ArticlePhysiological reports2015
Circulating angiotensin II deteriorates left ventricular function with sympathoexcitation via brain angiotensin II receptor.
Article in Physiological reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
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- Aorticorenal ganglion ablation: a potential neuromodulation approach for blood pressure control.Hypertension research : official journal of the Japanese Society of Hypertension · 2025Article
- Renal denervation for hypertensive heart disease and atrial fibrillation.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Review
- Renal denervation: a key approach to hypertension and cardiovascular disease.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Review
- ATRAP in the paraventricular nucleus of the hypothalamus as another key player in the control of sympathetic outflow.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Article
- The effects of renal denervation on blood pressure, cardiac hypertrophy, and sympathetic activity during the established phase of hypertension in spontaneously hypertensive rats.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Article
- An Insight on Multicentric Signaling of Angiotensin II in Cardiovascular system: A Recent Update.Frontiers in pharmacology · 2021Review
- Neurocardiac regulation: from cardiac mechanisms to novel therapeutic approaches.The Journal of physiology · 2020Review
- Angiotensin peptide synthesis and cyclic nucleotide modulation in sympathetic stellate ganglia.Journal of molecular and cellular cardiology · 2020Article
- TRPV1 (Transient Receptor Potential Vanilloid 1) Cardiac Spinal Afferents Contribute to Hypertension in Spontaneous Hypertensive Rat.Hypertension (Dallas, Tex. : 1979) · 2019Article
- Experimental models of cardiac physiology and pathology.Heart failure reviews · 2019Review
- Central Inhibition of Tumor Necrosis Factor Alpha Reduces Hypertension by Attenuating Oxidative Stress in the Rostral Ventrolateral Medulla in Renovascular Hypertensive Rats.Frontiers in physiology · 2019Article
- Disruption of Central Antioxidant Property of Nuclear Factor Erythroid 2-Related Factor 2 Worsens Circulatory Homeostasis with Baroreflex Dysfunction in Heart Failure.International journal of molecular sciences · 2018Article
- Angiotensin-(1-7) attenuates atrial tachycardia-induced sympathetic nerve remodeling.Journal of the renin-angiotensin-aldosterone system : JRAASArticle
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sympathoexcitation contributes to the progression of heart failure. Activation of brain angiotensin II type 1 receptors (AT1R) causes central sympathoexcitation. Thus, we assessed the hypothesis that the increase in circulating angiotensin II comparable to that reported in heart failure model affects cardiac function through the central sympathoexcitation via activating AT1R in the brain. In Sprague-Dawley rats, the subcutaneous infusion of angiotensin II for 14 days increased the circulating angiotensin II level comparable to that reported in heart failure model rats after myocardial infarction. In comparison with the control, angiotensin II infusion increased 24 hours urinary norepinephrine excretion, and systolic blood pressure. Angiotensin II infusion hypertrophied left ventricular (LV) without changing chamber dimensions while increased end-diastolic pressure. The LV pressure -: volume relationship indicated that angiotensin II did not impact on the end-systolic elastance, whereas significantly increased end-diastolic elastance. Chronic intracerebroventricular infusion of AT1R blocker, losartan, attenuated these angiotensin II-induced changes. In conclusion, circulating angiotensin II in heart failure is capable of inducing sympathoexcitation via in part AT1R in the brain, subsequently leading to LV diastolic dysfunction.
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