Angiotensin (1-7) vs NAD+

Binds Mas receptor (MasR), activating nitric oxide synthase and reducing oxidative stress. Opposes TGF-β and angiotensin II signaling to reduce fibrosis. Enhances insulin sensitivity and provides cardiovascular protection.

A heptapeptide formed from angiotensin II via ACE2 cleavage, or from angiotensin I via neprilysin. Acts as the endogenous counter-regulatory axis to angiotensin II — producing vasodilation, anti-fibrotic, and metabolic benefits via the Mas receptor.

NAD+ is a coenzyme central to cellular energy metabolism, serving as an electron carrier in glycolysis, the citric acid cycle, and oxidative phosphorylation. It is also a required substrate for sirtuins (SIRT1–7) and PARP enzymes, which regulate DNA repair, gene expression, and mitochondrial biogenesis. NAD+ levels decline measurably with age; IV or subcutaneous delivery aims to restore intracellular pools more directly than oral precursors such as NMN or NR.

NAD+ (nicotinamide adenine dinucleotide) is a coenzyme found in every cell, central to energy production, DNA repair, and sirtuin activation. While not a peptide in the traditional sense, it is widely administered by functional medicine and longevity providers via intravenous infusion or subcutaneous injection. Research interest centres on its role in mitochondrial health, cellular resilience, and neurological function as NAD+ levels decline with age.