title: Functional asymmetry in the descending cardiovascular pathways from dorsomedial hypothalamic nucleus.
abstract: Neurons in the dorsomedial hypothalamus (DMH) play a key role in mediating tachycardia elicited by emotional stress. DMH activation by microinjections of the GABA(A) antagonist evokes tachycardia and physiological changes typically seen in experimental stress. DMH inhibition abolishes the tachycardia evoked by stress. Based on anatomic evidences for lateralization in the pathways from DMH, we investigated a possible inter-hemispheric difference in DMH-evoked cardiovascular responses. In anesthetized rats we compared changes in heart rate (HR), renal sympathetic activity (RSNA), mesenteric blood flow (MBF) and tail vascular conductance produced by activation of right (R) and left (L) sides of the DMH. We also evaluated the tachycardia produced by air jet stress after inhibition of R or L DMH. There were always greater increases in RSNA when bicuculline was injected ipsilaterally to the side where these parameters were recorded (average DeltaRSNA: L=+50% and R=+26%; P<0.05). Compared to pre-injection values, right DMH activation caused pronounced decrease (0.87+/-0.1% vs. 0.4+/-0.11%/mm Hg; P<0.05), whereas bicuculline methiodide (BMI) into left DMH produced no significant changes (0.95+/-0.09% vs. 1.04+/-0.25%/mm Hg) in tail vascular conductance. R or L DMH disinhibition produced decreases in MBF, but no differences in the range of these changes were observed. Activation of the right DMH caused greater tachycardia compared to the left DMH activation (average DeltaHR: R=+92 bpm; L=+48 bpm; P<0.05). Tachycardia evoked by air jet stress was smallest after right DMH inhibition (average DeltaHR: R=+57 bpm and L=+134 bpm; P<0.05). These results indicate that the descending cardiovascular pathways from DMH are predominantly lateralized and the right DMH might exert a prominent control on heart rate changes during emotional stress.
authors.affiliation: Laboratório de Hipertensão, Departamento de Fisiologia e Biofísica, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Brazil.
authors.forename: C H
authors.initials: CH
authors.lastname: Xavier
authors.forename: E
authors.initials: E
authors.lastname: Nalivaiko
authors.forename: M I
authors.initials: MI
authors.lastname: Beig
authors.forename: G B
authors.initials: GB
authors.lastname: Menezes
authors.forename: D C
authors.initials: DC
authors.lastname: Cara
authors.forename: M J
authors.initials: MJ
authors.lastname: Campagnole-Santos
authors.forename: M A P
authors.initials: MA
authors.lastname: Fontes
mesh_terms: D000818:Animals; D017776:Autonomic Pathways / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D001640:Bicuculline / Q000494:pharmacology; D002320:Cardiovascular Physiological Phenomena; D004302:Dorsomedial Hypothalamic Nucleus / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D004525:Efferent Pathways / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D007839:Functional Laterality / Q000502:physiology*; D018756:GABA Antagonists / Q000494:pharmacology; D006339:Heart Rate / Q000502:physiology; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D012039:Regional Blood Flow / Q000502:physiology; D013152:Splanchnic Circulation / Q000502:physiology; D013315:Stress, Psychological / Q000503:physiopathology; D017779:Sympathetic Fibers, Postganglionic / Q000033:anatomy & histology / Q000502:physiology; D013564:Sympathetic Nervous System / Q000033:anatomy & histology / Q000502:physiology; D013610:Tachycardia / Q000503:physiopathology
chemical_list: D018756:GABA Antagonists; D001640:Bicuculline