ArticleAmerican journal of physiology. Heart and circulatory physiology2015
Macrophage depletion lowers blood pressure and restores sympathetic nerve α2-adrenergic receptor function in mesenteric arteries of DOCA-salt hypertensive rats.
Article in American journal of physiology. Heart and circulatory physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 37 citations in OpenAlex.
- Macrophage-Dependent Intercellular Crosstalk in Multiphenotypic Heart Failure With Preserved Ejection Fraction.Journal of the American Heart Association · 2026Review
- Polyethylene terephthalate microplastics impair erectile function through macrophage mediated cGAS-STING ferroptosis.iScience · 2026Article
- Article
- Immune profiling of murine cardiac leukocytes identifies triggering receptor expressed on myeloid cells 2 as a novel mediator of hypertensive heart failure.Cardiovascular research · 2023Article
- The immunology of heart failure with preserved ejection fraction.Clinical science (London, England : 1979) · 2023Review
- Role of monocytes/macrophages in renin-angiotensin system-induced hypertension and end organ damage.Frontiers in physiology · 2023Review
- Pathophysiology and genetics of salt-sensitive hypertension.Frontiers in physiology · 2022Review
- Mineralocorticoid receptor antagonists in diabetic kidney disease - mechanistic and therapeutic effects.Nature reviews. Nephrology · 2022Review
- Myeloid Angiotensin II Type 1 Receptor Mediates Macrophage Polarization and Promotes Vascular Injury in DOCA/Salt Hypertensive Mice.Frontiers in pharmacology · 2022Article
- Reversal of pulmonary arterial hypertension and neointimal formation by kinin B1 receptor blockade.Respiratory research · 2021Article
- Angiotensin-II activates vascular inflammasome and induces vascular damage.Vascular pharmacology · 2021Article
- Ablation of TRPV1-positive nerves exacerbates salt-induced hypertension and tissue injury in rats after renal ischemia-reperfusion via infiltration of macrophages.Clinical and experimental hypertension (New York, N.Y. : 1993) · 2021Article
- Aldosterone, Inflammation, Immune System, and Hypertension.American journal of hypertension · 2021Review
- Immunity and Hypertension.Acta physiologica (Oxford, England) · 2021Review
- Depletion of macrophages slows the early progression of renal injury in obese Dahl salt-sensitive leptin receptor mutant rats.American journal of physiology. Renal physiology · 2020Article
- Brain perivascular macrophages contribute to the development of hypertension in stroke-prone spontaneously hypertensive rats via sympathetic activation.Hypertension research : official journal of the Japanese Society of Hypertension · 2020Article
- Macrophage Depletion Improves Endothelial Insulin Resistance and Protects against Cardiovascular Injury in Salt-Sensitive Hypertension.BioMed research international · 2020Article
- Salt-sensitive increase in macrophages in the kidneys of Dahl SS rats.American journal of physiology. Renal physiology · 2019Article
- Inflammation in Salt-Sensitive Hypertension and Renal Damage.Current hypertension reports · 2018Review
- Deactivation of 12(S)-HETE through (ω-1)-hydroxylation and β-oxidation in alternatively activated macrophages.Journal of lipid research · 2018Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
We tested the hypothesis that vascular macrophage infiltration and O2 (-) release impairs sympathetic nerve α2-adrenergic autoreceptor (α2AR) function in mesenteric arteries (MAs) of DOCA-salt hypertensive rats. Male rats were uninephrectomized or sham operated (sham). DOCA pellets were implanted subcutaneously in uninephrectomized rats who were provided high-salt drinking water or high-salt water with apocynin. Sham rats received tap water. Blood pressure was measured using radiotelemetry. Treatment of sham and DOCA-salt rats with liposome-encapsulated clodronate was used to deplete macrophages. After 3-5, 10-13, and 18-21 days of DOCA-salt treatment, MAs and peritoneal fluid were harvested from euthanized rats. Norepinephrine (NE) release from periarterial sympathetic nerves was measured in vitro using amperometry with microelectrodes. Macrophage infiltration into MAs as well as TNF-α and p22(phox) were measured using immunohistochemistry. Peritoneal macrophage activation was measured by flow cytometry. O2 (-) was measured using dihydroethidium staining. Hypertension developed over 28 days, and apocynin reduced blood pressure on days 18-21. O2 (-) and macrophage infiltration were greater in DOCA-salt MAs compared with sham MAs after day 10. Peritoneal macrophage activation occurred after day 10 in DOCA-salt rats. Macrophages expressing TNF-α and p22(phox) were localized near sympathetic nerves. Impaired α2AR function and increased NE release from sympathetic nerves occurred in MAs from DOCA-salt rats after day 18. Macrophage depletion reduced blood pressure and vascular O2 (-) while restoring α2AR function in DOCA-salt rats. Macrophage infiltration into the vascular adventitia contributes to increased blood pressure in DOCA-salt rats by releasing O2 (-), which disrupts α2AR function, causing enhanced NE release from sympathetic nerves.
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