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Erratum for Buckler and Honoré, J Physiol 562 (1) 213-222.
Erratum for Bearden et al., J Physiol 561 (2) 535-545.
J Physiol Volume 562, Number 3, 977-978, February 1, 2005 DOI: 10.1113/jphysiol.2005.562001
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Errata

Shawn E Bearden2,1, Geoffrey W Payne1,2, Alia Chisty3 and Steven S Segal1,2,3

1 The John B. Pierce Laboratory
2 Department of Cellular & Molecular Physiology
3 Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, CT, USA

The paper by Bearden et al. (2004) contained an error in the first line of the summary and the author affiliations were incorrect. The correct versions are reproduced below. The publisher apologises for any confusion.

Physical work capacity diminishes with ageing, but little is known of how the microvascular supply to skeletal muscle fibres is affected. To test the hypothesis that ageing alters blood flow control, we investigated network architecture and vasomotor responses of arterioles in the gluteus maximus muscle of young (2–3 months), adult (12–14 months) and old (18–20 months) C57BL6 male mice (n = 83) (Young, Adult and Old, respectively). Microvascular casts revealed that the total number, length and surface area of arteriolar segments (diameter, 10–50 µm) were not significantly different across age-groups. However, for arterioles with diameter of 30 µm, tortuosity and branch angles increased with age (P < 0.05). In anaesthetized mice, second-order (2A) distributing arterioles had similar resting (17 ± 1 µm) and maximal (37 ± 1 µm) diameters and similar responsiveness to cumulative (10–10–10–4M) superfusion of acetylcholine or phenylephrine. With superfusate oxygen level raised from 0 to 21%, 2A arteriolar constriction in Young (11 ± 1 µm) was greater (P < 0.05) than Adult and Old (5 ± 1 µm). Observed 1 mm upstream from microiontophoresis of ACh (1 µA, 1 s), conducted vasodilatation was 10 ± 1 µm in Young, 17 ± 1 µm in Adult and 6 ± 1 µm in Old (P < 0.05). With muscle contractions (2, 4 and 8 Hz; 30 s) arteriolar diameter increased similarly across age-groups (6 ± 1, 11 ± 1 and 18 ± 1 µm, respectively). Muscle mass and active tension were similar across age-groups yet postcontraction vasodilatation recovered more rapidly in Old versus Adult and Young (P < 0.05). With arteriolar network architecture maintained during ageing, the impairment in conducted vasodilatation and attenuation of postcontraction vasodilatation may compromise exercise tolerance.

The paper by Buckler & Honoré (2005) contained an error on page 220. Figure 6 should have appeared as follows:



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  		Figure 6.  Effects of hypoxia and intracellular acidosis on mTREK-1
mTREK-1 currents recorded at room temperature in Hepes buffer. A, effects of 10 mM sodium propionate on membrane currents in air-equilibrated and nitrogen- equilibrated solutions. Upper panel, voltage clamp protocol; cells were held at –70 mV and subject to a 500 ms voltage from –100 mV to +70 mV at 0.1 Hz. Lower panel, membrane current. B, ramp currents from the experiment in A in air-equilibrated (Air) and nitrogen-equilibrated (N2) saline in the presence and absence of 10 mM propionate (Prop). C, mean (± S.E.M.) of mTREK-1 currents at 0 mV expressed relative to control (air equilibrated) in Hepes buffer at room temperature (n = 5).

 

References

Bearden SE, Payne GW, Chisty A & Segal SS (2004). Arteriolar network architecture and vasomotor function with ageing in mouse gluteus maximus muscle. J Physiol 561, 535–545.[Abstract/Free Full Text]

Buckler KJ & Honoré E (2005). The lipid-activated two-pore domain K+ channel TREK-1 is resistant to hypoxia: implication for ischaemic neuroprotection. J Physiol 562, 213–222.[Abstract/Free Full Text]





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