Interaction between AVP and sympathetic system in subtotal nephrectomy-saline hypertension: role of alpha and V1 receptors.
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 V1 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 V1 antagonist, (2) normotensive and hypertensive groups injected only phentolamine, (3) normotensive and hypertensive groups injected first V1 antagonist and then phentolamine, (4) normotensive and hypertensive groups injected first phentolamine and then V1 antagonist. Either V1 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 V1 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 V1 and alpha pressor activities contributes to the subtotal nephrectomy-saline hypertension and the augmentation of alpha pressor activity by vasopressin may participate in this contribution.
Ozaykan
B
B
Department of Physiology, Faculty of Medicine, University of Cukurova, Balcali, Adana, Turkey. bozaykan@mail.cu.edu.tr
Doğan
A
A
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D065092:Antidiuretic Hormone Receptor Antagonists; D001127:Arginine Vasopressin / Q000031:analogs & derivatives / Q000037:antagonists & inhibitors* / Q000378:metabolism*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D004039:Diet, Sodium-Restricted / Q000009:adverse effects*; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006727:Hormone Antagonists / Q000494:pharmacology; D006977:Hypertension, Renal / Q000188:drug therapy* / Q000503:physiopathology*; D008297:Male; D009392:Nephrectomy / Q000009:adverse effects*; D010646:Phentolamine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects* / Q000378:metabolism*; D017483:Receptors, Vasopressin / Q000187:drug effects* / Q000378:metabolism*; D017673:Sodium Chloride, Dietary / Q000009:adverse effects*; D013564:Sympathetic Nervous System / Q000187:drug effects* / Q000378:metabolism*; D013997:Time Factors
D000317:Adrenergic alpha-Antagonists; D065092:Antidiuretic Hormone Receptor Antagonists; D006727:Hormone Antagonists; D011942:Receptors, Adrenergic, alpha; D017483:Receptors, Vasopressin; D017673:Sodium Chloride, Dietary; C058531:argipressin, (1-beta-mercapto-beta,beta-cyclopentamethylenepropionic acid)-Sar(7)-; D001127:Arginine Vasopressin; D010646:Phentolamine