ArticleHypertension (Dallas, Tex. : 1979)2016
Selective Deletion of the Brain-Specific Isoform of Renin Causes Neurogenic Hypertension.
Article in Hypertension (Dallas, Tex. : 1979), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 46 citations in OpenAlex.
- The choroid plexus is a source of active renin in the central nervous system.Research square · 2026Article
- Definitive Evidence for the Identification and Function of Renin-Expressing Cholinergic Neurons in the Nucleus Ambiguus.Hypertension (Dallas, Tex. : 1979) · 2025Article
- Therapeutic Implications of Renin-Angiotensin System Modulators in Alzheimer's Dementia.Pharmaceutics · 2023Review
- Angiotensin II increases respiratory rhythmic activity in the preBötzinger complex without inducing astroglial calcium signaling.Frontiers in cellular neuroscience · 2023Article
- Renin-a in the Subfornical Organ Plays a Critical Role in the Maintenance of Salt-Sensitive Hypertension.Biomolecules · 2022Article
- Role of the renin-angiotensin system in the development of COVID-19-associated neurological manifestations.Frontiers in cellular neuroscience · 2022Review
- Methods for the ComprehensiveFrontiers in physiology · 2022Article
- Renal denervation based on experimental rationale.Hypertension research : official journal of the Japanese Society of Hypertension · 2021Review
- Article
- Failure to vasodilate in response to salt loading blunts renal blood flow and causes salt-sensitive hypertension.Cardiovascular research · 2021Article
- Studies of salt and stress sensitivity on arterial pressure in renin-b deficient mice.PloS one · 2021Article
- Angiotensin dependent and angiotensin independent protective effects of renin-b in H9c2 cells after anoxia.Scientific reports · 2020Article
- Increased Susceptibility of Mice Lacking Renin-b to Angiotensin II-Induced Organ Damage.Hypertension (Dallas, Tex. : 1979) · 2020Article
- Neuromodulation Therapy in Heart Failure: Combined Use of Drugs and Devices.The Journal of innovations in cardiac rhythm management · 2020Article
- Role of brain renin angiotensin system in neurodegeneration: An update.Saudi journal of biological sciences · 2020Review
- The Renin-Angiotensin System in the Central Nervous System and Its Role in Blood Pressure Regulation.Current hypertension reports · 2020Review
- Revisiting the Brain Renin-Angiotensin System-Focus on Novel Therapies.Current hypertension reports · 2019Review
- Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology.Physiological reviews · 2018Review
- Potential mechanisms of hypothalamic renin-angiotensin system activation by leptin and DOCA-salt for the control of resting metabolism.Physiological genomics · 2017Review
- Selective Deletion of Renin-b in the Brain Alters Drinking and Metabolism.Hypertension (Dallas, Tex. : 1979) · 2017Article
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9 authors at 1 institution in 1 country.
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Abstract
The renin-angiotensin system (RAS) in the brain is a critical determinant of blood pressure, but the mechanisms regulating RAS activity in the brain remain unclear. Expression of brain renin (renin-b) occurs from an alternative promoter-first exon. The predicted translation product is a nonsecreted enzymatically active renin whose function is unknown. We generated a unique mouse model by selectively ablating the brain-specific isoform of renin (renin-b) while preserving the expression and function of the classical isoform expressed in the kidney (renin-a). Preservation of renal renin was confirmed by measurements of renin gene expression and immunohistochemistry. Surprisingly, renin-b-deficient mice exhibited hypertension, increased sympathetic nerve activity to the kidney and heart, and impaired baroreflex sensitivity. Whereas these mice displayed decreased circulating RAS activity, there was a paradoxical increase in brain RAS activity. Physiologically, renin-b-deficient mice exhibited an exaggerated depressor response to intracerebroventricular administration of losartan, captopril, or aliskiren. At the molecular level, renin-b-deficient mice exhibited increased expression of angiotensin-II type 1 receptor in the paraventricular nucleus, which correlated with an increased renal sympathetic nerve response to leptin, which was dependent on angiotensin-II type 1 receptor activity. Interestingly, despite an ablation of renin-b expression, expression of renin-a was significantly increased in rostral ventrolateral medulla. These data support a new paradigm for the genetic control of RAS activity in the brain by a coordinated regulation of the renin isoforms, with expression of renin-b tonically inhibiting expression of renin-a under baseline conditions. Impairment of this control mechanism causes neurogenic hypertension.
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