ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2014
CNS neuroplasticity and salt-sensitive hypertension induced by prior treatment with subpressor doses of ANG II or aldosterone.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- Chronic intermittent hypoxia increases EPSC frequency in median preoptic nucleus neurons through BDNF-TrkB signaling in a sex-dependent manner.Journal of neurophysiology · 2026Article
- Central nervous system mechanisms of salt-sensitive hypertension.Physiological reviews · 2025Review
- The interaction of BDNF with estrogen in the development of hypertension and obesity, particularly during menopause.Frontiers in endocrinology · 2024Review
- Predator Scent-Induced Sensitization of Hypertension and Anxiety-like Behaviors.Cellular and molecular neurobiology · 2022Article
- Central Ang II (Angiotensin II)-Mediated Sympathoexcitation: Role for HIF-1α (Hypoxia-Inducible Factor-1α) Facilitated Glutamatergic Tone in the Paraventricular Nucleus of the Hypothalamus.Hypertension (Dallas, Tex. : 1979) · 2021Article
- Sympathetic Nervous System Contributions to Hypertension: Updates and Therapeutic Relevance.The Canadian journal of cardiology · 2020Review
- Central nervous system neuroplasticity and the sensitization of hypertension.Nature reviews. Nephrology · 2018Review
- ATAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
- Differential effects of long-term slow-pressor and subpressor angiotensin II on contractile and relaxant reactivity of resistance versus conductance arteries.Physiological reports · 2018Article
- Recent Advances in Neurogenic Hypertension: Dietary Salt, Obesity, and Inflammation.Hypertension (Dallas, Tex. : 1979) · 2017Review
- Central TrkB blockade attenuates ICV angiotensin II-hypertension and sympathetic nerve activity in male Sprague-Dawley rats.Autonomic neuroscience : basic & clinical · 2017Article
- A Single Angiotensin II Hypertensive Stimulus Is Associated with Prolonged Neuronal and Immune System Activation in Wistar-Kyoto Rats.Frontiers in physiology · 2017Article
- Possible role for brain prostanoid pathways in the development of angiotensin II-salt hypertension in rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Article
- Central Renin-Angiotensin System Activation and Inflammation Induced by High-Fat Diet Sensitize Angiotensin II-Elicited Hypertension.Hypertension (Dallas, Tex. : 1979) · 2016Article
- The roles of sensitization and neuroplasticity in the long-term regulation of blood pressure and hypertension.American journal of physiology. Regulatory, integrative and comparative physiology · 2015Review
- Estrogen regulation of the brain renin-angiotensin system in protection against angiotensin II-induced sensitization of hypertension.American journal of physiology. Heart and circulatory physiology · 2014Article
- Genetic knockdown of brain-derived neurotrophic factor in the nervous system attenuates angiotensin II-induced hypertension in mice.Journal of the renin-angiotensin-aldosterone system : JRAASArticle
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Although sensitivity to high dietary NaCl is regarded to be a risk factor for cardiovascular disease, the causes of salt-sensitive hypertension remain elusive. Previously, we have shown that rats pretreated with subpressor doses of either ANG II or aldosterone (Aldo) show sensitized hypertensive responses to a mild pressor dose of ANG II when tested after an intervening delay. The current studies investigated whether such treatments will induce salt sensitivity. In studies employing an induction-delay-expression experimental design, male rats were instrumented for chronic mean arterial pressure (MAP) recording. In separate experiments, ANG II, Aldo, or vehicle was delivered either subcutaneously or intracerebroventricularly during the induction. There were no sustained differences in BP during the delay prior to being given 2% saline. While consuming 2% saline during the expression, both ANG II- and Aldo-pretreated rats showed significantly greater hypertension. When hexamethonium was used to assess autonomic control of MAP, no differences in the decrease of MAP in response to ganglionic blockade were detected during the induction. However, during the expression, the fall was greater in sensitized rats. In separate experiments, brain tissue that was collected at the end of delay showed increases in message or activation of putative markers of neuroplasticity (i.e., brain-derived neurotrophic factor, p38 mitogen-activated protein kinase, and cAMP response element-binding protein). These experiments demonstrate that prior administration of nonpressor doses of either ANG II or Aldo will induce salt sensitivity. Collectively, our findings indicate that treatment with subpressor doses of ANG II and Aldo initiate central neuroplastic changes that are involved in hypertension of different etiologies.
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