Excessive salt intake linked to cognitive disorders and high blood pressure

The involvement of angiotensin II (Ang II)-a hormone that plays a key role in regulating blood pressure and fluid balance-and its receptor “AT1”, as well as that of the physiologically important lipid molecule prostaglandin E2 and its receptor “EP1” in hypertension and neurotoxicity is well-recognized. However, the involvement of these systems in HS-mediated hypertension and emotional/cognitive impairment remains elusive.

A recent study published in the British Journal of Pharmacology thoroughly evaluated the aspects of HS-mediated hypertension and emotional/cognitive impairment. According to the published data, the addition of excessive phosphates to the protein “tau” is primarily responsible for this emotional and cognitive consequences. The findings are particularly noteworthy because tau is a key protein of the Alzheimer's disease.

The team first loaded laboratory mice with an HS solution (2% NaCl in drinking water) for 12 weeks and monitored their blood pressure. Next, they also studied the involvement of the Ang II-AT1 and PGE2-EP1 systems in the HS-induced hypertension and neuronal/behavioral impairment.

The brains of the experimental mice had several biochemical alternations. At the molecular level, besides the addition of phosphates to tau, the researchers also observed a decrease in the phosphate groups linked to a key enzyme called “CaMKII”-a protein involved in brain signaling. Moreover, changes in the levels of “PSD95”-a protein that plays a vital role in the organization and function of brain synapses were also evident. Interestingly, the biochemical changes were reversed after the administration of the antihypertensive drug “losartan.” A similar reversal was observed after knocking out the EP1 gene.

Reference:

High salt induces cognitive impairment via the interaction of angiotensin II-AT1 and prostaglandin E2-EP1 systems,British Journal of Pharmacology,DOI: https://doi.org/10.1111/bph.16093