Related Experiment Video
Updated: May 13, 2026
Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice
Published on: September 28, 2015
Apelin elevates blood pressure in ICR mice with L‑NAME‑induced endothelial dysfunction
Katsumasa Nagano1, Junji Ishida, Madoka Unno
1Life Science Center, Tsukuba Advanced Research Alliance, Graduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba 305‑8577, Japan.
Insights
Apelin normally lowers blood pressure, but in mice with vascular damage, it temporarily increased it. This suggests apelin acts as a vasopressor peptide in conditions of endothelial dysfunction.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
- Pharmacology
Background:
- Apelin, the endogenous ligand for the APJ receptor, is expressed in cardiovascular tissues.
- Apelin typically activates endothelial nitric oxide synthase (eNOS) to lower blood pressure.
- The role of apelin in regulating blood pressure during pathological conditions remains unclear.
Purpose of the Study:
- To investigate the effect of apelin on blood pressure in a mouse model of chronic vascular endothelial dysfunction.
Main Methods:
- Peripheral vascular damage and hypertension were induced in mice using chronic administration of NG-nitro-L-arginine methyl ester (L-NAME).
- Vascular endothelial function and aortic gene expression (VCAM-1, PAI-1, eNOS) were assessed.
- The blood pressure response to apelin was evaluated after L-NAME withdrawal.
Main Results:
- L-NAME treatment induced hypertension, endothelial damage, and impaired vasodilation with reduced eNOS expression.
- While apelin lowered blood pressure in control mice, it transiently elevated blood pressure in L-NAME-treated mice.
- Apelin's effect shifted from hypotensive to vasopressor in the context of endothelial dysfunction.
Conclusions:
- Apelin can function as a vasopressor peptide under pathological conditions characterized by vascular endothelial dysfunction.
- These findings highlight a context-dependent role for apelin in blood pressure regulation.
- Further research is warranted to explore apelin's therapeutic potential in cardiovascular diseases.
Abstract:
Apelin is the endogenous ligand of APJ, which belongs to the family of G protein‑coupled receptors. Apelin and APJ are highly expressed in various cardiovascular tissues, including the heart, kidney and vascular endothelial and smooth muscle cells. Although apelin exerts hypotensive effects via activation of endothelial nitric oxide synthase (eNOS), the ability of apelin to regulate blood pressure under pathological conditions is poorly understood. In the current study, NG‑nitro‑L‑arginine methyl ester (L‑NAME), a potent NOS inhibitor, was administered chronically, to induce peripheral vascular damage in mice. L‑NAME‑treated mice exhibited hypertension, increased vascular cell adhesion molecule‑1 and plasminogen activator inhibitor‑1 mRNA levels in the aorta and impaired vasodilatation associated with decreased aortic eNOS expression, consistent with endothelial damage. Three days following withdrawal of L‑NAME treatment, the blood pressure response to apelin stimulation was assessed. Although apelin reduced blood pressure in non‑treated mice, it was found to transiently elevate blood pressure in L‑NAME‑treated mice. These results indicate that apelin functions as a vasopressor peptide under pathological conditions, including vascular endothelial dysfunction in mice.
More Related Videos
Related Concept Videos
01:30Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors
01:30Antihypertensive Drugs: Angiotensin II Receptor Blockers