By Gabor M. Rubanyi M.D., Ph.D. (auth.), Ellis R. Levin M.D., Jerry L. Nadler M.D. (eds.)
Endocrinology of Cardiovascular Function is a becoming inauguration to the Endocrine replace Series. the purpose of those guides is to supply the clinician with innovative, but succinct, entry to the newest advances in endocrinology. traditionally, our figuring out of hormonal disturbances used to be constrained to the classical secretory glands and their ambitions. As Endocrinology of Cardiovascular Function so aptly exhibits, endocrinology isn't any longer limited by means of our early physiologic knowing of glandular affliction. Endocrinology ofCardiovascular Function has set the normal of excellence for the long run volumes during this sequence.
Shlomo Melmed, M.D. sequence Editor, Endocrine Update
progress elements comparable to IGF-1 play vital roles in cardiovascular mobile hypertrophy and the reaction to acute vascular harm. From one other point of view, conventional endocrine hormones, corresponding to estrogen, were came upon to take part in fighting the advance of atherosclerosis in ladies, appearing via novel mechanisms on course vascular cells. different `endocrine' hormones, reminiscent of PTHRP and adrenomedullin, additionally modulate cardiovascular and renovascular dynamic states, suggesting new roles for those peptides as vasodilators. This multi-authored textual content is devoted to highlighting rising and critical new information about the endocrinology of the cardiovascular method.
Ellis R. Levin, M.D.
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Extra info for Endocrinology of Cardiovascular Function
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This data suggests that smooth muscle cell proliferation, in response to vascular injury, is reduced in response to E. This same study showed that steady state cmyc mRNA levels are significantly greater in intact carotid arteries from nongonadectomized male than non-gonadectomized female rats. In response to balloon injury, steady state c-myc mRNA levels rose more rapidly, and to a greater degree in intact male than female rats. This suggests that c-myc mRNA may be negatively regulated by E. This is in agreement with data from our laboratory that demonstrated that E, as well as P, can inhibit serum or ET-1-induced steady state cmyc mRNA levels in cultured human umbilical vein smooth muscle cells (18).