By Michael Bader

Content material:
Chapter 1 Glucocorticoids and Mineralocorticoids (pages 1–37): Eilidh Craigie, John J. Mullins and Matthew A. Bailey
Chapter 2 intercourse Steroid Hormones (pages 39–64): Vera Regitz?Zagrosek, Eva Becher, Shokoufeh Mahmoodzadeh and Carola Schubert
Chapter three Angiotensins (pages 65–100): Robson Augusto Souza Dos Santos, Anderson Jose Ferreira and Ana Cristina Simoes e Silva
Chapter four Kinins (pages 101–123): Suzana Macedo de Oliveira, Kely de Picoli Souza, Michael Bader and Joao Bosco Pesquero
Chapter five Natriuretic Peptides (pages 125–141): Paula M. Bryan and Lincoln R. Potter
Chapter 6 Endothelins (pages 143–167): Gian Paolo Rossi and Teresa M. Seccia
Chapter 7 Adrenomedullin (pages 169–191): Istvan Szokodi and Heikki Ruskoaho
Chapter eight Apelin and Vasopressin (pages 193–208): Xavier Iturrioz, Annabelle Reaux?Le Goazigo, Francoise Moos and Catherine Llorens?Cortes
Chapter nine Serotonin (pages 209–231): Prof. Dr. Michael Bader
Chapter 10 Adrenaline and Noradrenaline (pages 233–250): Nadine Beetz and Lutz Hein
Chapter eleven Dopamine (pages 251–293): Pedro Gomes and Patriio Soares?da?silva
Chapter 12 Histamine (pages 295–314): Izabela Rozenberg, Felix C. Tanner and Thomas F. Luscher
Chapter thirteen Prostaglandins and Leukotrienes (pages 315–331): Katharina Lotzer and Andreas J. R. Habenicht
Chapter 14 Cytochrome P450?Dependent Eicosanoids (pages 333–372): Wolf?Hagen Schunck and Cosima Schmidt
Chapter 15 Nucleotides and the Purinergic procedure (pages 373–393): Vera Jankowski and Joachim Jankowski
Chapter sixteen Nitric Oxide (pages 395–406): Valerie B. Schini?Kerth and Paul M. Vanhoutte
Chapter 17 Acetylcholine (pages 407–424): Maria Claudia Irigoyen, Catarina S. Porto, Pedro Paulo Soares, Fernanda Consolin?Colombo and Antonio Claudio Nobrega

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

Sample text

This feedback loop is so persuasive that it can, under conditions of sodium depletion for example, uncouple the secretion of aldosterone from control by Ang II [21]. Thus, the sodium-retaining (and pressor) effects of Ang II may be more important for blood pressure homeostasis than the effects of aldosterone on either the kidney or the vasculature, with the latter acting principally as a regulator of potassium [20]. 3). ACTH is synthesized by the posterior pituitary mainly in response to two synergistic factors – CRH and antidiuertic hormone (ADH or vasopressin), both of which produced in the paraventricular nucleus of the hypothalamus.

This produced a 30% reduction in mortality and a 35% lower frequency of hospitalization versus placebo-treated patients. Further verification of the beneficial effects of MR blockade and aldosterone antagonism was provided by the EPHESUS study in which eplerenone, an antagonist at MR more selective than spironolactone, was administered to patients who had suffered an acute myocardial infarction. Again, the results of MR blockade were particularly positive in terms of patient morbidity and mortality.

In contrast a pathological role for MR activation, particularly in the setting of mineralocorticoid excess or salt loading, has been demonstrated since the 1940s. In the early 1990s a study by Brilla and Weber investigated the effects of mineralocorticoid excess with relation to cardiovascular function, observing that rats exposed to high levels of both aldosterone and salt developed hypertension and cardiac fibrosis [94]. This triggered resurgence in clinical interest with data suggesting that actual mineralocorticoid excess was associated with cardiac abnormalities [95].

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