Hemodynamic and renal effects of bosentan and losartan in endothelin-1 and angiotensin II induced hypertensive rats

Abstract EN

Endothelin-1 (ET-1) and Angiotensin II (Ang II) have great roles in the development of hypertension.

The present study was designed to investigate the short term hemodynamic and renal effects of bosentan and losartan in ET-1 and Ang II infused rats.

The study included two experiments.

First experiment included: Group 1 saline infusion, Group 2 ET-1 infusion, Group 3 Bosentan + ET-1, and Group 4 Losartan + ET-1.

While second experiment includes: Group 1 Saline infusion, Group 2 Ang II infusion, Group 3 Losartan + Ang II, and Group 4 Bosentan + Ang II.

Blood pressure was monitored every ten minutes for sixty minutes after equilibration period and urine samples were taken every twenty minutes.

Mean arterial pressure (MAP) significantly raised after thirty minutes in ET-1 infusion.

Bosentan slightly decreased MAP, while losartan infusion significantly reduced it.

Furthermore, Ang II significantly decreased H.R at 10 minute after infusion.

Neither losartan nor bosentan significantly changed serum NO level as compared with ET-1 and AngII infused rats.

Serum calcium concentration significantly elevated in ET-1 induced hypertensive rats as compared with saline group.

Sodium excretion rate tended to increase significantly in losartan group at twenty minutes and in bosentan group in both twenty and sixty minutes as compared with ET-1 group.

Furthermore, potassium excretion rate significantly increased in both time intervals.

In conclusions: Intravenous infusion of ET-1 could increase MAP.

Surprisingly, losartan rather than bosentan caused significantly reduction in MAP in ET-1 induces hypertension rats.

In contrast to bosentan administration, which caused a slight decrease in K+ excretion rate, bolus infusion of losartan significantly elevated it as compared with Ang II infused rats.