Relationships between kallikrein secretion, kallikrein excretion and β‐adrenoceptors in kidney cortical slices from neurogenic hypertensive dogs

• Published in: British journal of pharmacology 1995-09, Vol.116 (1), p.1704-1710
• Main Authors: Damase‐Michel, Christine, Bompart, Guy, Durrieu, Geneviève, Montastruc, Jean‐Louis, Montastruc, Paul, Girolami, Jean‐Pierre
• Format: Article
• Language: English
• Subjects: Animals; Arterial hypertension. Arterial hypotension; Biological and medical sciences; Blood and lymphatic vessels; Blood Pressure - physiology; Cardiology. Vascular system; Catecholamines - blood; Denervation; Disease Models, Animal; Dogs; Experimental diseases; experimental hypertension; Heart Rate - physiology; Hypertension - physiopathology; Hypertension - urine; Kallikrein; Kallikreins - metabolism; Kallikreins - urine; Kidney Cortex - metabolism; Kidney Cortex - physiopathology; Kidney Cortex - ultrastructure; Male; Medical sciences; Proteinuria - urine; Receptors, Adrenergic, beta - physiology; sinoaortic denervation; Sinus of Valsalva - innervation; β‐adrenoceptors
• ISSN: 0007-1188; 1476-5381
• DOI: 10.1111/j.1476-5381.1995.tb16395.x

1 Sinoaortic denervation (SAD) in dogs is characterized by an increase in blood pressure and heart rate as well as the development of renal morphological lesions similar to those observed in essential hypertension in human subjects. To assess the effect of SAD on the secretion of kallikrein kinin systems (KKS), we studied the in vitro secretion of kallikrein by renal cortical slices of normal and neurogenic hypertensive dogs (1 and 18 months after SAD). The method using renal cortical slices allowed the study of secretion of kallikrein independently of renal perfusion pressure. The number of renal β‐adrenoceptors was measured by [125I]‐cyanopindolol binding. 2 SAD was associated with a marked increase in urinary kallikrein excretion at one month and a significant decrease at 18 months when compared with controls. Both changes were statistically significant (P