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(Hypertension. 2004;43:1153.)
© 2004 American Heart Association, Inc.

In Memoriam

Richard D. Bukoski, PhD

(1954–2004)

Harvey Sparks; Julius C. Allen; Donald J. DiPette

Michigan State University, East Lansing, Michigan
Baylor College of Medicine, Houston, Texas
Texas A&M University of Health Science Center Temple, Texas

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

Richard Bukoski, PhD, a member of the American Physiological Society since 1980, died of natural causes on March 2, 2004. He is survived by his wife Heidi, his parents, and his four children, Conrad, Jacob, Isaac, and Sarah-Anne. At the time of his death, Dick was Professor of Biology and director of the Cardiovascular Disease Research Program at the Biomedical, Biotechnology Research Institute at North Carolina Central University (NCCU), Durham.

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Dr Bukoski’s research, which has been supported by National Institutes of Health (NIH) funding since 1988, had the long-range goal of understanding the molecular mechanisms that link whole animal Ca²⁺ homeostasis with vascular function. Among his accomplishments were description of the effects of 1,25 (OH)₂ vitamin D₃ and noncalcemic analogues of the secosteroid on vascular smooth muscle phenotype, intracellular Ca²⁺ metabolism, and contractility; the demonstration of a Ca²⁺-activated, perivascular sensory nerve dependent vasodilator system in isolated arteries; the finding that sensory nerves express a Ca²⁺ sensing receptor that is homologous with that initially described in the parathyroid gland; and providing the first evidence that an endocannabinoid-like ligand may serve as the transmitter that is released from perivascular nerves in response to elevation of extracellular Ca²⁺. More recently, his group found that dorsal root ganglion calcium sensing receptor cDNA arises from tissue-specific alternative splicing of a single gene, that its amino acid sequence is homologous to other known calcium sensing receptors, and that it undergoes differential posttranslational processing relative to the thyroparathyroid calcium sensing receptor and is functionally . . . [Full Text of this Article]