These aren't the best papers/articles to support this argument, but they'll have to do for now.
Lack of noreinephrine activity (due to block or shortage) causes MS symptoms. Aldosterone blocks NE. Also, aldosterone causes release of bnp (link in first thread post under how complicated can this get). Bnp decreases the release of NE. So, aldosterone both blocks and indirectly reduces secretion of NE.
Other interesting leads regarding NO, etc but no time to chase them right now.http://www.cbucommons.ca/psych/courses/ ... sclerosis/
Elevated aldosterone levels in heart failure may have a detrimental effect on the autonomic nervous system. First, aldosterone infusion directly reduced baroreceptor discharge from the carotid sinus in dog ［5］. Second, aldosterone blunts the human baroreflex response ［6,7］. Third, aldosterone may potentiate the effects of catecholamine ［8］. Fourth, aldosterone blocks myocardial uptake of norepinephrine (NA) in vivo in an animal model ［9］.
Mechanisms of spironolactone include following aspects ［11~13］, antagonizing over-activated renin-angiotensin-system (RAS), decreasing the heart burden by diuresis, decreasing incidence of arrhythmia and sudden death from low blood potassium and magnesium, inhibiting ventricle remodeling, alleviating fibrosis of myocardial and vascular which lead to arrhythmia, increasing synthesis of nitric oxide (NO) by melioration of vascular endothelial function, increasing activity of vagus nerves and circadian rhythms of HRV, decreasing the incidence of sudden death by increase of myocardial NA uptake.http://www.experts.scival.com/uic/pubDe ... n&u_id=612
A study by Polak, Kalinin and Feinstein (2010) looked at the reduction of the neurotransmitter norepinephrine (NE), found in the central nervous system, and damage to the locus coeruleus (LC), which produces norepinephrine in the brain stem. Neurotransmitters such as norepinephrine are chemicals used by neurons, or brain cells, to communicate with each other. The study was directed towards patients with multiple sclerosis and animals with experimental autoimmune encephalomyelitis (EAE, an animal model of MS where experimenters immunize animals and they develop symptoms closely related to MS, though the two are not exactly the same). For this study, infant female mice were injected with specific chemicals to induce EAE. After 60 days they then measured the NE levels in these mice, as well as the NE levels of humans suffering from MS. They found that both groups demonstrated reduced NE levels when compared to control groups, and the humans showed evidence of inflammation in and around the LC. These results are comparable to other studies in suggesting an alteration of NE levels in EAE cases. This suggests that loss of NE production is the cause of the decreased quantity, as opposed to other possibilities including increased metabolism or increased reuptake (reabsorption of the NE by the cells that released it). While it still can’t be determined whether low levels of norepinephrine are the cause of MS, they are at least responsible for several symptoms including memory problems, depression, and lack of arousal. Therefore, defining the cause of lowered norepinephrine levels is extremely important for these patients. http://link.springer.com/article/10.102 ... 9?LI=true#
A study by Simonini and colleagues (2009) attempted to see whether increasing levels of NE in the CNS would provide any benefit in neurological diseases such as MS by decreasing inflammation. In this study, researchers injected infant female mice with EAE and altered their NE levels within the CNS in a controlled setting. Researchers used lesions in the locus coeruleus to reduce NE levels in of mice by administering a toxin that acts specifically on LC neurons. Mice were then given a reuptake inhibitor, which decreases the natural reabsorbtion of their NE. Researchers noted that after 3 weeks, there had been no changes in the severity of their EAE. Researchers then tested to see if giving the mice a precursor of NE, which their body would then turn into excess NE, would have any effects on their symptoms. They found that this neutralized their symptoms, but did not change the clinical severity of their EAE. Researchers then tested a combination of the reuptake inhibitor combined with the precursor to see if that would provide any advantage. The results of this combination proved to be quite substantial. The severity of EAE was considerably enhanced, suggesting that increasing CNS NE levels can have meaningful positive effects on EAE severity, although to achieve the full desired effects they require the combination treatment.
We previously demonstrated that atrial natriuretic factor and B- and C-type natriuretic peptides (ANF, BNP, and CNP, respectively) modified catecholamine metabolism by increasing the neuronal uptake and decreasing the neuronal release of norepinephrine in the rat hypothalamus