A study published in the journal Nature shows that inhibiting CD38 synthesis or supplementing NMN can increase the level of 

NAD+ in the body, thereby inhibiting the production of extracellular vesicles, and achieving the purpose of delaying vascular 

cell aging and preventing cardiovascular disease.

Excessive blood pressure will lead to a phenomenon called "Vascular Remodeling", that is, the phenomenon of changes in the 

physiological structure of the vascular wall thickness, lumen diameter and vascular elasticity, especially the decline of lumen 

diameter and vascular elasticity may lead to further aggravation of hypertension, thus falling into a vicious cycle.

In 2021, a research team from Sichuan University found that in a mouse model of hypertension induced by angiotensin II, a 

series of vascular remodeling processes occur in the blood vessel wall of mice, accompanied by accelerated aging; Treatment 

with NMN (nicotinamide mononucleotide) can increase the level of NAD+ (nicotinamide adenine dinucleotide) in vascular cells, 

and effectively inhibit the phenomenon of vascular aging and remodeling. The study was published in Signal Transduction and 

Targeted Therapy, a subsidiary of the journal Nature.

In the experiment, the researchers injected angiotensin II into young mice 8 to 10 weeks old (about 18 years old in humans) for 

four consecutive weeks, making the blood pressure of the mice continue to rise during this time, and the vascular wall thickening 

and vascular elasticity are reduced. The researchers also found that these phenomena were closely related to the presence of CD38 

protein, a consumer of NAD+, and that when mice were treated with a CD38 inhibitor (compound 78c), both elevated blood pressure 

and vascular remodeling were effectively alleviated.

In addition to inhibiting CD38 protein, giving mice 300mg/kg/ day of NMN orally (translated to about 1.35g/ day in humans) can also 

reduce blood pressure and inhibit vascular remodeling.

Notably, in cell culture experiments, the researchers found that high blood pressure caused vascular smooth muscle cells in mice to 

age faster, These senescent cells release senescence associated small extracellular vesicles (SA-sEVs) and further accelerate the aging 

of surrounding cells. However, the addition of NAD+ or CD38 inhibitors in the medium can inhibit this process.

In summary, this study found that hypertension would lead to the remodeling of blood vessels in mice, such as thickening of tube walls 

and decreasing elasticity, and accelerate the aging of vascular smooth muscle cells, which would also release tiny vesicles to further affect 

surrounding cells. The inhibition of NAD+ consuming enzyme CD38, or NMN and other CD38 inhibitors, can effectively alleviate these 

symptoms. This may mean that raising NAD+ levels can help combat the damage that high blood pressure causes to blood vessels.