Nitric Oxide Levels May Impact Severity of Heart Disease


Published Date : May 15, 2018

In a new study undertaken by researchers from the School of Medicine - Case Western Reserve University suggests that nitric oxide many have a major role in how medicines for heart failure function, often maximizing the benefits of the drugs while also improving the function of the heart. In turn, it has also been found that the deficiency of nitric oxide could be an underlying reason resulting in hear failure while orienting the effects of drugs towards side effects and more harmful pathways.

The study shows that the key heart receptors that respond to medicines, knows as G protein-coupled receptors or GPCRs, do not function without nitric oxide. These receptors reside on the surface of cells and are presently the targets for nearly 1/3rd of all FDA-approved heart drugs. When heart drugs are attached to these receptors, they have an influence on the protein pathways that are located inside the cells. One pathway activates the G proteins in the cells, which are of therapeutic benefits and the other pathway triggers the activation of arrestins, which can lead to side effects. According to the study, nitric oxide helps in determining that the beneficial pathway is activated.

The results suggest that the severity of heart failure could see variations based on the levels of nitric oxide in the body. Low levels of the compound make it difficult for the heart to go back to its normal contractibility and increase heart beats, thus it could fail. As the body has hundreds of GPCRs, the findings of the study could have universal appeal. According to the researchers, managing the level of nitric oxide in the body could help all varieties of existing drugs work in a better way leading to fewer side effects.

This suggestion stems from the observation that GPCR signaling across all types of cells and tissues is regulated by nitric oxide. This may also have a direct impact on a number of diseases and the expected response to therapeutic agents.