MORIMOTO Satoshi    Department   School of Medicine(Tokyo Women's Medical University Hospital), School of Medicine    Position   Associate Professor
Article types	Original article
Language	English
Peer review	Peer reviewed
Title	Blockade of angiotensin II receptors inhibits the increase in blood pressure induced by insulin.
Journal	Formal name：Journal of cardiovascular pharmacology Abbreviation：J Cardiovasc Pharmacol ISSN code：01602446/01602446
Domestic / Foregin	Foregin
Volume, Issue, Page	31(2),pp.248-52
Author and coauthor	Nakata T, Takeda K, Hatta T, Kiyama M, Moriguchi J, Miki S, Kawa T, Morimoto S, Nakamura K, Uchida A, Itoh H, Sasaki S, Nakagawa M
Publication date	1998/02
Summary	To elucidate whether hyperinsulinemia increases blood pressure by increasing sympathetic outflow via the activation of the central angiotensin system, insulin was infused into urethane-anesthetized rats intravenously (i.v.) or intracerebroventricularly (i.c.v.) under euglycemic conditions. Infusion (i.v.) of insulin elicited pressor effects in a dose-dependent manner (13, 20, and 40 mU/min). Although depressor responses to i.v. injections of hexamethonium were significantly greater in insulin-infused than in saline-infused rats, i.v. captopril and d(CH2)5Tyr(Me)-arginine vasopressin did not show any differences between the groups. Infusions (i.c.v.) of insulin (8 mU/10 microl) also induced cardiovascular acceleration and augmented the depressor response to i.v. hexamethonium in insulin-infused rats. The i.c.v. pretreatment with the angiotensin II antagonist losartan inhibited the pressor responses to both the i.c.v. and i.v. infusion of insulin. These results suggest that the increase in blood pressure induced by euglycemic hyperinsulinemia is elicited by sympathetic activation and that hyperinsulinemia stimulates the angiotensin system in the brain to increase sympathetic nerve activity.
DOI	10.1097/00005344-199802000-00010
PMID	9475266