ArticlePloS one2014
Neuroendocrine humoral and vascular components in the pressor pathway for brain angiotensin II: a new axis in long term blood pressure control.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 41 citations in OpenAlex.
- Ouabain-induced hypertension in rats: Mechanisms, variability and translational implications.Experimental physiology · 2026Review
- Impact of the diverse cardiotonic steroids on beta-amyloid precursor protein level.Frontiers in pharmacology · 2025Article
- Mechanisms mediating effects of cardiotonic steroids in mammalian blood cells.Frontiers in pharmacology · 2025Review
- Sensational site: the sodium pump ouabain-binding site and its ligands.American journal of physiology. Cell physiology · 2024Review
- Review
- NO-induced vasodilation correlates directly with BP in smooth muscle-Na/Ca exchanger-1-engineered mice: elevated BP does not attenuate endothelial function.American journal of physiology. Heart and circulatory physiology · 2021Article
- Reply: "Comment on: Endogenous Ouabain and Related Genes in the Translation from Hypertension to Renal Diseases".International journal of molecular sciences · 2019Article
- Arterial Stiffness in Hypertension: an Update.Current hypertension reports · 2018Review
- Reply to "Letter to the editor: Comments on Blaustein (2018): 'The pump, the exchanger, and the holy spirit: origins and 40-year evolution of ideas about the ouabain-NaAmerican journal of physiology. Cell physiology · 2018Article
- Central and peripheral slow-pressor mechanisms contributing to Angiotensin II-salt hypertension in rats.Cardiovascular research · 2018Article
- The pump, the exchanger, and the holy spirit: origins and 40-year evolution of ideas about the ouabain-NaAmerican journal of physiology. Cell physiology · 2018Review
- How does pressure overload cause cardiac hypertrophy and dysfunction? High-ouabain affinity cardiac NaAmerican journal of physiology. Heart and circulatory physiology · 2017Review
- Update on angiotensin II: new endocrine connections between the brain, adrenal glands and the cardiovascular system.Endocrine connections · 2017Review
- Personalized Management of Cardiovascular Disorders.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2017Review
- Pivotal role of α2 NaThe Journal of physiology · 2016Review
- Low dose ouabain stimulates NaK ATPase α1 subunit association with angiotensin II type 1 receptor in renal proximal tubule cells.Biochimica et biophysica acta · 2016Article
- Endogenous Ouabain: Recent Advances and Controversies.Hypertension (Dallas, Tex. : 1979) · 2016Review
- Lanosterol Synthase Gene Polymorphisms and Changes in Endogenous Ouabain in the Response to Low Sodium Intake.Hypertension (Dallas, Tex. : 1979) · 2016Article
- Arterial α2-Na+ pump expression influences blood pressure: lessons from novel, genetically engineered smooth muscle-specific α2 mice.American journal of physiology. Heart and circulatory physiology · 2015Article
- Endogenous cardiotonic steroids in kidney failure: a review and an hypothesis.Advances in chronic kidney disease · 2015Review
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Central nervous system (CNS) administration of angiotensin II (Ang II) raises blood pressure (BP). The rise in BP reflects increased sympathetic outflow and a slower neuromodulatory pressor mechanism mediated by CNS mineralocorticoid receptors (MR). We investigated the hypothesis that the sustained phase of hypertension is associated also with elevated circulating levels of endogenous ouabain (EO), and chronic stimulation of arterial calcium transport proteins including the sodium-calcium exchanger (NCX1), the type 6 canonical transient receptor potential protein (TRPC6), and the sarcoplasmic reticulum calcium ATPase (SERCA2). Wistar rats received a chronic intra-cerebroventricular infusion of vehicle (C) or Ang II (A, 2.5 ng/min, for 14 days) alone or combined with the MR blocker, eplerenone (A+E, 5 µg/day), or the aldosterone synthase inhibitor, FAD286 (A+F, 25 µg/day). Conscious mean BP increased (P<0.05) in A (123 ± 4 mm Hg) vs all other groups. Blood, pituitary and adrenal samples were taken for EO radioimmunoassay (RIA), and aortas for NCX1, TRPC6 and SERCA2 immunoblotting. Central infusion of Ang II raised plasma EO (0.58 ± 0.08 vs C 0.34 ± 0.07 nM (P<0.05), but not in A + E and A + F groups as confirmed by off-line liquid chromatography (LC)-RIA and LC-multistage mass spectrometry. Two novel isomers of EO were elevated by Ang II; the second less polar isomer increased >50-fold in the A+F group. Central Ang II increased arterial expression of NCX1, TRPC6 and SERCA2 (2.6, 1.75 and 3.7-fold, respectively; P<0.01)) but not when co-infused with E or F. Adrenal and pituitary EO were unchanged. We conclude that brain Ang II activates a CNS-humoral axis involving plasma EO. The elevated EO reprograms peripheral ion transport pathways known to control arterial Na(+) and Ca(2+) homeostasis; this increases contractility and augments sympathetic effects. The new axis likely contributes to the chronic pressor effect of brain Ang II.
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