Download Cardiovascular Hormone Systems: From Molecular Mechanisms to by Michael Bader PDF

By Michael Bader

Edited by way of a well known scientist within the box with greater than 2 hundred excessive profile medical courses to his identify, this can be the 1st booklet to supply a finished assessment of all cardiovascular hormone structures. essentially established, the textual content covers steroid and peptide hormones, amines, and arachidonic acid metabolites, besides as nucleotides, nitric oxide, and acetylcholine. a necessary reference for researchers engaged on the cardiovascular procedure and similar illnesses.

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Extra resources for Cardiovascular Hormone Systems: From Molecular Mechanisms to Novel Therapeutics

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This results in a compensatory increase in adrenal ACTH secretion through hyperactivation of the HPA axis, leading to increased levels of circulating glucocorticoids, mineralocorticoids and androgens. A number of mutations in the human GR (hGR) gene LBD or DBD have been identified as underlying molecular mechanisms of familial GRS [162]. Although the different locations of these GRS mutations within the hGR gene result in variable clinical phenotypes, some phenotypes are more persistently expressed than others.

This is NO-dependent in conduit vasculature, but not in resistance vessels. More recently, experiments have described direct effects of aldosterone on VSMCs. By improving the coupling of α1adrenoceptors to downstream signaling pathways, mineralocorticoids improve vascular tone [124]. The molecular mechanism of aldosterone’s action in the vasculature involves genomic effects but these are observed more than 2 h after exposure. e. prior to the onset of de novo protein synthesis) suggests nongenomic action in the vasculature [104].

CAH (OMIM +201910) is an autosomal recessive disorder of cortisol synthesis in which patients have low levels of cortisol and accumulation of DOC and 11deoxycorticosterone. Approximately 11% of CAH arises from mutations in CYP11B1, the majority being caused by loss of 21-hydroxylase function. Regardless of genetic causality, CAH is associated with neonatal lethality, perhaps leading to an underestimation of the prevalence of the syndrome. Hypertension (DOC is a potent mineralocorticoid, see below) and symptoms of androgen excess, such as precocious puberty and the development of intersexual genitalia, are also features.

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