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(Hypertension. 2005;46:452.)
© 2005 American Heart Association, Inc.

In Memoriam

Sandford Lloyd Skinner (1933–2005)

Duncan J. Campbell; Colin I. Johnston; Darren J. Kelly; Eugenie R. Lumbers; Joël Ménard; James W. Ryan; Jennifer L. Wilkinson-Berka

St. Vincent’s Institute of Medical Research Fitzroy, Victoria, Australia
Baker Heart Research Institute Prahran, Victoria, Australia
Department of Medicine The University of Melbourne St. Vincent’s Hospital Fitzroy, Victoria, Australia
Department of Physiology and Pharmacology The University of New South Wales Sydney, New South Wales, Australia
Hôpital Européen Georges Pompidou Centre d’Investigations Cliniques Paris, France
Augusta, Georgia
Department of Physiology The University of Melbourne Parkville, Victoria, Australia

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Sandford Lloyd ("Sandy") Skinner, one of the pillars of the renin-angiotensin system, died on May 29, 2005, after a long illness. Sandy was a gentleman, scientist, teacher, and family man who touched the lives of the many who were fortunate to know him.

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Sandy was born in Clare, South Australia, on August 6, 1933. He graduated MBBS from The University of Adelaide in 1957. Following his medical studies, he researched the effects of vasoactive substances on the circulation and respiration of humans in the Department of Physiology, The University of Adelaide, for which he was awarded an MD degree in 1962. He also reported the artifactual elevation of plasma potassium levels during venepuncture.¹ His first postdoctoral position during 1962–1963 was at the Cleveland Clinic working with Irvine Page and James McCubbin. This was the start of his life-long passion for the renin-angiotensin system. At the Cleveland Clinic he performed seminal studies demonstrating the role of the baroreceptor mechanism of control of renin release.² Importantly, his studies demonstrated that renin release could be stimulated by reduction in renal perfusion pressure within the physiological range without significant change in renal blood flow, thus demonstrating that renin release was caused by a baroreceptor mechanism and not renal ischemia. He also showed that renal compression could stimulate renin release. These studies were important in showing that variation in renin release may have a physiological, rather than an entirely pathological, function. After the Cleveland Clinic he spent 12 months during 1963 and 1964 in Sir . . . [Full Text of this Article]