ReviewFrontiers in physiology2019
Mechanisms Responsible for Genetic Hypertension in Schlager BPH/2 Mice.
Review in Frontiers in physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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30 citing papers in PubMed, 37 citations in OpenAlex.
- Hypertension and brain damage: evidence from rodent models.Laboratory animal research · 2026Review
- Peripartum dapagliflozin improves late-life maternal cardiovascular outcomes in a murine model of superimposed preeclampsia.American journal of obstetrics and gynecology · 2025Article
- Hypertensive BPH/2J mice exhibit sex-specific heart failure progression and late-life microvascular rarefaction.American journal of physiology. Heart and circulatory physiology · 2025Article
- Cullin-3 regulates the renal baroreceptor machinery that controls renin gene expression.JCI insight · 2025Article
- The pathogenesis of cerebral small vessel disease and vascular cognitive impairment.Physiological reviews · 2025Review
- Differential composition of lymphocyte subpopulations and activation between the hypertensive Bph/2 and normotensive Bpn/3 mouse strains.Frontiers in immunology · 2025Article
- Malaria and Hypertension: What Is the Direction of Association?Function (Oxford, England) · 2024Article
- The P2Y6 Receptor as a Potential Keystone in Essential Hypertension.Function (Oxford, England) · 2024Article
- α1Journal of the American Heart Association · 2024Article
- Review
- Pathophysiology of cerebral small vessel disease: a journey through recent discoveries.The Journal of clinical investigation · 2024Review
- Hypertension Increases Susceptibility to Experimental Malaria in Mice.Function (Oxford, England) · 2024Article
- Reprogramming endothelial and vascular smooth muscle cells to prevent and treat hypertension.Medical hypotheses · 2023Article
- Cardiovascular characterisation of a novel mouse model that combines hypertension and diabetes co-morbidities.Scientific reports · 2023Article
- Neurogenic Hypertension, the Blood-Brain Barrier, and the Potential Role of Targeted Nanotherapeutics.International journal of molecular sciences · 2023Review
- Mouse models of cerebral injury and cognitive impairment in hypertension.Frontiers in aging neuroscience · 2023Review
- The Role of the Paraventricular-Coerulear Network on the Programming of Hypertension by Prenatal Undernutrition.International journal of molecular sciences · 2022Review
- Left Atrial Myocardium in Arterial Hypertension.Cells · 2022Review
- Bone marrow endothelial dysfunction promotes myeloid cell expansion in cardiovascular disease.Nature cardiovascular research · 2022Article
- Oral Lisinopril Raises Tissue Levels of ACE2, the SARS-CoV-2 Receptor, in Healthy Male and Female Mice.Frontiers in pharmacology · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been 45 years since Gunther Schlager used a cross breeding program in mice to develop inbred strains with high, normal, and low blood pressure (BPH/2, BPN/3, and BPL/1 respectively). Thus, it is timely to gather together the studies that have characterized and explored the mechanisms associated with the hypertension to take stock of exactly what is known and what remains to be determined. Growing evidence supports the notion that the mechanism of hypertension in BPH/2 mice is predominantly neurogenic with some of the early studies showing aberrant brain noradrenaline levels in BPH/2 compared with BPN/3. Analysis of the adrenal gland using microarray suggested an association with the activity of the sympathetic nervous system. Indeed, in support of this, there is a larger depressor response to ganglion blockade, which reduced blood pressure in BPH/2 mice to the same level as BPN/3 mice. Greater renal tyrosine hydroxylase staining and greater renal noradrenaline levels in BPH/2 mice suggest sympathetic hyperinnervation of the kidney. Renal denervation markedly reduced the blood pressure in BPH/2 but not BPN/3 mice, confirming the importance of renal sympathetic nervous activity contributing to the hypertension. Further, there is an important contribution to the hypertension from miR-181a and renal renin in this strain. BPH/2 mice also display greater neuronal activity of amygdalo-hypothalamic cardiovascular regulatory regions. Lesions of the medial nucleus of the amygdala reduced the hypertension in BPH/2 mice and abolished the strain difference in the effect of ganglion blockade, suggesting a sympathetic mechanism. Further studies suggest that aberrant GABAergic inhibition may play a role since BPH/2 mice have low GABA
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