Kacie M Dickinson, Peter M Clifton, and Jennifer B Keogh:
Endothelial function is impaired after a high-salt meal in healthy subjects.
Am J Clin Nutr March 2011 vol. 93 no. 3 500-505 http://ajcn.nutrition.org/content/93/3/500.full
From this:
« Overall FMD (flow-mediated dilatation) was reduced 2 h postprandially. FMD was significantly more impaired after the HSM (high-salt meal) than after the LSM (low-salt meal) at 30 min … »
« An HSM (65 mmol Na = 3,8 g NaCl), which reflects the typical amount of salt consumed in a commonly eaten meal, can significantly suppress brachial artery FMD within 30 min. These results suggest that high salt intakes have acute adverse effects on vascular dilatation in the postprandial state. »
« We speculate that one of these possible mechanisms by which salt impairs endothelial function is via an alteration in plasma sodium. Two studies have reported responses to oral salt loading over a postprandial time period, which showed a rise in plasma sodium in response to 100 mmol Na (5.8 g salt) loading in healthy persons of 3 mmol/L, which occurred within 2–3 h of consuming the test meal [16, 17]. It has been postulated that a high salt intake may acutely impair vascular function by raising plasma sodium by as much as 3 mmol/L. »
« It appears that higher salt intakes have acute adverse effects on vascular dilatation in the postprandial phase. »

Indisputable: Impaired vascular function = impaired oxygen supply. And less oxygen = less energy.

Nedergaard et al.: Acid-induced death in neurons and glia.
The Journal of Neuroscience, August 1991, 11(8): 2489-2497
facweb.northseattle.edu/.../Flow%20of%20Energy_04_Acid-Induced%20Cell%20Death.pdf
https://www.researchgate.net/publication/21285911
From the article: « Cerebral hypoxia-ischemia induces lactic acid formation trough the accentuation of anaerobic glycolysis. The magnitude of this lactic acid accumulation depends largely upon the preischemic glucose and glycogen concentrations of the affected tissue (Smith et al., 1986). Local accumulation of lactic acid to cytotoxic levels may play a causal role in the genesis of brain infarction following cerebral ischemia (Meyerand Yamaguchi, 1977; Siemkowitz and Hansen, 1978; Pulsinelli et al., 1982; Nedergaard, 1987). Several authors have addressed directly the issue of acid-induced cell death. »
And the excess sodium intake (floor gas Na-K pump) also induces lactic acid formation by switching the anaerobic glycolysis (SICAG) on. And our cells are dying, even in our brain. The salted humanity degenerates and will be idiotic.

And one 41 years old article:
W J Oliver, E L Cohen, J V Neel: Blood pressure, sodium intake, and sodium related hormones in the Yanomamo Indians, a « no-salt » culture.
Circulation. 1975; 52: 146-151
http://circ.ahajournals.org/content/52/1/146
circ.ahajournals.org/.../146.full.pdf+html
https://www.researchgate.net/publication/22023760

A very important new research article:

Herman Pontzer, Ramon Durazo-Arvizu, Lara R. Dugas, Jacob Plange-Rhule, Pascal Bovet, Terrence E. Forrester, Estelle V. Lambert, Richard S. Cooper, Dale A. Schoeller, Amy Luke:
Constrained Total Energy Expenditure and Metabolic Adaptation to Physical Activity in Adult Humans
Current biology: CB January 2016 DOI: 10.1016/j.cub.2015.12.046
www.cell.com/.../S0960-9822(15)01577-8
https://www.researchgate.net/publication/292208779
Including (now) 2 comments.

More evidences and references:

Z. Sandor: Re: The scientific report guiding the US dietary guidelines: is it scientific? BMJ (online) 25 September 2015
http://www.bmj.com/content/351/bmj.h4962/rr-5
https://www.researchgate.net/publication/282672806

Z. Sandor: Entropy and sodium intakes, the wicked problems of health sciences
Science 2.0 (9 September 2013)
www.science20.com/entropy_and_sodium_intakes_wicked_problems_health_sciences-120016