Akademik Veri Yönetim Sistemi
JOURNAL OF THE AUTONOMIC NERVOUS SYSTEM, cilt.78, ss.165-171, 2000 (SCI-Expanded)
The development process of subtotal nephrectomy-salt hypertension is still unclear. The aim of the present study was to determine the role of the interaction between vasopressin and sympathetic system in the development of this hypertension by using AVP V-1 antagonist and alpha blocker phentolamine under anesthesia condition. For this purpose, we carried out about 73% subtotal nephrectomy on male Wistar rats. One group of these rats (normotensive group) was given a low-salt diet and the other group (hypertensive group) was given a high-salt diet for 4 weeks. Finally, eight groups of rats were formed according to the kind(s) of the injected drug(s): (1) normotensive and hypertensive groups injected only V-1 antagonist, (2) normotensive and hypertensive groups injected only phentolamine, (3) normotensive and hypertensive groups injected first V-1 antagonist and then phentolamine, (4) normotensive and hypertensive groups injected first phentolamine and then V-1 antagonist. Either V-1 or alpha blockage separately led to a higher reduction in the mean blood pressure (MAP) of the hypertensives than, of the normotensives (p < 0.05). The combined blockage of V-1 and alpha receptors, also caused a higher decrease in the MAP of hypertensive group than, of normotensive group, not depending on the order of the injections (p < 0.01). The heart rate increase recorded as a response to the phentolamine injection in normotensive group, did not develop in hypertensive group (p < 0.05). There was no significant difference between the two groups with regard to plasma electrolytes and osmolality. A positive correlation was found between systolic blood pressure and plasma osmolality in hypertensive group (r = 0.40, p < 0.05), but not in normotensive group. We conclude that the increase in V-1 and alpha presser activities contributes to the subtotal nephrectomy-saline hypertension and the augmentation of alpha presser activity by vasopressin may participate in this contribution. (C) 2000 Published by Elsevier Science B.V. All rights reserved.