Research Article

Controlled Hemorrhage Sensitizes Angiotensin II-Elicited Hypertension through Activation of the Brain Renin-Angiotensin System Independently of Endoplasmic Reticulum Stress

Figure 7

Schematic representation of controlled hemorrhage-induced hypertensive response sensitization (HTRS) through upregulation of renin-angiotensin system (RAS) prohypertensive effects and downregulation of RAS antihypertensive effects in the peripheral and central nervous system (CNS) network controlling sympathetic nervous system (SNS) drive and blood pressure (BP) including the paraventricular nucleus of hypothalamus (PVN). Endoplasmic reticulum stress (ERS) does not appear to mediate the induction and maintenance of a sensitized state after hypotensive hemorrhage although activation of ERS results in sensitization of angiotensin II-elicited hypertension in the present study.