ABSTRACT
Neurons in the nucleus rostral ventrolateral (RVL), a major site of the antihypertensive sympathoinhibitory action of clonidine are responsive to a wealth of other pharmacologic agents involved in the central regulation of arterial blood pressure (AP). Its pivotal role in governing the discharge of sympathetic preganglionic neurons suggests that sympathoexcitatory neurons in the RVL, and their inputs from cardiorespiratory receptors, somatic receptors and those from the brain itself, could contribute to exaggerated sympathetic tone, leading to the circulatory changes involved in the expression and maintenance of certain types of hypertension. The regulation of AP and respiration by nicotinic acetylcholine receptors on the ventral surface of the medulla underlying the RVL was described by Feldberg. Investigation of the cardiovascular responses to cerebral ischemia by Dampney and Moon (1980) demonstrated that lesions of the rostral ventrolateral medulla (VLM) not only abolished the pressor response to cerebral ischemia, but also lowered arterial blood pressure (AP) to spinal levels.
