Logo image
Back
Amphetamine-induced sensitization of hypertension and lamina terminalis neuroinflammation
Journal article   Open access   Peer reviewed

Amphetamine-induced sensitization of hypertension and lamina terminalis neuroinflammation

Seth W Hurley, Terry G Beltz, Fang Guo, Baojian Xue and Alan Kim Johnson
American journal of physiology. Regulatory, integrative and comparative physiology, Vol.318(3), pp.R649-R656
03/01/2020
DOI: 10.1152/AJPREGU.00233.2019
PMCID: PMC7099466
PMID: 32048863
url
https://doi.org/10.1152/AJPREGU.00233.2019View
Published (Version of record) Open Access

Abstract

Psychomotor stimulants are prescribed for many medical conditions, including obesity, sleep disorders, and attention-deficit/hyperactivity disorder. However, despite their acknowledged therapeutic utility, these stimulants are frequently abused, and their use can have both short- and long-term negative consequences. Although stimulants such as amphetamines acutely elevate blood pressure, it is unclear whether they cause any long-term effects on cardiovascular function after use has been discontinued. Previous work in our laboratory has demonstrated that physiological and psychosocial stressors will produce sensitization of the hypertensive response, a heightened pressor response to a hypertensinogenic stimulus delivered after stressor exposure. Here, we tested whether pretreatment with amphetamine for 1 wk can sensitize the hypertensive response in rats. We found that repeated amphetamine administration induced and maintained sensitization of the pressor response to angiotensin II following a 7-day delay after amphetamine injections were terminated. We also found that amphetamine pretreatment altered mRNA expression for molecular markers associated with neuroinflammation and renin-angiotensin-aldosterone system (RAAS) activation in the lamina terminalis, a brain region implicated in the control of sympathetic nervous system tone and blood pressure. The results indicated amphetamine upregulated mRNA expression underlying neuroinflammation and, to a lesser degree, message for components of the RAAS in the lamina terminalis. However, we found no changes in mRNA expression in the paraventricular nucleus. These results suggest that a history of stimulant use may predispose individuals to developing hypertension by promoting neuroinflammation and upregulating activity of the RAAS in the lamina terminalis.
 Amphetamine - pharmacology Angiotensin II - pharmacology Animals Blood Pressure - drug effects Blood Pressure - physiology Central Nervous System Stimulants - pharmacology Diet, High-Fat Disease Models, Animal Hypertension - chemically induced Hypertension - physiopathology Hypothalamus - drug effects Hypothalamus - metabolism Inflammation - drug therapy Paraventricular Hypothalamic Nucleus - drug effects Rats

Details

Metrics

27 Record Views
6 Times Cited - Web of Science
Logo image