The involvement of angiotensin II (Ang II)– a hormonal agent that plays a key role in managing blood pressure and fluid balance– and its receptor “AT1”, as well as that of the physiologically essential lipid molecule prostaglandin E2 (PGE2 and its receptor “EP1” in hypertension and neurotoxicity is well-recognized. Nevertheless, the involvement of these systems in HS-mediated hypertension and emotional/cognitive impairment stays elusive.
To this end, a current research study published in the British Journal of Pharmacology completely evaluated the aspects of HS-mediated hypertension and emotional/cognitive problems. The research study was performed by a team of teaming up scientists from Japan, and has actually demonstrated how high blood pressure, mediated by the crosstalk in between Ang II-AT1 and PGE2-EP1 triggers cognitive and psychological dysfunction.
Author Hisayoshi Kubota from Fujita Health Universitys Graduate School of Health Science remarks, “Excessive salt intake is thought about a risk factor for hypertension, cognitive dysfunction, and dementia. Studies focusing on the interaction between the main and peripheral worried system have not sufficiently examined this association.”
According to the published information, the addition of excessive phosphates to the protein “tau” is primarily accountable for these cognitive and emotional effects. Due to the fact that tau is a crucial protein of Alzheimers illness, the findings are particularly noteworthy.
The group initially loaded laboratory mice with an HS solution (2% NaCl in drinking water) for 12 weeks and monitored their high blood pressure. “The effects of HS intake on emotional/cognitive function and tau phosphorylation were also examined in 2 essential areas of the mouse brain– the prefrontal cortex and the hippocampus,” describes Prof. Mouri. Next, they likewise studied the involvement of the Ang II-AT1 and PGE2-EP1 systems in HS-induced hypertension and neuronal/behavioral impairment.
At the molecular level, besides the addition of phosphates to tau, the researchers likewise observed a decrease in the phosphate groups linked to a key enzyme called “CaMKII”– a protein involved in brain signaling. Modifications in the levels of “PSD95”– a protein that plays an important role in the organization and function of brain synapses (the connection between brain cells)– were likewise obvious.
Overall, these findings recommend that angiotensin II-AT1 and prostaglandin E2-EP1 systems could be unique restorative targets for hypertension-induced dementia.
Prof. Mouri concludes by stating, “This study is of specific social and financial importance because the yearly social cost of dementia treatment in Japan is surging like never previously”. Establishing healing and preventive drugs for dementia appears important for Japans rapidly aging population.”
Reference: “High salt induces cognitive disability through the interaction of the angiotensin II-AT1 and prostaglandin E2-EP1 systems” by Hisayoshi Kubota, Kazuo Kunisawa, Bolati Wulaer, Masaya Hasegawa, Hitomi Kurahashi, Takatoshi Sakata, Hiroyuki Tezuka, Masanori Kugita, Shizuko Nagao, Taku Nagai, Tomoyuki Furuyashiki, Shuh Narumiya, Kuniaki Saito, Toshitaka Nabeshima and Akihiro Mouri, 19 April 2023, British Journal of Pharmacology.DOI: 10.1111/ bph.16093.
The research study was funded by the Japan Society for the Promotion of Science, the Japan Science and Technology Agency, Fujita Health University, the Smoking Research Foundation, and the Takeda Science Foundation.
Defined as a deterioration of cognitive functions such as thinking, keeping in mind, and reasoning, dementia is extremely typical in Japan. With an ever-increasing aging population worldwide, the seriousness for the advancement of preventive procedures and restorative drugs for dementia is escalating.
The connection between cognitive problems and excessive consumption of table salt, a staple in food spices, is well developed. High salt (HS) consumption can likewise lead to high blood pressure. Next, they likewise studied the involvement of the Ang II-AT1 and PGE2-EP1 systems in HS-induced hypertension and neuronal/behavioral problems.
A current research study carried out by Japanese scientists has revealed that the interaction of angiotensin II-AT1 and prostaglandin E2-EP1 systems, amplified by high salt intake, triggers hypertension that causes cognitive and psychological problems, which involves changes to tau protein and other enzymes in the brain. These findings, which were reversed by antihypertensive medication and genetic modification, suggest new potential healing targets for hypertension-induced dementia, which is especially substantial given the rising cost of dementia treatment in aging societies like Japan.
Scientists have actually pinpointed 2 essential physiological mechanisms that are included in hypertension induced by high salt consumption and cognitive and psychological disability.
Defined as a degeneration of cognitive functions such as thinking, keeping in mind, and reasoning, dementia is highly common in Japan. As it stands, there is a distinct lack of satisfaction with the treatment of this condition, offered the lack of any alleviative drug therapy. With an ever-increasing aging population worldwide, the urgency for the development of preventive steps and restorative drugs for dementia is intensifying.
The connection between cognitive disability and excessive intake of table salt, a staple in food spices, is well established. High salt (HS) intake can also result in high blood pressure. To avoid negative health effects, the World Health Organization supporters for a constraint on salt usage to under 5 g daily.
