Regulation of Aldosterone Biosynthesis: Physiological and Clinical Aspects

ISBN-13: 9783642831225 / Angielski / Miękka / 2011 / 364 str.

J. Rg M. Ller

Opis

Sixteen years is a long time, not only in human life but also in the rapid history of contemporary endocrinology. Since the publication of the first edition of this monograph, numerous new lines of research and discoveries have greatly contrib uted to our knowledge of the physiological and pathological regulation of aldos terone biosynthesis in man and animals. The first reports about a sensitive ra dioimmunoassay for plasma aldosterone and about a preparation of dispersed zona glomerulosa cells were published in 1970 (Mayes et al. 1970; Haning et al. 1970). These two developments alone turned out to have a tremendous impact on research in aldosterone physiology (for reviews see Coghlan et al. 1979b; J. F. Tait et al. 1980b). In 1971, atrial natriuretic peptides, somatostatin, and the precursor molecule of ACTH had not yet been discovered. Angiotensin antagonists and con verting-enzyme inhibitors were not yet available. The clinical syndrome of hypo reninemic hypo aldosteronism was unknown. The possible roles of prostaglandins and dopamine in the control of aldosterone pwduction had not been considered. Cyclic AMP was then the only substance with a clearly established second-mes senger function.

Spis treści

1 Zona Glomerulosa of the Adrenal Cortex: Source of Aldosterone.- 2 Pathway of Aldosterone Biosynthesis.- 2.1 Classical Pathway and Alternative Pathways.- 2.2 Corticosterone as an Intermediate Product.- 2.3 18-Hydroxycorticosterone: Intermediate Product or By-product?.- 2.4 Alternative Pathway Through 18-Hydroxy-11-deoxycorticosterone?.- 2.5 Deoxycorticosterone Secretion.- 3 Aldosterone Biosynthesis by Cell-Free Systems.- 4 Substances Directly Influencing Aldosterone Biosynthesis in Shortterm Incubation or Perfusion Experiments.- 4.1 Angiotensins.- 4.1.1 Angiotensin II.- 4.1.2 Angiotensin III.- 4.1.3 Angiotensin I and Des-asp1-angiotensin I.- 4.1.4 Synthetic Angiotensin Analogues.- 4.1.5 Adrenocortical Angiotensin Receptors.- 4.2 Monovalent Cations.- 4.2.1 Sodium.- 4.2.2 Potassium.- 4.2.3 Ammonium, Rubidium, and Cesium.- 4.2.4 Lithium.- 4.2.5 Hydrogen Ions.- 4.3 Divalent Cations.- 4.3.1 Calcium.- 4.3.2 Substances Affecting Transport and Second-Messenger Functions of Calcium.- 4.3.3 Magnesium.- 4.4 ACTH, ACTH-related Peptides, and Other Pituitary Hormones.- 4.4.1 ACTH.- 4.4.2 ACTH-related Pituitary Peptides.- 4.4.3 Prolactin.- 4.4.4 Aldosterone-Stimulating Factor.- 4.4.5 Vasopressin.- 4.5 Amines.- 4.5.1 Serotonin.- 4.5.2 Serotonin-Related Indole Derivatives.- 4.5.3 Serotonin Antagonists.- 4.5.4 Dopamine, Dopaminergic Agonists, and Dopamine Antagonists.- 4.5.5 Histamine and Histamine Antagonists.- 4.5.6 Adrenergic Agonists and Antagonists.- 4.6 Prostaglandins and Inhibitors of Prostaglandin Biosynthesis.- 4.6.1 Prostaglandins.- 4.6.2 Inhibitors of Prostaglandin Biosynthesis.- 4.7 Aldosterone-Inhibiting Peptides.- 4.7.1 Atrial Natriuretic Peptides.- 4.7.2 Adrenal-Medullary Inhibitory Factor.- 4.7.3 Somatostatin.- 4.8 Specific Inhibitors of Steroidogenic Enzymes.- 4.8.1 Metyrapone.- 4.8.2 Su-8000, Su-9055, and Su-10603.- 4.8.3 Aminoglutethimide.- 4.8.4 Cyanosteroids.- 4.8.5 Spirolactones.- 4.9 Inhibitors of RNA or Protein Synthesis.- 4.9.1 Actinomycin D.- 4.9.2 Cycloheximide.- 4.9.3 Puromycin and Chloramphenicol.- 4.10 Steroid Hormones.- 4.10.1 Corticosteroids and Gestagens.- 4.10.2 Androgens and Estrogens.- 4.11 Ouabain.- 4.12 Miscellaneous Biological Substances with Direct Stimulatory or Inhibitory Effects on Aldosterone Biosynthesis.- 4.13 Site of Action of Stimulators or Inhibitors in the Biosynthetic Pathway.- 4.13.1 “Early Steps” and “Late Steps”.- 4.13.2 Endogenous Steroid Output.- 4.13.3 Conversion of Labeled Precursors.- 4.13.4 Experiments with Unlabeled Precursors.- 4.13.5 Experiments with Inhibitors of Steroidogenic Enzymes.- 4.14 Primary Effects and Intracellular Mediation.- 4.14.1 General Considerations.- 4.14.2 Cyclic AMP.- 4.14.3 Cyclic GMP.- 4.14.4 Calcium.- 4.14.5 Phospholipid Metabolism.- 4.14.6 Intracellular Potassium and (Na, K)-ATPase.- 5 Alterations in Aldosterone Biosynthesis and Secretion in Long-Term Experiments and Diseases.- 5.1Alterations in Sodium Intake or in Sodium Balance.- 5.1.1 “Sodium Deficiency”.- 5.1.2 Morphological and Histochemical Changes.- 5.1.3 Altered Sensitivity of the Zona Glomerulosa to.- Aldosterone-Stimulating Substances.- 5.1.4 Sites of Action in the Biosynthetic Pathway.- 5.1.5 Role of the Renin-Angiotensin System.- 5.1.6 Role of Plasma Potassium Concentration.- 5.1.7 Role of Plasma Volume.- 5.1.8 Role of Plasma Sodium Concentration.- 5.1.9 Involvement of the Central Nervous System.- 5.2 Alterations in Potassium Intake or in Potassium Balance.- 5.2.1 General Considerations.- 5.2.2 Morphological Changes.- 5.2.3 Duration of Stimulatory Effects of Potassium.- 5.2.4 Alterations in Zona Glomerulosa Sensitivity.- 5.2.5 Site of Action in the Biosynthetic Pathway.- 5.2.6 Potassium-Induced Mitochondrial Protein.- 5.2.7 Potassium Intake and the Renin-Angiotensin System.- 5.3 Exogenous Angiotensin or Renin.- 5.3.1 Aldosterone Stimulation by Pressor and Nonpressor Doses.- 5.3.2 Selectivity of Aldosterone Stimulation.- 5.3.3 Persistence of Aldosterone Stimulation.- 5.3.4 Effects on Angiotensin II Receptors and on Steroidogenic Enzymes.- 5.3.5 Effects on Sodium Balance.- 5.3.6 Renal Arterial Infusion of Angiotensin II.- 5.3.7 Immunization Against Renin or Angiotensin.- 5.3.8 Morphological and Histochemical Alterations of the Adrenal Cortex.- 5.4 Pharmacological Blockade of the Renin-Angiotensin System.- 5.4.1 Angiotensin Antagonists.- 5.4.2 Converting-Enzyme Inhibitors.- 5.4.3 Beta-Adrenergic Blocking Agents.- 5.4.4 Inhibitors of Prostaglandin Synthesis.- 5.5 Role of the Kidneys.- 5.5.1 Renovascular Hypertension.- 5.5.2 Renal Denervation, Kidney Transplantation, and Unilateral Nephrectomy.- 5.5.3 Renal Failure and Hemodialysis.- 5.5.4 Bilateral Nephrectomy.- 5.5.5 Primary Reninism.- 5.5.6 Hyporeninemic Hypoaldosteronism.- 5.6 Role of the Pituitary Gland.- 5.6.1 Hypophysectomy and Hypopituitarism.- 5.6.2 Adrenocorticotropin (ACTH).- 5.6.3 ACTH-Related Pituitary Peptides.- 5.6.4 Glucocorticoids.- 5.6.5 Growth Hormone.- 5.6.6 Prolactin.- 5.6.7 Thyroid Hormones.- 5.6.8 Vasopressin.- 5.7 Dopaminergic Regulation of Aldosterone Secretion.- 5.7.1 General Considerations.- 5.7.2 Experiments with Metoclopramide.- 5.7.3 Other Dopamine Antagonists.- 5.7.4 Dopamine and l-Dopa.- 5.7.5 Bromocriptine.- 5.8 Role of the Central Nervous System.- 5.8.1 General Considerations.- 5.8.2 Electrical and Humoral Stimulation of the Central Nervous System.- 5.8.3 Brain Lesions.- 5.8.4 Hypothalamic Factors.- 5.8.5 Pineal Gland.- 5.8.6 Spinal Cord Transection.- 5.8.7 Manic-depressive Psychosis.- 5.9 Normal Life.- 5.9.1 Fetal Development.- 5.9.2 Infancy and Childhood.- 5.9.3 Age.- 5.9.4 Diurnal Rhythms.- 5.9.5 Posture.- 5.9.6 Exercise.- 5.9.7 Heat and Cold.- 5.9.8 Altitude.- 5.9.9 Fasting and Refeeding.- 5.10 Estrogens and Progestogens.- 5.10.1 Exogenous Estrogens.- 5.10.2 Exogenous Progestogens.- 5.10.3 Oral Contraceptive Medication.- 5.10.4 Menstrual Cycle.- 5.10.5 Pregnancy.- 5.11 Aspects of Negative Feedback Regulation.- 5.11.1 Mineralocorticoids.- 5.11.2 Licorice and Carbenoxolone.- 5.11.3 Pseudohyperaldosteronism (Liddle’s Syndrome).- 5.11.4 Acquired Forms of Primary Hypoaldosteronism.- 5.11.5 Congenital Deficiencies of Steroidogenic Enzymes.- 5.11.6 Pseudohypoaldosteronism.- 5.11.7 Spirolactones.- 5.11.8 Heparin and Heparinoids.- 6 Conclusions.- 6.1 Multiplicity of Aldosterone-Stimulating Substances.- 6.2 “Adrenoglomerulotropins”.- 6.3 Physiological Inhibitors of Aldosterone Biosynthesis.- 6.4 The Shrinking Black Box.- 6.5 Long-Term Regulation of Late Steps in Aldosterone Biosynthesis.- 6.6 A Matter of Time.- 6.7 Enzymology of the Final Steps in Aldosterone Biosynthesis.- 6.8 Predominance of the Renin-Angiotensin System in the Physiological Control of Aldosterone Secretion?.- 6.9 Multifactorial Control of Aldosterone Biosynthesis.- References.

O autorze

Jürg Müller, Dr. sc. tech. ETH, seit 2005 Geschäftsführer der MKR Partner, Solothurn. Frühere Tätigkeiten: 1972 1978 Abteilungsleiter Systemanalyse bei der BBC Schweiz, 1978 1990 Direktor der Cement- und Kalkfabrik Wildegg und des Kraftwerks Rüchlig in Aarau, 1991 2004 Generaldirektor der Papierfabrik Biberist.