title: Reduced reactivity of renal microvessels to pressure and angiotensin II in fawn-hooded rats.
abstract: Fawn-Hooded rats possess an increased risk to develop glomerular damage. Both an impaired control of preglomerular resistance and an elevated postglomerular resistance have been implicated. In the present study, we directly assessed the myogenic reactivity of distal interlobular arteries and afferent arterioles from hypertensive and normotensive Fawn-Hooded rats compared with Sprague-Dawley and Wistar rats, which are known to be resistant for developing renal disease. Pressure-response curves were made in isolated perfused hydronephrotic kidneys from these rats. In addition, increasing concentrations of angiotensin II were added to the perfusate to determine the reactivity of interlobular arteries, afferent arterioles, and efferent arterioles to this peptide. Preglomerular vessels from hypertensive and normotensive Fawn-Hooded rats exhibited an impaired reactivity to both pressure and angiotensin II compared with that of Sprague-Dawley and Wistar rats. Basal efferent arteriolar diameters were similar among the 4 strains of rat. In addition, efferent arterioles from hypertensive and normotensive Fawn-Hooded rats displayed a reduced sensitivity to angiotensin II. Our observations demonstrate that in Fawn-Hooded rats, 2 components of preglomerular resistance control are impaired: the myogenic and the angiotensin II response. In addition, efferent arteriolar reactivity to angiotensin II is not elevated but lowered in these rats. Therefore, a deficit in preglomerular resistance control is the most important intrinsic factor involved in the increased susceptibility of Fawn-hooded rats to develop renal disease.
authors.affiliation: Laboratory for Physiology, Vrije Universiteit Medical Center, Amsterdam, The Netherlands. w.van_rodijnen.physiol@med.vu.nl
authors.forename: William F
authors.initials: WF
authors.lastname: van Rodijnen
authors.forename: Ton A
authors.initials: TA
authors.lastname: van Lambalgen
authors.forename: Geert-Jan
authors.initials: GJ
authors.lastname: Tangelder
authors.forename: Richard P E
authors.initials: RP
authors.lastname: van Dokkum
authors.forename: Abraham P
authors.initials: AP
authors.lastname: Provoost
authors.forename: Piet M
authors.initials: PM
authors.lastname: ter Wee
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D001160:Arterioles / Q000187:drug effects / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D006869:Hydronephrosis / Q000503:physiopathology; D006973:Hypertension / Q000503:physiopathology*; D007668:Kidney / Q000098:blood supply*; D008297:Male; D010477:Perfusion; D051381:Rats; D017207:Rats, Sprague-Dawley; D017208:Rats, Wistar; D012077:Renal Artery / Q000187:drug effects / Q000502:physiology; D012079:Renal Circulation / Q000187:drug effects* / Q000502:physiology*
chemical_list: D000804:Angiotensin II