title: Vascular reactivity of rabbit isolated renal and femoral resistance arteries in renal wrap hypertension.
abstract: In rabbits with cellophane renal wrap hypertension, hindquarter and total vascular resistance changes to pressor and depressor agents are amplified compared to those of normotensive rabbits. The aim of the present study was to evaluate the in vitro pharmacodynamics of hypertensive and normotensive rabbit small artery segments isolated from the renal and hindquarter vascular beds. Using wire myography, the full range (Emax) and sensitivity (EC50) to a range of agonists of segments of renal interlobar (≈ 600 µm i.d.), renal arcuate (≈ 250 µm i.d.) and deep femoral branch (≈ 250 µm i.d.) arteries were assessed under normalised conditions of passive tension. Interlobar arteries from hypertensive rabbits were more sensitive (EC50) than those from normotensive rabbits to noradrenaline (6-fold), methoxamine (3-fold) and angiotensin II (3-fold). Arcuate artery reactivity was largely unaffected by hypertension. Deep femoral arteries from hypertensive rabbits had enhanced sensitivity only to noradrenaline (2-fold) and methoxamine (4-fold). Sensitivity to relaxation by acetylcholine was unaffected by hypertension in all arteries. Deep femoral arteries from hypertensive rabbits were more sensitive to sodium nitroprusside than normotensive counterparts. Adenosine caused little relaxation in renal arteries, but full relaxation in deep femoral arteries, unaltered by hypertension. This study found substantial heterogeneity in the pharmacodynamic profile of vessels isolated from different vascular beds and between arterial segments within the kidney. These profiles were differentially affected by hypertension suggesting that hypertension per se is not a resultant of general vascular dysfunction.
authors.affiliation: Cardiovascular Therapeutics Unit, Department of Pharmacology and Therapeutics, University of Melbourne, Victoria 3010, Australia. Electronic address: khammy@sund.ku.dk.
authors.forename: Makhala M
authors.initials: MM
authors.lastname: Khammy
authors.affiliation: Cardiovascular Therapeutics Unit, Department of Pharmacology and Therapeutics, University of Melbourne, Victoria 3010, Australia. Electronic address: jamesaa@unimelb.edu.au.
authors.forename: James A
authors.initials: JA
authors.lastname: Angus
authors.affiliation: Cardiovascular Therapeutics Unit, Department of Pharmacology and Therapeutics, University of Melbourne, Victoria 3010, Australia. Electronic address: cewright@unimelb.edu.au.
authors.forename: Christine E
authors.initials: CE
authors.lastname: Wright
mesh_terms: D000818:Animals; D001794:Blood Pressure; D004195:Disease Models, Animal; D005260:Female; D005263:Femoral Artery / Q000378:metabolism / Q000503:physiopathology*; D006977:Hypertension, Renal / Q000503:physiopathology*; D008297:Male; D011817:Rabbits; D011956:Receptors, Cell Surface / Q000378:metabolism; D012077:Renal Artery / Q000378:metabolism / Q000503:physiopathology*; D014655:Vascular Resistance; D014661:Vasoconstriction; D014664:Vasodilation
chemical_list: D011956:Receptors, Cell Surface
keywords: Acetylcholine bromide (PubChem CID: 65551); Deep femoral artery; Maximum effective active pressure; Page hypertension; Pharmacodynamics; Renal arcuate artery; Renal interlobar artery; Vascular reactivity; [−]-noradrenaline bitartrate (PubChem CID: 297812); adenosine (PubChem CID: 60961); and sodium nitroprusside (PubChem CID: 11963622); angiotensin II amide (PubChem CID: 5890); endothelin-1 (PubChem CID: 16132423); methoxamine hydrochloride (PubChem CID: 6081)