title: Ca(2+) sensitisation of force production by noradrenaline in femoral conductance and resistance arteries from rats with postinfarction congestive heart failure.
abstract: In this study we tested the hypothesis that arterial myofilament Ca(2+) sensitivity and/or the Ca(2+) sensitising effect of noradrenaline (NA) is enhanced in post-infarction congestive heart failure (CHF), which could contribute to the high peripheral vascular resistance in this condition. Femoral skeletal muscle resistance and conductance arteries (mean lumen diameters of 159 and 519 microm) from rats with CHF and sham-operated control rats were used. Isometric tension development and intracellular free calcium concentration ([Ca(2+)](i)) were measured simultaneously in isolated vessel segments using wire myography and the FURA-2 fluorescence technique. In conductance and resistance arteries, the resting levels of [Ca(2+)](i) and tension in physiological saline solution (PSS) and active tension in response to single doses of 125 mM K(+) (KPSS) were unaffected by CHF. During cumulative application of extracellular Ca(2+) to arteries depolarised with 125 mM K(+) or activated with 30 microM NA, [Ca(2+)](i) and vessel wall tension were similar in CHF and control rats. However, the conductance arteries showed significantly higher calcium sensitivity than resistance arteries in these experiments. We conclude that an abnormality in the sensitivity of the contractile apparatus to Ca(2+), or in NA-induced Ca(2+) sensitisation in arterial vascular smooth muscle cells is unlikely to contribute to the ubiquitously elevated vascular resistance associated with CHF. However, our data demonstrate significant differences in vascular Ca(2+) handling, myofilament Ca(2+) sensitivity and tension development between resistance and conductance arteries, regardless of CHF.
authors.affiliation: Department of Cardiology, The Danish National Hospital (Rigshospitalet), Blegdamsvej 9, Copenhagen, DK-2100, Denmark.
authors.forename: Simon
authors.initials: S
authors.lastname: Trautner
authors.forename: Ole
authors.initials: O
authors.lastname: Amtorp
authors.forename: Soren
authors.initials: S
authors.lastname: Boesgaard
authors.forename: Claus B
authors.initials: CB
authors.lastname: Andersen
authors.forename: Henrik
authors.initials: H
authors.lastname: Galbo
authors.forename: Stig
authors.initials: S
authors.lastname: Haunsoe
authors.forename: Majid
authors.initials: M
authors.lastname: Sheykhzade
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D005263:Femoral Artery / Q000187:drug effects* / Q000378:metabolism; D006333:Heart Failure / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D009119:Muscle Contraction; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism; D009203:Myocardial Infarction / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D009638:Norepinephrine / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D014655:Vascular Resistance; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
chemical_list: D014662:Vasoconstrictor Agents; D002118:Calcium; D009638:Norepinephrine