ArticleInternational journal of hypertension2012
Upregulation of the Renin-Angiotensin-aldosterone-ouabain system in the brain is the core mechanism in the genesis of all types of hypertension.
Article in International journal of hypertension, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Aldosterone in the brain and cognition: knowns and unknowns.Frontiers in endocrinology · 2024Review
- The Brain-Heart Axis: Neuroinflammatory Interactions in Cardiovascular Disease.Current cardiology reports · 2023Review
- Role of Inflammatory Processes in the Brain-Body Relationship Underlying Hypertension.Current hypertension reports · 2023Review
- Endogenous Digitalis-like Factors as a Key Molecule in the Pathophysiology of Pregnancy-Induced Hypertension and a Potential Therapeutic Target in Preeclampsia.International journal of molecular sciences · 2023Review
- Effects of renal denervation on endogenous ouabain in spontaneously hypertensive rats.Acta cirurgica brasileira · 2023Article
- Implications of testicular ACE2 and the renin-angiotensin system for SARS-CoV-2 on testis function.Nature reviews. Urology · 2022Review
- Rapeseed (canola) oil aggravates metabolic syndrome-like conditions in male but not in female stroke-prone spontaneously hypertensive rats (SHRSP).Toxicology reports · 2022Article
- Parental Renovascular Hypertension-Induced Autonomic Dysfunction in Male Offspring Is Improved by Prenatal or Postnatal Treatment With Hydrogen Sulfide.Frontiers in physiology · 2019Article
- Resistant Hypertension: Mechanisms and Treatment.Current hypertension reports · 2017Review
- Pivotal role of α2 NaThe Journal of physiology · 2016Review
- Endogenous Ouabain: Recent Advances and Controversies.Hypertension (Dallas, Tex. : 1979) · 2016Review
- Direct anti-inflammatory effects of angiotensin-(1-7) on microglia.Journal of neurochemistry · 2016Article
- Brain inflammation and hypertension: the chicken or the egg?Journal of neuroinflammation · 2015Review
- Direct pro-inflammatory effects of prorenin on microglia.PloS one · 2014Article
- Age-related autoregulatory dysfunction and cerebromicrovascular injury in mice with angiotensin II-induced hypertension.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2013Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Basic research using animal models points to a causal role of the central nervous system in essential hypertension; however, since clinical research is technically difficult to perform, this connection has not been confirmed in humans. Recently, renal nerve ablation in humans proved to continuously decrease blood pressure in resistant hypertension. Furthermore, when electrical stimulation was continuously applied to the carotid baroreceptor nerve of human adults, their blood pressure lowered. These findings promoted the concept that the central nervous system may actually be involved in the pathogenesis of essential hypertension, which is closely associated with excess sodium intake. We have demonstrated that endogenous digitalis plays a key role in hypertension associated with excess sodium intake via sympathetic activation in rats. Increased sodium concentration inside the brain activates epithelial sodium channels and the renin-angiotensin-aldosterone system in the brain. Aldosterone releases ouabain from neurons in the paraventricular nucleus in the hypothalamus. Angiotensin II and aldosterone of peripheral origin reach the brain to augment sympathetic outflow. Collectively essential hypertension associated with excess sodium intake and obesity, renovascular hypertension, and primary aldosteronism and pseudoaldosteronism all seem to have a common cause originating from the central nervous system.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.