By Michael Bader
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 method (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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Additional resources for Cardiovascular Hormone Systems: From Molecular Mechanisms to Novel Therapeutics
Whether this is a species difference or reﬂects the sensitivity of enzyme expression to conditions of culture remains uncertain and resolution awaits the development of reliable antibodies. Physiologically adrenal steroids – both aldosterone and glucocorticoids – potentiate the action of vasoconstrictors. This effect was ﬁrst described in the 1950s for catecholamines but is also true for other vasoactive agents, notably Ang II . There is some evidence to suggest that the potentiating effect of corticosteroids differs throughout the vasculature.
4 GR Polymorphisms Glucocorticoid variation also exists in the general population, as has been experimentally shown by varied responses to dexamethasone (asynthetic glucocorticoid that has no afﬁnity for the MR) by an elderly experimental cohort . Several GR polymorphisms have been identiﬁed that seem to be associated with altered glucocorticoids sensitivity and metabolic parameters (for review, see ). The N363S polymorphism has been shown to increase glucose sensitivity and the insulin response to dexamethasone, as well as an increased body mass index (BMI).
Mutations in CYP11B2 cause the autosomal disorder of corticosterone methyoxidase deﬁciency (CMO), types 1 and 2 . In CMO1 (OMIM #203400), there is no enzyme activity and aldosterone is undetectable. Patients have marked growth retardation and fail to thrive. Altered renal electrolyte balance leads to hyponatremia and hyperkalemia, and hypotension is evident. This is presumably secondary to volume depletion; however, since activation of MR in vascular smooth muscle potentiates the action of vasoconstrictors (see below), a contribution of vasodilation to the hypotension cannot be discounted.
Cardiovascular Hormone Systems: From Molecular Mechanisms to Novel Therapeutics by Michael Bader