title: Endothelin-1 facilitates synaptic transmission in the nucleus tractus solitarii in normotensive rats but not in spontaneously hypertensive rats.
abstract: We previously demonstrated that endothelin-1 (ET-1) increases the neuronal activity of neurons in the nucleus tractus solitarii (NTS) and augments the response to glutamate (Glu), using in vitro brainstem slice preparations of normotensive Wistar-Kyoto (WKY) rats. This study was designed to determine whether the effects of ET-1 on neuronal activity and synaptic transmission in the NTS are altered in spontaneously hypertensive rats (SHR). Experiments were performed with WKY rats and age-matched SHR. We recorded the extracellular single unit of neuronal activity of NTS neurons in response to electrical stimulation of the solitary tracts using in vitro brainstem slice preparations. ET-1 or Glu was iontophoretically applied to the recording neurons. ET-1 increased the neuronal activity of NTS neurons in SHR as well as WKY. The magnitude of the increase in the neuronal activity evoked by Glu was augmented by application of ET-1 in WKY rats (6.1 +/- 0.6 to 11.1 +/- 1.7 spikes/s, p < 0.05) but not in SHR (5.6 +/- 0.5 to 5.6 +/- 0.6 spikes/s). These results indicate that ET-1 increases the neuronal activity of the NTS in both SHR and WKY. However, the increase in neuronal activity in response to Glu is augmented by ET-1 in WKY but not in SHR, suggesting that reflex control is impaired in SHR.
authors.affiliation: Research Institute of Angiocardiology and Cardiovascular Clinic, Kyushu University School of Medicine, Fukuoka, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Hirooka
authors.forename: M
authors.initials: M
authors.lastname: Shihara
authors.forename: K
authors.initials: K
authors.lastname: Eshima
authors.forename: N
authors.initials: N
authors.lastname: Hori
authors.forename: A
authors.initials: A
authors.lastname: Takeshita
mesh_terms: D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D001794:Blood Pressure / Q000502:physiology; D004558:Electric Stimulation; D065128:Endothelin Receptor Antagonists; D019332:Endothelin-1 / Q000494:pharmacology*; D018698:Glutamic Acid / Q000494:pharmacology; D006339:Heart Rate / Q000502:physiology; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology*; D066298:In Vitro Techniques; D007478:Iontophoresis; D008297:Male; D008839:Microelectrodes; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D010456:Peptides, Cyclic / Q000494:pharmacology; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D044022:Receptor, Endothelin A; D015398:Signal Transduction / Q000187:drug effects; D017552:Solitary Nucleus / Q000187:drug effects / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects*
chemical_list: D000959:Antihypertensive Agents; D065128:Endothelin Receptor Antagonists; D019332:Endothelin-1; D010456:Peptides, Cyclic; D044022:Receptor, Endothelin A; D018698:Glutamic Acid; C072247:cyclo(Trp-Asp-Pro-Val-Leu)