title: Exercise pressor reflex function is altered in spontaneously hypertensive rats.
abstract: In hypertension, exercise elicits excessive elevations in mean arterial pressure (MAP) and heart rate (HR) increasing the risk for adverse cardiac events and stroke during physical activity. The exercise pressor reflex (a neural drive originating in skeletal muscle), central command (a neural drive originating in cortical brain centres) and the tonically active arterial baroreflex contribute importantly to cardiovascular control during exercise. Each of these inputs potentially mediates the heightened cardiovascular response to physical activity in hypertension. However, given that exercise pressor reflex overactivity is known to elicit enhanced circulatory responses to exercise in disease states closely related to hypertension (e.g. heart failure), we tested the hypothesis that the exaggerated cardiovascular response to exercise in hypertension is mediated by an overactive exercise pressor reflex. To test this hypothesis, we used a rat model of exercise recently developed in our laboratory that selectively stimulates the exercise pressor reflex independent of central command and/or the arterial baroreflex. Activation of the exercise pressor reflex during electrically induced static muscle contraction in the absence of input from central command resulted in significantly larger increases in MAP and HR in male spontaneously hypertensive rats as compared to normotensive Wistar-Kyoto rats over a wide range of exercise intensities. Similar findings were obtained in animals in which input from both central command and the arterial baroreflex were eliminated. These findings suggest that the enhanced cardiovascular response to exercise in hypertension is mediated by an overactive exercise pressor reflex. Potentially, effective treatment of exercise pressor reflex dysfunction may reduce the cardiovascular risks associated with exercise in hypertension.
authors.affiliation: Department of Physical Therapy, Allied Health Sciences School, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9174, USA. scott.smith@utsouthwestern.edu
authors.forename: Scott A
authors.initials: SA
authors.lastname: Smith
authors.forename: Maurice A
authors.initials: MA
authors.lastname: Williams
authors.forename: Anna K
authors.initials: AK
authors.lastname: Leal
authors.forename: Jere H
authors.initials: JH
authors.lastname: Mitchell
authors.forename: Mary G
authors.initials: MG
authors.lastname: Garry
mesh_terms: D000818:Animals; D001158:Arteries / Q000294:innervation; D017704:Baroreflex; D001794:Blood Pressure; D004452:Echocardiography; D004558:Electric Stimulation; D005730:Ganglionic Blockers / Q000494:pharmacology; D018738:Hexamethonium / Q000494:pharmacology; D006973:Hypertension / Q000000981:diagnostic imaging / Q000503:physiopathology*; D008297:Male; D009119:Muscle Contraction; D018482:Muscle, Skeletal / Q000503:physiopathology; D010805:Physical Conditioning, Animal; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D013562:Sympathectomy; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000503:physiopathology; D016277:Ventricular Function, Left
chemical_list: D005730:Ganglionic Blockers; D018738:Hexamethonium