Aims: 

Endogenous peptide endothelin-1 (ET-1) is known as a potential marker and probable participant of various cardiovascular disorders. In kidneys, ET-1 inhibits water and Na reabsorption. Urinary ET-1 is believed to have renal origin. The aim of the research is to determine whether ET-1 plays any role in the development of experimental renovascular hypertension.

Methods: 

Male Wistar rats were divided into 4 groups. Groups H and HI were subjected to right nefrectomy. The clip was placed on left renal artery. Groups S, SI underwent sham operation. After the operation groups HI and SI were administered to endothelin-converting enzyme inhibitor PP36 with drinking water for 4 weeks. Blood pressure was controlled with the tail-cuff method. 4 weeks after the operation the rats were sacrificed by rapid neck dislocation, blood samples for ET-1 measurement were collected. The rats from H and S groups underwent urine collection before and 4 weeks after the operation.

Results: 

By the 4^th week after the operation mean blood pressure rise in group HI was significantly higher than in H group (63±6 vs 41±7 mmHg, p< 0.05). Plasma ET-1 concentration in group SI was 17% lower than in S group (median 14.8 (11–19) vs 17.8 (15–26) fmol/ml, p< 0.05), the concentration in group HI was also decreased compared to H group (16.2 (11–26) vs 18.9 (10–23) fmol/ml, not significant). After the operation ET-1 excretion rate significantly rised in H group, in S group it was unaltered (median augmentation 647.3 (range 193–1172) vs 0.9 ((-130)-310) fmol/kg*day, p< 0.05).

Conclusion: 

We suppose, ET-1 excretion rise may be a compensatory mechanism, aimed to promote water excretion by rats with one kidney. Water and Na retention could be one of the reasons why hypertension is more pronounced while administering PP36.