scispace - formally typeset
D

David A. Low

Researcher at Liverpool John Moores University

Publications -  136
Citations -  2966

David A. Low is an academic researcher from Liverpool John Moores University. The author has contributed to research in topics: Orthostatic vital signs & Blood pressure. The author has an hindex of 30, co-authored 128 publications receiving 2543 citations. Previous affiliations of David A. Low include Imperial College London & Brunel University London.

Papers
More filters
Journal ArticleDOI

Postural tachycardia syndrome—current experience and concepts

TL;DR: The characteristics and neuroepidemiology of PoTS are described, and possible pathophysiological mechanisms of this syndrome are outlined, as well as current and investigational treatments.
Journal ArticleDOI

Hemodynamic responses to heat stress in the resting and exercising human leg: insight into the effect of temperature on skeletal muscle blood flow

TL;DR: The findings suggest that local hyperthermia also induces vasodilatation of the skeletal muscle microvasculature, thereby contributing to heat stress and exercise hyperemia.
Journal ArticleDOI

Autonomic dysfunction in parkinsonian disorders: assessment and pathophysiology

TL;DR: The aim of this review is to describe aspects of autonomic dysfunction, including symptoms, assessment and pathophysiology, resulting from autonomic impairment in PD and other parkinsonian syndromes.
Journal ArticleDOI

Skin blood flow and local temperature independently modify sweat rate during passive heat stress in humans

TL;DR: Testing the hypotheses that decreased skin blood flow and decreased local temperature each independently attenuate sweating demonstrates that local cooling attenuates sweating by independent effects of decreased skinBlood flow and decreases local skin temperature.
Journal ArticleDOI

Heat stress enhances arterial baroreflex control of muscle sympathetic nerve activity via increased sensitivity of burst gating, not burst area, in humans

TL;DR: The primary finding of this investigation is that, at rest, whole‐body heating enhanced arterial baroreflex control of MSNA through increased sensitivity of a ‘gating’ mechanism, as indicated by an increase in the slope of the relationship between burst incidence and diastolic blood pressure.