Vascular Angiotensin II Receptors and Sodium Balance in Rats: ROLE OF KIDNEYS AND VASCULAR RENIN ACTIVITY

• Published in: Circulation research 1975-07, Vol.37 (1), p.96-100
• Main Authors: Swales, John D, Tange, John D, Thurston, Herbert
• Format: Article
• Language: English
• Subjects: Angiotensin II - immunology; Angiotensin II - pharmacology; Angiotensin II - physiology; Animals; Female; Immune Sera; Kidney - physiology; Male; Nephrectomy; Pressoreceptors - drug effects; Rabbits - immunology; Rats; Renin - blood; Renin - physiology; Sodium - metabolism; Sodium Chloride - administration & dosage
• ISSN: 0009-7330; 1524-4571
• DOI: 10.1161/01.RES.37.1.96

The relationship between the vascular response to angiotensin II and sodium balance was studied by measuring the volume of specific antiserum needed to block the pressor response to a standard dose of angiotensin II in rats. In normal rats, sodium depletion reduced the volume of antiserum required to prevent a pressor response to 50 ng of angiotensin II from 0.32 to 0.22 ml; sodium loading increased the volume required to 0.65 ml. After bilateral nephrectomy, there was a progressive increase in the antibody requirement to a maximum of 0.63 ml at 6 hours. At this stage, there was no change in the blocking requirement with sodium depletion by either pretreatment with a low-salt diet (0.60 ml) or peritoneal dialysis (0.62 ml). The pressor response to a 50-ng bolus of angiotensin II was closely correlated with the antibody requirement in all experiments (r = + 0.93). These observations indicate that sodium-induced changes in the vascular response to angiotensin II require the presence of kidney tissue. We suggest that such changes in response are mediated by alterations in vascular renin which generates angiotensin II at an arteriolar site that is not accessible to antibody molecules. This locally formed angiotensin II reduces the number of receptors free to respond to circulating angiotensin II and raises the threshold of the pressor response.