title: New method for imaging innervation of the renal preglomerular vasculature. Alterations in hypertensive rats.
abstract: OBJECTIVE
  To develop a new method for viewing adrenergic innervation along renal preglomerular vessels; to assess nerve densities and vascular lesions along arcuate arteries (ArcA), arcuate arterial branches (ArcB), and interlobular arteries (ILA) in spontaneously hypertensive rats (SHR) and in angiotensin II (AngII) and in N(G)-nitro-L-arginine methyl ester (L-NAME) hypertensive rats.
  
  
  METHODS
  Preglomerular vasculatyres were isolated after HCl maceration and were immunostained against synaptophysin, a membrane protein of synaptic vesicles. Lesions were stained with Sudan black. Longitudinal nerve densities and relative frequencies of ArcA, ArcB, and ILA endowed with sudanophilic lesions were assessed separately.
  
  
  RESULTS
  Synaptophysin immunostaining revealed the vascular neural plexus. Nerves were adrenergic, as the plexus was destroyed by treatment with 6-hydroxy dopamine. Vascular lesions were not seen in SHR, and increased nerve density was observed along ArcA and ILA. In L-NAME- and AngII-hypertensive rats, vascular lesions affected predominantly ArcB and ILA, and nerve density was reduced by 12% and 28% (ArcA), 37% and 31% (ArcB), and by 55% and 34% (ILA), respectively, versus normotensive controls. Endothelin-1 receptor blockade did not affect AngII-induced hypertension but prevented both lesion development and reduction of density of the vascular neural plexus.
  
  
  CONCLUSIONS
  The method we have devised provides a direct en face view of the vascular adrenergic innervation of isolated preglomerular vasculature. Measurements in hypertensive rat models suggest a link between vascular lesions and reduction in nerve density in hypertension. Endothelin-1 likely plays a key role in mediation both vascular injury and altered vascular nerve density in hypertension.
authors.affiliation: Groupe Rein et Hypertension, Institut Universitaire de Recherche Clinique, Montpellier, France. casellas@iurc1.iurc.montp.inserm.fr
authors.forename: D
authors.initials: D
authors.lastname: Casellas
authors.forename: N
authors.initials: N
authors.lastname: Bouriquet
authors.forename: A
authors.initials: A
authors.lastname: Artuso
authors.forename: B
authors.initials: B
authors.lastname: Walcott
authors.forename: L C
authors.initials: LC
authors.lastname: Moore
mesh_terms: D000320:Adrenergic Fibers / Q000378:metabolism / Q000473:pathology; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001158:Arteries / Q000294:innervation / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D006973:Hypertension / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D007150:Immunohistochemistry; D007668:Kidney / Q000098:blood supply* / Q000294:innervation* / Q000378:metabolism; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D016708:Synaptophysin / Q000378:metabolism
chemical_list: D016708:Synaptophysin; D000804:Angiotensin II; D019331:NG-Nitroarginine Methyl Ester