title: Mesenteric small artery changes after vasoconstrictor infusion in young rats.
abstract: We evaluated whether chronic alpha 1-adrenergic stimulation, angiotensin II (AII), or increased blood pressure (BP) alters resistance arterial structure and function. Structural parameters and wall tension were recorded in mesenteric small arteries (MrA) isolated from 6-week-old normotensive Wistar Kyoto rats that had been infused for 4 days with saline (WKY), 2 mg/kg/day phenylephrine (WKY + PHE), or 0.3 mg/kg/day AII (WKY + AII) and from saline-infused spontaneously hypertensive rats (SHR). During the experimental period, systolic BP (SBP) did not change in WKY but increased in WKY + PHE, WKY + AII, and SHR. Relative cardiac mass did not differ between SHR and WKY, but was increased in WKY + PHE and WKY + AII. Stiffness and optimal lumen diameter of MrA did not differ between WKY and SHR and were not altered in WKY + PHE or WKY + AII. Maximal contractile responses and sensitivities for vasconstrictors and calcium in vessels of WKY + AII and SHR did not differ from those in WKY. In vessels of WKY + PHE, maximal responses to vasoconstrictors and sensitivities for norepinephrine (NE) and PHE were reduced. Relaxing responses to isoproterenol (ISO) and Na-nitroprusside did not differ between SHR and WKY and were not altered in WKY + PHE and WKY + AII. Those to acetylcholine (ACh) were reduced in WKY + PHE. Media cross-sectional area and media thickness were significantly larger in WKY + AII and SHR as compared with WKY but were not altered in WKY + PHE. These data indicate that in young rats AII leads to small artery hypertrophy and that neither increased BP or increased vasconstriction appear to be involved therein. Chronic alpha 1-adrenergic stimulation, on the other hand, did not modify small artery structure but resulted in nonselective reduction of arterial smooth muscle contractile reactivity.
authors.affiliation: Department of Pharmacology, University of Limburg, Maastricht, The Netherlands.
authors.forename: H C
authors.initials: HC
authors.lastname: Boonen
authors.forename: M J
authors.initials: MJ
authors.lastname: Daemen
authors.forename: P H
authors.initials: PH
authors.lastname: Eerdmans
authors.forename: G E
authors.initials: GE
authors.lastname: Fazzi
authors.forename: E M
authors.initials: EM
authors.lastname: van Kleef
authors.forename: P M
authors.initials: PM
authors.lastname: Schiffers
authors.forename: J G
authors.initials: JG
authors.lastname: De Mey
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D004730:Endothelium, Vascular / Q000502:physiology; D006439:Hemodynamics / Q000187:drug effects; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D008638:Mesenteric Arteries / Q000187:drug effects* / Q000502:physiology; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D009126:Muscle Relaxation / Q000187:drug effects / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology; D010656:Phenylephrine / Q000494:pharmacology; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects*; D014655:Vascular Resistance / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
chemical_list: D011942:Receptors, Adrenergic, alpha; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D010656:Phenylephrine