Essential hypertension as a result of neurochemical changes at the rostral ventrolateral medulla
Related Experiment Video
Updated: May 7, 2026

Mesenteric Artery Contraction and Relaxation Studies Using Automated Wire Myography
Published on: September 22, 2011
Ajith J Thomas1, Bradley A Gross, Anila Jacob
1Department of Neurological Surgery, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.
Abstract:
Acute ischemia of the brainstem has been known to produce hypertension. After an initial review of central nervous system mechanisms contributing to systemic hypertension and the impact of the rostral ventrolateral medulla (RVLM) on arterial pressure, the authors propose that essential hypertension involves neurochemical changes at the level of the RVLM which are triggered by cerebral ischemia. Experimental and clinical data are presented to show that there is a link between ischemia of the brainstem and chronic hypertension. Atherosclerosis of the cerebral circulation leads to ischemia of the RVLM and other regions with autonomic function. This ischemic process results in increased availability of angiotensin II in the RVLM, which maintains the chronic hypertensive state via either direct stimulation of the RVLM or exacerbation of brainstem ischemia due to increased vasoconstriction.
More Related Videos
Related Concept Videos
Hypertension and Regulation of Blood Pressure
Hypertension II: Pathophysiology
Neural Regulation of Blood Pressure
Baroreceptor Reflex
Baroreceptors, located in the carotid sinuses and aortic arch, detect changes in blood pressure. When blood pressure rises, these stretch-sensitive receptors...
Hormonal Regulation of Blood Pressure
Epinephrine and Norepinephrine
The adrenal medulla releases epinephrine and norepinephrine, catecholamines that enhance and extend the sympathetic or "fight or flight" physiological response. These hormones escalate heart rate and the force of contraction while...
Hormonal Regulation
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

