Norepinephrine Content in Brainstem and Hypothalamic Nuclei of Borderline and Wistar-Kyoto Rats Consuming High Salt for Varying Durations

Introduction: Both electrolytic lesions and electrical stimulation of the brain are classic methods for examining the role of the central nervous system (CNS) in control of cardiovascular function. For example, Doba and Reis (13) showed that bilateral electrolytic lesions of the nuclei tracti solitarii (NTS) in the rat at the level of the obex result in an immediate and marked elevation in arterial blood pressure. Death typically results in a matter of days. Ernsberger, Azar and Azar (14) revealed that radiofrequency lesions of the paraventricular and suprachiasmatic nl!clei prevented a rise in blood pressure (BP) in salt-sensitive rats fed a high salt (8%) diet for 15 weeks. Electrical stimulation of the C1 region of the rostral ventrolateral medulla (RVLM) elicits a pressor response (46). More recently, newer techniques in the brain sciences, originally developed in the study of other neural systems, have been applied to central control of cardiovascular function. For example, microinjection of the excitatory amino acid glutamate into catecholamine-containing neurons of the RVLM produces an increase in blood pressure (36). A couple of points worth developing further are, first, that norepinephrine (NE) appears to be an important neurotransmitter in control of cardiovascular function and, second, that many of the structures studied receive direct or indirect projections from limbic system structures. Thus, there is the possibility that stressors might alter cardiovascular function sufficiently to lead to a disease state such as hypertension. However, as we shall see, this is a fairly new area of research, and results are far from conclusive. Many years ago, Hilton (20) revealed the importance of the hypothalamus in the cardiovascular component of the fight-or-flight response. It is noteworthy that many hypothalamic nuclei contain NE and interact extensively with brainstem structures that eventually form the final common pathway to the intermediolateral cell column of the spinal cord, the point of origin of preganglionic sympathetic nervous system neurons. For example, Bennaroch et al (4) showed that reduction of NE in the anterior hypothalamus induced an increase in arterial BP and heart rate, while clonidine, an NE agonist, administered after NE depletion caused hypotension in Wistar-Kyoto (WKY) rats. This suggests that NE has a tonic depressor effect in the anterior hypothalamus. However, NE does not always have an inhibitory effect as was shown in the study of Bachelard et al (3), where microinjection of NE into the paraventricular nuclei of Long-Evans rats produced dose-dependent increases in BP, …