Kidney in Essential Hypertension : Proceedings of the Course on the Kidney in Essential Hypertension Held at New Orleans, Louisiana, March 18–19, 1983

The kidney, similar to the heart, plays a three-fold role in essential hypertension. First, it participates in the patho­ genesis of arterial hypertension. Second, it suffers as a target organ of long-standing hypertension, and third, it experiences the effects of antihypertensive therapy. Perhaps most contested at the present time is the involvement of the kidney in the patho­ genesis of essential hypertension. More than a century ago, William Osler put forward three basic hypotheses about the "genuine contracted kidney. "l 1. "The hypertrophy can be regarded as an effect to overcome a sort of stop-cock action of the vessels when under the influence of an irritating ingredient in the blood greatly contracted and increased the peripheral resistance. " Clearly this hypothesis of an "irritating ingredient" is perhaps the most convincing nowadays, and numerous attempts have been made to identify a specific vasoconstrictive agent in the blood in essential hypertension. 2. "The obliteration of a large number of capillary territories in the kidney materially raised the arterial pressure. An additional factor of dimin­ ished excretion of water also heightened the pressure within the blood vessel. " Today we know that fluid volume overload in the presence of reduced renal mass seems to be the most likely mechanism accoun­ ting for renal parenchymal hypertension and, as shown by Guyton's group, for certain forms of experimental hypertension. 3. Front Matter....Pages i-xii The Relation of a Circulating Sodium Transport Inhibitor to Essential Hypertension....Pages 1-14 Atrial Natriuretic Factor....Pages 15-23 The Physiology and Cell Biology of the Renin-Angiotensin System in Hypertension....Pages 25-41 Prostaglandins and Hypertension....Pages 43-54 Kallikrein and Kinins in Epithelial Ion Transport....Pages 55-64 Renal Afferent Nerves: Evidence for a Role in Cardiovascular Regulation and the Pathogenesis of Experimental Hypertension....Pages 65-75 Renal Blood Flow and Function in Essential Hypertension....Pages 77-85 The Kidney and Experimental Hypertension....Pages 87-103 Determinants of Exaggerated Natriuresis in Arterial Hypertension....Pages 105-123 Renal Hemodynamics in Obese and Lean Essential Hypertensive Patients....Pages 125-129 Sodium and Water Excretion in Patients with Congestive Heart Failure and Cirrhosis....Pages 131-147 Comparison of Renal Hemodynamics in Black and White Patients with Essential Hypertension....Pages 149-156 Effects of Beta-Adrenergic Antagonists and Diuretics on Kidney Function in Hypertensive Patients....Pages 157-169 Effects of Central Alpha-Adrenoceptor Agonists and Adrenergic-Neuronal Blocking Agents on the Kidney....Pages 171-191 Effects of Alpha 1 -Adrenoceptor Antagonists and Directly Acting Vasodilators on the Kidney....Pages 193-207 Diuretics and the Kidney....Pages 209-225 Converting Enzyme Inhibition and the Kidney: Effect on Potassium Homeostasis and Renal Function....Pages 227-234 Systemic and Renal Hemodynamic Effects of Enalapril in Patients with Essential Hypertension....Pages 235-245 Antihypertensive Treatment in Renal Failure....Pages 247-259 The kidney, similar to the heart, plays a three-fold role in essential hypertension. First, it participates in the pathoƯ genesis of arterial hypertension. Second, it suffers as a target organ of long-standing hypertension, and third, it experiences the effects of antihypertensive therapy. Perhaps most contested at the present time is the involvement of the kidney in the pathoƯ genesis of essential hypertension. More than a century ago, William Osler put forward three basic hypotheses about the "genuine contracted kidney. "l 1. "The hypertrophy can be regarded as an effect to overcome a sort of stop-cock action of the vessels when under the influence of an irritating ingredient in the blood greatly contracted and increased the peripheral resistance." Clearly this hypothesis of an "irritating ingredient" is perhaps the most convincing nowadays, and numerous attempts have been made to identify a specific vasoconstrictive agent in the blood in essential hypertension. 2. "The obliteration of a large number of capillary territories in the kidney materially raised the arterial pressure. An additional factor of diminƯ ished excretion of water also heightened the pressure within the blood vessel." Today we know that fluid volume overload in the presence of reduced renal mass seems to be the most likely mechanism accounƯ ting for renal parenchymal hypertension and, as shown by Guyton's group, for certain forms of experimental hypertension. 3