by ICV infusion of RU-28318, Tempol or losartan. Aldo increased expression of AT1R and angiotensin-converting enzyme (ACE) mRNA in hypothalamic tissue. RU-28318 minimized and Tempol prevented the increase in AT1R mRNA; RU-28318 prevented the increase in ACE mRNA. Losartan had no effect on AT1R or ACE mRNA. Immunohistochemistry revealed Aldo-induced increases in dihydroethidium staining (indicating oxidative stress) and Fra-like activity (indicating neuronal excitation) in neurons of the hypothalamic paraventricular nucleus (PVN). RU-28318 prevented the increases in superoxide and Fra-like activity in PVN; Tempol and losartan minimized these effects. Acute ICV infusions of sarthran (AT1R antagonist) or Tempol produced greater sympathoinhibition in Aldo-treated than in Veh-treated rats. Thus aldosterone upregulates key elements of brain RAS and induces oxidative stress in the hypothalamus. Aldosterone may increase sympathetic nerve activity by these mechanisms.

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