Key result
Vasopressin levels were elevated in rats with BEA-induced renal medullary damage (2 vs 0.8 pg/ml, P<0.05), but there was no evidence that it contributed to the rise in blood pressure.
Why the study?
Does a specific V1 receptor AVP antagonist reduce blood pressure in rats with BEA-induced renal medullary damage?
Does a specific V1 receptor AVP antagonist reduce blood pressure in rats with BEA-induced renal medullary damage?
Absolute Event Rate: 2% vs 0.8%
p-value: p=<0.05
Vasopressin does not contribute to the rise in blood pressure produced by chemical renal medullectomy in rats, despite elevated plasma levels.
Vasopressin does not mediate BP rise in this rat model despite elevation; leaves open its role in other hypertension contexts.
The induction of selective renal medullary damage by 2-bromoethylamine hydrobromide (BEA) results in polyuria and raised blood pressure. In view of the likely elevation of plasma vasopressin we have investigated the role of vasopressin (AVP) in the elevated blood pressure in this model. Plasma vasopressin levels in BEA pretreated rats were raised significantly (2 +/- 0.6 pg/ml vs 0.8 +/- 0.1 in normal rat, P less than 0.05) but not to pressor levels. In addition, pressor responsiveness was investigated in renal medullary damaged rats. There was a reduced response to vasopressin and noradrenaline but no alteration with angiotensin II. A specific V1, receptor AVP antagonist [d(CH2)5Tyr(Me)AVP] produced no fall in blood pressure but returned the noradrenaline dose-response curve to normal. This suggests an interaction between vasopressin and the sympathetic nervous system in this model. Thus there is no evidence that vasopressin contributes to the rise in blood pressure produced by chemical renal medullectomy and other mechanisms have to be sought.
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Russell et al. (1986) studied Selective renal medullary damage and hypertension. 2-bromoethylamine hydrobromide (BEA) vs. Normal rats was evaluated on Plasma vasopressin levels (p=<0.05). Vasopressin levels were elevated in rats with BEA-induced renal medullary damage (2 vs 0.8 pg/ml, P<0.05), but there was no evidence that it contributed to the rise in blood pressure.
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