The Central Peptidergic Stimulation Syndrome: A Role for Brain Peptides in Central Mechanisms of Blood Pressure Regulation

Angiotensin II (ANG II) and enkephalins (ENK) occur in brain tissue and they increase blood pressure when injected into the brain ventricles. Stimulation of ANG II receptors by exogenous administration of the peptide or endogenous stimulation of its biosynthesis leads to the release of antidiuretic hormone (ADH) and adrenocorticotropic hormone (ACTH) and to an increase of sympathetic tone (“central peptidergic stimulation syndrome”). ENK produce similar humoral effects and the humoral pattern of increased ADH, ACTH and sympathetic tone has also been found in spontaneously hypertensive rats (SHR). It is concluded that central peptidergic stimulation can contribute to be maintenance of high blood pressure in SHR. Such a conclusion is supported by the fact that 1) SHR are supersensitive to intraventricular ANG II and ENK, 2) in SHR the brain renin-angiotensin system (RAS) is stimulated while plasma renin is decreased, and 3) intraventricular ANG II receptor blockade results in the lowering of blood pressure in SHR.