Voluntary Exercise Prevents Hypertensive Response Sensitization Induced by Angiotensin II.

Exercise training has profound effects on the renin-angiotensin system, inflammatory cytokines and oxidative stress, all of which affect autonomic nervous system activity and regulate blood pressure (BP) in both physiological and pathophysiological states. Using the Induction-Delay-Expression paradigm, our previous studies demonstrated that various challenges (stressors) during Induction resulted in hypertensive response sensitization (HTRS) during Expression. The present study tested whether voluntary exercise would protect against subpressor angiotensin (ANG) II-induced HTRS in rats.

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

Hemorrhagic shock is associated with activation of renin-angiotensin system (RAS) and endoplasmic reticulum stress (ERS). Previous studies demonstrated that central RAS activation produced by various challenges sensitizes angiotensin (Ang) II-elicited hypertension and that ERS contributes to the development of neurogenic hypertension. The present study investigated whether controlled hemorrhage could sensitize Ang II-elicited hypertension and whether the brain RAS and ERS mediate this sensitization.

[Changes of protein kinase C activity in experimental presyrinx state in rabbits].

Objective: To investigate the changes of protein kinase C (PKC) activity and its role in the development of presyrinx state in rabbits.

Methods: Presyrinx state was established in 56 rabbits by intra-cisternal injection of kaolin. At 1, 3, 7, 14, and 21 days after the injection, the water content in the upper cervical spinal cord was measured, its pathological changes observed microscopically and the PKC activity determined with substrate phosphorolysis kinase assay.