Abstract
The present study was performed to explore a possible vascular interplay between nitric oxide (NO) and calcitonin gene-related peptide (CGRP). We examined factors affecting CGRP release by the NO donor, nitroglycerin (NTG) and the potential involvement of endothelial NO synthase (eNOS) using eNOS knockout (-/-) vs. wild-type (+/+) mice. In the female eNOS (+/+) mice, but not in males, in vitro NTG (0.73 mM) induced significant increases in the release of CGRP-like immunoreactivity (CGRP-LI) from the aorta and the heart but not from the small intestine. In eNOS (-/-) mice, NTG incubation did not induce any CGRP-LI changes in either gender. These results suggest that NTG-induced CGRP release is eNOS-dependent and tissue- and gender-selective. The functional implication of this NO-CGRP interaction was further examined by testing the anti-aggregatory action of acetylcholine (Ach). Ach-induced platelet inhibition was significantly enhanced by the addition of aorta segments of either gender. However, the female aorta segments exhibited a greater platelet inhibitory effect, which could be reversed by the blockade of either CGRP or eNOS. Our study revealed a novel eNOS-dependent interaction between NO and CGRP, and the possible participation of regulatory peptides in affecting platelet function and possibly cardiovascular protection in females.
Original language | English (US) |
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Pages (from-to) | 115-122 |
Number of pages | 8 |
Journal | Regulatory Peptides |
Volume | 110 |
Issue number | 2 |
DOIs | |
State | Published - Jan 31 2003 |
Externally published | Yes |
Keywords
- Acetylcholine
- Knockout
- Nitroglycerin
- Platelet inhibition
- Vasculature
ASJC Scopus subject areas
- Biochemistry
- Physiology
- Endocrinology
- Clinical Biochemistry
- Cellular and Molecular Neuroscience