ArticleCirculation research2009
Shift to an involvement of phosphatidylinositol 3-kinase in angiotensin II actions on nucleus tractus solitarii neurons of the spontaneously hypertensive rat.
Article in Circulation research, 2009. 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, 33 citations in OpenAlex.
- Angiotensin II Disrupts Axo-Axonal Interaction-Mediated Vasorelaxation in Basilar Arteries of Normotensive and Hypertensive Rats.Biomedicines · 2026Article
- The Cholinergic Amelioration of Sepsis-Induced Baroreflex Dysfunction and Brainstem Inflammation Is Negated by Central Adenosine A3 Receptors.Pharmaceuticals (Basel, Switzerland) · 2025Article
- NLRP4 renders pancreatic cancer resistant to olaparib through promotion of the DNA damage response and ROS-induced autophagy.Cell death & disease · 2024Article
- Neurogenic Hypertension, the Blood-Brain Barrier, and the Potential Role of Targeted Nanotherapeutics.International journal of molecular sciences · 2023Review
- Six Decades of History of Hypertension Research at the University of Toledo: Highlighting Pioneering Contributions in Biochemistry, Genetics, and Host-Microbiota Interactions.Current hypertension reports · 2022Review
- Hypertension in chronic kidney disease: What lies behind the scene.Frontiers in pharmacology · 2022Review
- Role of PI3-Kinase in Angiotensin II-Induced Cardiac Hypertrophy: Class I Versus Class III.Frontiers in pharmacology · 2021Article
- NOX Modifiers-Just a Step Away from Application in the Therapy of Airway Inflammation?Antioxidants & redox signaling · 2015Review
- Multiscale model of dynamic neuromodulation integrating neuropeptide-induced signaling pathway activity with membrane electrophysiology.Biophysical journal · 2015Article
- Angiotensin-II-derived reactive oxygen species on baroreflex sensitivity during hypertension: new perspectives.Frontiers in physiology · 2013Article
- Differences in oxidative stress status and expression of MKP-1 in dorsal medulla of transgenic rats with altered brain renin-angiotensin system.American journal of physiology. Regulatory, integrative and comparative physiology · 2012Article
- Timing and efficacy of alternative methods of sympathetic blockade.Current hypertension reports · 2012Review
- Angiotensin-(1-7) attenuates the chronotropic response to angiotensin II via stimulation of PTEN in the spontaneously hypertensive rat neurons.American journal of physiology. Heart and circulatory physiology · 2012Article
- Autonomic-immune-vascular interaction: an emerging concept for neurogenic hypertension.Hypertension (Dallas, Tex. : 1979) · 2011Review
- 20-HETE increases NADPH oxidase-derived ROS production and stimulates the L-type Ca2+ channel via a PKC-dependent mechanism in cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2010Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
rationaleCentral angiotensin (Ang) II inhibits baroreflex and plays an important role in the pathogenesis of hypertension. However, the underlying molecular mechanisms are still not fully understood.
objectiveOur objective in the present study was to characterize the signal transduction mechanism of phosphatidylinositol 3-kinase (PI3K) involvement in Ang II-induced stimulation of central neuronal activity in cultured neurons and Ang II-induced inhibition of baroreflex in spontaneously hypertensive rats (SHR) versus WKY rats. METHODS AND
resultsApplication of Ang II to neurons produced a 42% greater increase in neuronal firing in cells from the SHR than the WKY rat. Although the Ang II-mediated increase in firing rate was abolished entirely by the protein kinase (PK)C inhibitor GF109230 in the WKY, blockade of both PKC and PI3K activity was necessary in the SHR. This was associated with an increased ability of Ang II to stimulate NADPH oxidase-reactive oxygen species (ROS)-mediated signaling involving phosphorylation of the p47phox subunit of the NADPH oxidase and was dependent on the activation of PI3K in the SHR. Inhibition of PI3K resulted in the reduction of levels of p47phox phosphorylation, NADPH oxidase activity, ROS levels, and ultimately neuronal activity in cells from the SHR but not the WKY rat. In addition, in working heart-brainstem preparations, inhibition of PKC activity in the nucleus of the solitary tract in situ abolished the Ang II-mediated depression of cardiac and sympathetic baroreceptor reflex gain in the WKY. In contrast, PKC inhibition in the nucleus of the solitary tract of SHR only partially reduced the effect of Ang II on the baroreceptor reflex gain.
conclusionsThese observations demonstrate that PI3K in the cardiovascular brainstem regions of the SHR may be selectively involved in Ang II-mediated signaling that includes a reduction in baroreceptor reflex function, presumably via a NADPH-ROS mediated pathway.
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