Circulating angiotensin II deteriorates left ventricular function with sympathoexcitation via brain angiotensin II receptor. Issue 8 (19th August 2015)

• Record Type: Journal Article
• Authors: Shinohara, Keisuke; Kishi, Takuya; Hirooka, Yoshitaka; Sunagawa, Kenji
• Is Part Of: Physiological reports. Volume 3:Issue 8(2015:Aug.)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2015-08-19
• Subjects: Physiology -- Periodicals; 571
• DOI: 10.14814/phy2.12514
• Languages: English
• ISSNs: 2051-817X

Abstract

<abstract abstract-type="main" id="phy212514-abs-0001"> <title>Abstract</title> <p>Sympathoexcitation contributes to the progression of heart failure. Activation of brain angiotensin II type 1 receptors (AT<sub>1</sub>R) 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 AT<sub>1</sub>R 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<bold>–</bold>volume relationship indicated that angiotensin II did not impact on the end‐systolic elastance, whereas significantly increased end‐diastolic elastance. Chronic intracerebroventricular infusion of AT<sub>1</sub>R blocker, losartan, attenuated these angiotensin II‐induced changes. In conclusion, circulating angiotensin II in heart failure is capable of inducing sympathoexcitation via in part AT<sub>1</sub>R in the brain, subsequently leading to LV diastolic dysfunction.</p> </abstract>