ArticleClinical science (London, England : 1979)2022
Hypertension induces gonadal macrophage imbalance, inflammation, lymphangiogenesis, and dysfunction.
Article in Clinical science (London, England : 1979), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Blood pressure reduction and anti-inflammatory macrophage augmentation attenuate uterine immune dysregulation and inflammation in mice with salt-sensitive hypertension.Clinical science (London, England : 1979) · 2025Article
- Hypertension: a lymphatic disease?Clinical science (London, England : 1979) · 2025Review
- Sodium-Directed Crosstalk Between Immune Cells and Lymphatic Vessels.Current hypertension reports · 2025Review
- High-intensity interval training reduces inflammatory mediator levels in the testes of spontaneously hypertensive rats.Animal reproduction · 2025Article
- Systemic alpha-1 adrenergic receptor inhibition reduces sperm damage in adult and aging spontaneously hypertensive rats.Scientific reports · 2024Article
- Differential changes in end organ immune cells and inflammation in salt-sensitive hypertension: effects of lowering blood pressure.Clinical science (London, England : 1979) · 2024Article
- Differential changes in end organ immune cells and inflammation in salt-sensitive hypertension: effects of increasing M2 macrophages.Clinical science (London, England : 1979) · 2024Article
- The aging ovary impairs acute stroke outcomes.Journal of neuroinflammation · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Hypertension (HTN) is associated with gonadal dysfunction and impaired reproductive health in both men and women. An imbalance in the systemic and renal proinflammatory (M1)/anti-inflammatory (M2) macrophage ratio, increased inflammation, and inflammation-associated lymphangiogenesis have been observed in animals with HTN. However, the impact of HTN on gonadal macrophages, inflammation, and lymphatics remains obscure. We hypothesized that salt-sensitive HTN (SSHTN) and HTN alters gonadal macrophage polarization, which is associated with inflammation, inflammation-associated lymphangiogenesis, and reproductive dysfunction. Flow cytometry analyses revealed a significant increase in M1 macrophages in the testes of SSHTN and nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced HTN (LHTN) mice, with a concurrent decrease in M2 macrophages in SSHTN mice yet an increase in M2 macrophages in LHTN mice. Ovaries from SSHTN mice exhibited an increase in M1 and a decrease in M2 macrophages, while ovaries from LHTN mice had a significant increase in M2 and a decrease in M1 macrophages. Gene expression patterns of proinflammatory cytokines revealed gonadal inflammation in all hypertensive mice. Increased lymphatic vessel density in the gonads of both male and female hypertensive mice was confirmed by immunofluorescence staining for lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1). HTN adversely affected the expression pattern of steroidogenic enzymes, hormone receptors, and secretory proteins in both the testes and ovaries. In line with these results, male hypertensive mice also presented with decreased sperm concentration, and increased percentage of sperm with abnormal morphology, damaged acrosome, and nonfunctional mitochondrial activity. These data demonstrate that HTN alters gonadal macrophage polarization, which is associated with gonadal inflammation, inflammation-associated lymphangiogenesis, and dysfunction.
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