Brain RAS: Hypertension and Beyond

Call for Papers

Cardiac output and vascular resistance, that control blood pressure (BP), are regulated through neural, humoral, and local tissue factors. The sympathetic and renin-angiotensin system (RAS) plays major roles. Vasopressin and vasodepressor hormones are also involved.

Angiotensin and its metabolites act as endocrine, paracrine, autocrine, and intracrine regulators.

The clinical efficiency of renin/ACE inhibitors and angiotensin receptors blockers and the presence of their targets in the brain illustrate the interaction with peripheral RAS. The brain RAS regulates blood pressure through sympathetic activation and vasopressin release. Transgenic animal models over- or underexpressing RAS components in a tissue-specific manner illustrate how brain and peripheral RAS interact.

All the constituents of the RAS occur in the brain. In addition, the AT1, AT2, AT4/IRAP, and Mas receptors, aldosterone-synthesizing enzyme are present. Aminopeptidases and other angiotensin-degrading enzymes, for example, ACE2, endopeptidase which form fragments such as Ang III, Ang IV, Ang 2-10, change BP regulation. Ang III in the brain may promote hypertension and Ang IV affects vasopressinase activity. Moreover, the interconnection between neurotransmitters and brain RAS influences behavior and neurological diseases, for example, Parkinson’s and Alzheimer’s. AT1 receptors stimulate DOPA release in the striatum whereas AT2 receptors may decrease dopamine synthesis. Intracerebroventricular infusion of a selective renin inhibitor, aliskiren, reduces salt-induced sympathetic activity and hypertension in Dahl salt-sensitive rats and improves spatial memory and reduces depression in aging Alzheimer’s patients.

We invite contributions of original and review articles regarding the interrelationship of brain, hypertension, and behavior in animal models as well as in patients. Potential topics include, but are not limited to:

• Brain RAS and sympathetic activity
• Brain RAS; angiotensin processing; brain RAS and aldosterone; the prorenin receptor; roles of angiotensin metabolites; inhibitors of brain RAS
• Brain RAS and Dopamine
• Brain RAS and inflammation
• Brain RAS and behavior, obesity, Parkinson’s or Alzheimer’s disease, stress, anxiety, mental retardation

Before submission authors should carefully read over the journal's Author Guidelines, which are located at http://www.hindawi.com/journals/ijht/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/ according to the following timetable:

Lead Guest Editor

• Marc de Gasparo, Rue es Planches 5, 2842 Rossemaison, Switzerland

Guest Editors

• Robert C. Speth, Department of Pharmaceutical Sciences, College of Pharmacy, Nova Southeastern University, Fort Lauderdale, FL 33328-2018, USA
• Ovidiu C. Baltatu, Center of Biomedical Engineering, University Camilo Castelo Branco, Rod. Presidente Dutra Km 138, 12247-004 São José dos Campos, SP, Brazil
• Patrick Vanderheyden, Department of Molecular and Biochemical Pharmacology, Vrije Universiteit Brussel, Pleinlaan 2, 1050 Brussels, Belgium