title: Interactions of sympathetic nerves with capsaicin-sensitive sensory nerves: neurogenic mechanisms for phenol-induced hypertension in the rat.
abstract: BACKGROUND
  Previous investigations have shown that norepinephrine is capable of inhibiting neurotransmission in capsaicin-sensitive sensory nerves via a prejunctional mechanism. The alteration in the activity of sympathetic or capsaicin-sensitive sensory nerves in the development of phenol-induced hypertension was observed separately in rats.
  
  
  METHODS
  In the present study, we examined interactions of adrenergic nerves with capsaicin-sensitive sensory nerves in phenol-induced hypertensive rats. Blood pressure, the synthesis and release of calcitonin gene-related peptide (CGRP) and the content of nerve growth factor in (NGF) arteries were determined.
  
  
  RESULTS
  Intrarenal injection of phenol caused a permanent elevation of blood pressure concomitantly with a decrease in the concentration of CGRP in plasma, the content of CGRP in dorsal root ganglia and the density of CGRP-containing nerves in the mesenteric artery, and vascular NGF content. Chronic treatment with prazosin (an alpha1-adrenoreceptor antagonist, 3 mg/kg per day) failed to alter the synthesis and release of CGRP and vascular NGF content, even though it completely normalized blood pressure. However, treatment with yohimbine (an alpha2-adrenoreceptor antagonist, 5 mg/kg per day) significantly increased CGRP level and vascular NGF content. Combined administration of prazosin and yohimbine not only significantly elevated the synthesis and release of CGRP and arterial NGF content, but also completely normalized blood pressure.
  
  
  CONCLUSIONS
  These results indicate that the decreased production and release of CGRP and reduced vascular NGF content are attributed to the activation of alpha2-adrenoreceptors in phenol-induced hypertensive rats.
authors.affiliation: Department of Pharmacology, School of Pharmaceutical Sciences, Central South University, Changsha, Hunan, China.
authors.forename: Pan-Yue
authors.initials: PY
authors.lastname: Deng
authors.forename: Jing
authors.initials: J
authors.lastname: Yu
authors.forename: Feng
authors.initials: F
authors.lastname: Ye
authors.forename: Dai
authors.initials: D
authors.lastname: Li
authors.forename: Dan
authors.initials: D
authors.lastname: Luo
authors.forename: Wei-Jun
authors.initials: WJ
authors.lastname: Cai
authors.forename: Jian-Wei
authors.initials: JW
authors.lastname: Zhang
authors.forename: Xue-Gang
authors.initials: XG
authors.lastname: Luo
authors.forename: Han-Wu
authors.initials: HW
authors.lastname: Deng
authors.forename: Yuan-Jian
authors.initials: YJ
authors.lastname: Li
mesh_terms: D000818:Animals; D001011:Aorta / Q000294:innervation / Q000502:physiology; D001794:Blood Pressure; D015740:Calcitonin Gene-Related Peptide / Q000378:metabolism; D002211:Capsaicin; D004195:Disease Models, Animal; D005727:Ganglia, Spinal / Q000166:cytology; D006973:Hypertension / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology*; D008297:Male; D008638:Mesenteric Arteries / Q000294:innervation / Q000502:physiology; D020932:Nerve Growth Factor / Q000378:metabolism; D009475:Neurons, Afferent / Q000187:drug effects / Q000502:physiology*; D019800:Phenol; D051381:Rats; D017207:Rats, Sprague-Dawley; D012597:Sclerosing Solutions; D013564:Sympathetic Nervous System / Q000166:cytology / Q000502:physiology*
chemical_list: D012597:Sclerosing Solutions; D019800:Phenol; D020932:Nerve Growth Factor; D015740:Calcitonin Gene-Related Peptide; D002211:Capsaicin