title: Cardiovascular Alterations during the Interictal Period in Awake and Pithed Amygdala-Kindled Rats.
abstract: Epileptic seizures are often accompanied by increased sympathetic cardiovascular activity (even interictally), but it remains unknown whether this increased activity is of central and/or peripheral origin. Hence, this study investigated the cardiovascular alterations produced by amygdala kindling in awake and pithed Wistar rats. Blood pressure (BP) and heart rate (HR) were initially recorded by tail cuff plethysmography in awake control, sham-operated and amygdala-kindled rats before and 24 hr after the kindling process. The after-discharge threshold (ADT) was measured under different conditions to correlate brain excitability with BP and HR in kindled rats. Twenty-four hours after the last kindling seizure, (i) HR, systolic and diastolic BP were increased and (ii) only higher HR values correlated with lower ADT values. Forty-eight hr after the last kindled seizure, all rats were pithed and prepared for analysing the tachycardic, vasopressor and vasodepressor responses by (i) stimulation of the sympathetic or sensory vasodepressor CGRPergic out-flows (stimulus-response curves, S-R curves) and (ii) intravenous injections of noradrenaline or α-CGRP (dose-response curves, D-R curves). Interestingly, (i) the tachycardic S-R and D-R curves were attenuated, whilst the CGRPergic S-R and D-R curves were potentiated in kindled rats, and (ii) the vasopressor noradrenergic S-R and D-R curves were not significantly different in all groups. Therefore, the kindling process may be associated with overstimulation in the central sympathetic and sensory out-flows interictally, producing (i) peripheral attenuation of cardiac sympathetic out-flow and β-adrenoceptor activity and (ii) peripheral potentiation of vasodepressor sensory CGRPergic out-flow and CGRP receptor activity.
authors.affiliation: Department of Pharmacobiology, Cinvestav-Coapa, Tlalpan, Mexico City, Mexico.
authors.forename: Inna
authors.initials: I
authors.lastname: Ruiz-Salinas
authors.affiliation: Department of Pharmacobiology, Cinvestav-Coapa, Tlalpan, Mexico City, Mexico.
authors.forename: Luisa
authors.initials: L
authors.lastname: Rocha
authors.affiliation: Department of Pharmacobiology, Cinvestav-Coapa, Tlalpan, Mexico City, Mexico.
authors.forename: Bruno A
authors.initials: BA
authors.lastname: Marichal-Cancino
authors.affiliation: Department of Pharmacobiology, Cinvestav-Coapa, Tlalpan, Mexico City, Mexico.
authors.forename: Carlos M
authors.initials: CM
authors.lastname: Villalón
mesh_terms: D000283:Administration, Intravesical; D000679:Amygdala / Q000503:physiopathology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D015740:Calcitonin Gene-Related Peptide / Q000494:pharmacology; D002319:Cardiovascular System / Q000503:physiopathology*; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation; D004827:Epilepsy / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics; D007696:Kindling, Neurologic; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D014662:Vasoconstrictor Agents / Q000494:pharmacology
chemical_list: D014662:Vasoconstrictor Agents; D015740:Calcitonin Gene-Related Peptide; D009638:Norepinephrine