title: Myogenic and flow-mediated responses in isolated mesenteric small arteries from pregnant and nonpregnant rats.
abstract: OBJECTIVE
  Responses to pressure, agonist-induced constriction, endothelium-dependent vasodilators, and shear stress were investigated in resistance-sized mesenteric arteries in vitro from late-pregnant and nonpregnant rats.
  
  
  METHODS
  Myogenic tone was determined in arteries mounted on a pressure myograph by evaluating the response to incremental increases in luminal pressure in resting arteries and arteries preconstricted with norepinephrine (10(-6) mol/L). Flow-mediated dilation was also investigated in the presence and absence of a nitric oxide synthase inhibitor, L-N(omega)-nitro-L-arginine methyl ester. Constrictor responses to norepinephrine (10(-9) to 10(-5) mol/L), were examined with a small vessel myograph. Responses of preconstricted arteries to acetylcholine (10(-9) to 10(-5) mol/L), bradykinin (10(-9) to 10(-5) mol/L), and sodium nitroprusside (10(-9) to 10(-5) mol/L) were also assessed.
  
  
  RESULTS
  Myogenic tone was only demonstrable in response to increasing pressure when arteries were preconstricted with norepinephrine (10(-6) mol/L) and was similar in arteries from both pregnant and nonpregnant rats. Flow-mediated dilation was greater in pregnant rats and was reduced by L-N(omega)-nitro-L-arginine methyl ester. Arteries from the pregnant rats demonstrated a reduced constrictor response to norepinephrine. Responses to acetylcholine were similar in both groups, but arteries from the pregnant rats showed enhanced relaxation to bradykinin.
  
  
  CONCLUSIONS
  The data substantiate previous studies indicating reduced constrictor responses in pregnancy but provide no evidence to suggest that blunted myogenic responses contribute to reduced vascular resistance in pregnancy. The results indicate that flow-mediated nitric oxide release may contribute to vasodilation in pregnant rats. Different responses to two endothelium-dependent vasodilators suggest that specific alterations in signal transduction pathways may influence nitric oxide synthesis in pregnancy.
authors.affiliation: Division of Obstetrics and Gynaecology, United Medical School of Guys' and St. Thomas' Hospital, London, United Kingdom.
authors.forename: J G
authors.initials: JG
authors.lastname: Learmont
authors.forename: A P
authors.initials: AP
authors.lastname: Cockell
authors.forename: G A
authors.initials: GA
authors.lastname: Knock
authors.forename: L
authors.initials: L
authors.lastname: Poston
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001920:Bradykinin / Q000494:pharmacology; D005260:Female; D066298:In Vitro Techniques; D008638:Mesenteric Arteries / Q000502:physiology*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D009638:Norepinephrine / Q000494:pharmacology; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000502:physiology*; D051381:Rats; D012039:Regional Blood Flow; D014661:Vasoconstriction; D014664:Vasodilation
chemical_list: D019001:Nitric Oxide Synthase; D000109:Acetylcholine; D001920:Bradykinin; D019331:NG-Nitroarginine Methyl Ester; D009638:Norepinephrine