title: Large blood pressure variability and hypertensive cardiac remodeling--role of cardiac inflammation.
abstract: An increase in short-term blood pressure (BP) variability is a characteristic feature of hypertensive patients, especially in elderly patients. There is increasing evidence that large BP variability aggravates hypertensive target organ damage and is an independent risk factor for the cardiovascular events in elderly hypertensive patients. However, little is known about the underlying mechanism. We have created a rat model of a combination of hypertension and large BP variability by performing sinoaortic denervation (SAD) in spontaneously hypertensive rats (SHRs). SAD aggravates left ventricular (LV)/myocyte hypertrophy and myocardial fibrosis to a greater extent and impairs LV systolic function without changing mean BP in SHR. SAD upregulates cardiac monocyte chemoattractant protein-1 and transforming growth factor-beta, and induces macrophage infiltration. Cardiac angiotensinogen expression is increased and the angiotensin II type 1 receptor is activated by SAD. A subdepressor dose of angiotensin receptor blocker abolishes SAD-induced inflammatory changes and cardiac remodeling and subsequently prevents systolic dysfunction in SHR+SAD. Accordingly, it is suggested that cardiac inflammation via activation of the cardiac angiotensin II system would play a role in the aggravation of cardiac remodeling and dysfunction in hypertensives with large BP variability.
authors.affiliation: Department of Internal Medicine, Division of Cardio-Vascular Medicine, Kurume University School of Medicine, Kurume, Japan. naikai@med.kurume-u.ac.jp
authors.forename: Hisashi
authors.initials: H
authors.lastname: Kai
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kudo
authors.forename: Narimasa
authors.initials: N
authors.lastname: Takayama
authors.forename: Suguru
authors.initials: S
authors.lastname: Yasuoka
authors.forename: Hidemi
authors.initials: H
authors.lastname: Kajimoto
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Imaizumi
mesh_terms: D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D001794:Blood Pressure; D004195:Disease Models, Animal; D005355:Fibrosis; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D008264:Macrophages / Q000378:metabolism; D009205:Myocarditis / Q000150:complications / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D011918:Rats, Inbred SHR; D044140:Receptor, Angiotensin, Type 1 / Q000378:metabolism; D013562:Sympathectomy; D013997:Time Factors; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling
chemical_list: D044140:Receptor, Angiotensin, Type 1; D000804:Angiotensin II