Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 1998 Jan-Feb;4(1):3-24.
doi: 10.1093/humupd/4.1.3.

Role of nitric oxide in the biology, physiology and pathophysiology of reproduction

Affiliations
Free article
Review

Role of nitric oxide in the biology, physiology and pathophysiology of reproduction

M Rosselli et al. Hum Reprod Update. 1998 Jan-Feb.
Free article

Abstract

Following its benchmark discovery, nitric oxide (NO) is now known to play important functional roles in a variety of physiological systems. Within the vasculature, NO induces vasodilation, inhibits platelet aggregation, prevents neutrophil/platelet adhesion to endothelial cells, inhibits smooth muscle cell proliferation and migration, regulates programmed cell death (apoptosis) and maintains endothelial cell barrier function. NO generated by neurons acts as a neurotransmitter, whereas NO generated by macrophages in response to invading microbes acts as an antimicrobial agent. Because neurons, blood vessels and cells of the immune system are integral parts of the reproductive organs, and in view of the important functional role that NO plays in those systems, it is likely that NO is an important regulator of the biology and physiology of the reproductive system. Indeed, in the past 10 years, NO has established itself as a polyvalent molecule which plays a decisive role in regulating multiple functions within the female as well as the male reproductive system. This review provides an overview of the role of NO in various reproductive organs under physiological and pathological conditions.

PubMed Disclaimer

Publication types

MeSH terms