title: Oestrogen modulates vascular adrenergic reactivity of the spontaneously hypertensive rat.
abstract: BACKGROUND
  Male spontaneously hypertensive rats (SHRs) show an increased vascular neurogenic response compared with normotensive Wistar-Kyoto (WKY) control rats.
  
  
  OBJECTIVE
  To study the vascular adrenergic response in hypertensive and normotensive female rats, with a focus on the influence of oestrogen.
  
  
  METHODS
  Female SHRs and WKY rats were allocated randomly to a control group or to groups to undergo ovariectomy or ovariectomy combined with oestrogen supplementation (17beta-oestradiol 150 microg/kg per day) for either 1 day (group 1E2) or 10 days (group 10E2). Mean arterial pressure (MAP) was recorded and small mesenteric arteries were mounted in a Multi Myograph 610M. Vascular reactivities to transmural nerve stimulation (TNS), exogenous noradrenaline and acetylcholine were analysed.
  
  
  RESULTS
  MAP was significantly greater in SHRs than in WKY rats in all groups studied. Sensitivity to cumulative TNS (0.12-32 Hz) did not differ between vessels from control SHRs and WKY rats, expressed as the frequency giving 50% of maximal neurogenic response (Ef(50): 4.1 +/- 1.1 and 4.0 +/- 1.6 Hz, respectively). However, there was a greater reactivity to TNS in ovariectomized SHRs than in ovariectomized WKY rats (Ef(50) 1.8 +/- 0.7 and 6.8 +/- 2.2 Hz, respectively; P < 0.05). Oestradiol treatment significantly decreased the sensitivity to TNS in ovariectomized SHRs (P < 0.05), and after 10 days the frequency-response curves were almost identical (Ef(50) 6.3 +/- 1.9 Hz for group 10E2 SHRs and 5.6 +/- 0.8 Hz for group 10E2 WKY rats). The increased adrenergic reactivity in ovariectomized SHRs was inhibited by prazosin, an alpha(1)-adrenergic antagonist, and could not be explained by differences in endothelial function or sensitivity to applied noradrenaline.
  
  
  CONCLUSIONS
  Increased adrenergic reactivity is not present in small arteries from female SHRs. The findings of this study suggest that oestrogen acts on prejunctional mechanisms, reducing full expression of hypertension and peripheral vascular pathology.
authors.affiliation: Clinical Experimental Research Laboratory, Heart and Lung Institute, Sahlgrenska University Hospital/Ostra, Sweden.
authors.forename: Lisa
authors.initials: L
authors.lastname: Brandin
authors.forename: Göran
authors.initials: G
authors.lastname: Bergström
authors.forename: Karin
authors.initials: K
authors.lastname: Manhem
authors.forename: Helena
authors.initials: H
authors.lastname: Gustafsson
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects* / Q000502:physiology*; D004558:Electric Stimulation; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology; D004967:Estrogens / Q000494:pharmacology*; D005260:Female; D006973:Hypertension / Q000503:physiopathology*; D008638:Mesenteric Arteries / Q000187:drug effects / Q000294:innervation / Q000502:physiology; D009638:Norepinephrine / Q000494:pharmacology*; D010052:Ovariectomy; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D011942:Receptors, Adrenergic, alpha / Q000502:physiology; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D000316:Adrenergic alpha-Agonists; D004967:Estrogens; D011942:Receptors, Adrenergic, alpha; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D000109:Acetylcholine; D009638:Norepinephrine