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Alpha adrenergic receptor regulation of blood flow during passive leg movement: The impact of age.
Author(s) -
La Salle D. Taylor,
Cerbie James,
Alpenglow Jeremy,
Jarret Catherine,
Craig Jesse C.,
Broxterman Ryan M.,
Richardson Russell S.,
Trinity Joel D.
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.06548
Subject(s) - phenylephrine , phentolamine , propranolol , medicine , vasodilation , endocrinology , agonist , vasomotor , adrenergic , vasoconstriction , saline , adrenergic receptor , alpha (finance) , blood flow , antagonist , methoxamine , receptor , blood pressure , surgery , construct validity , patient satisfaction
Passive leg movement (PLM) evokes a robust and transient increase in limb blood flow (LBF). The magnitude of this response is attenuated with aging and this reduction has been largely attributed to diminished nitric oxide (NO) bioavailability. Importantly, aging is also associated with heightened sympathetic activity and altered vasomotor tone, which may contribute to the age‐related reduction in PLM. Therefore, this study sought to determine the contribution of α‐adrenergic signaling to the PLM‐induced LBF response in aging. The central hypothesis is that aging is associated with sympathetically‐mediated restraint of the LBF during PLM. Following intravenous infusion of the β‐blocker propranolol, five young (24±6 yr) and five old (68±4 yr) healthy male subjects underwent PLM during intra‐arterial infusion of saline (CON; control), phenylephrine (PE; α1‐adrenergic receptor agonist) and phentolamine (PHEN; nonspecific α‐adrenergic receptor antagonist). LBF through the common femoral artery was determined second‐by‐second by Doppler ultrasound. Compared with CON, PE did not reduce baseline LBF in the young (CON: 251±11; PE: 193±18 ml/min, p=0.23) or old (CON: 265±18; PE: 239±36 ml/min, p=0.74); however, PHEN increased baseline LBF in both the young (PHEN: 725 ± 63 ml/min, p<0.01 vs. CON) and the old (PHEN: 680 ± 122 ml/min, p<0.01 vs. CON). During PLM in the young, PE reduced the peak change in LBF (ΔPeak LBF ) (CON: 595±67; PE: 393±46 ml/min, p=0.038) while PHEN increased the ΔPeak LBF (827 ± 89 ml/min, p=0.02 vs. CON). In contrast, in the old, no changes in ΔPeak LBF in response to PE or PHEN were evident (CON: 342±17; PE: 311±22, PHEN: 378±65 ml/min, p=0.37 for the treatment effect). The magnitude of α‐adrenergic receptor contribution (PHEN ΔPeak LBF – PE ΔPeak LBF ) was different between young and old (young: 434±97; old: 67±75 ml/min, p=0.02). The overall hyperemic response, assessed by the LBF area under the curve (LBF AUC ) during PLM, was not different when comparing CON (127 ± 23 ml/min) to PE (67 ± 19 ml/min, p=0.22) nor PHEN (210 ± 31 ml/min, p=0.095) in the young; however, LBF AUC was significantly different between PE and PHEN (p=0.02). Neither PE nor PHEN altered the LBF AUC in the old (CON: 82 ± 17, PE: 65 ± 9, PHEN: 127 ± 32 ml/min, p=0.29 for the treatment effect). Although both groups exhibited robust increases in baseline LBF after adrenergic receptor inhibition, only the young demonstrated alterations to the PLM response following stimulation and inhibition of adrenergic receptors. In line with previous findings, we observed sympathetic restraint of resting LBF in both young and old individuals. However, the age related reduction in ΔPeak LBF and LBF AUC during PLM in old individuals does not appear to be associated with augmented sympathetic regulation of vasomotor tone.