Key result
Intravenously administered endothelin-1 caused dose-dependent increases in mean arterial blood pressure and regional vascular resistances in pigs, with the kidney being most sensitive.
Endothelin-1 induces potent, dose-dependent vasoconstriction across multiple vascular beds in vivo, particularly in the renal circulation.
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Renal vasculature may be most vulnerable to endothelin-1; leaves open translation to human disease and targeted therapies.
The actions of endothelin-1 (ET-1) on vascular resistances were investigated and characterized in anesthetized pigs in vivo. Intravenously administered ET-1 (2-400 pmol/kg) caused dose-dependent increases in mean arterial blood pressure accompanied by a reduction in heart rate. ET-1 also increased renal, coronary, femoral, and bronchial vascular resistances. The kidney was about 10 times more sensitive to ET-1 than the other regions. The ET-1-induced vasoconstriction in the kidney was attenuated by nifedipine (100 micrograms/kg). The responses to ET-1 in the femoral and bronchial vascular beds were biphasic with an initial decrease followed by an increase in vascular resistance at high doses. It is concluded that ET-1 causes dose-dependent vasoconstriction in several vascular beds in vivo with the most pronounced effects in the renal circulation.
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Pernow et al. (1989) studied this question. Endothelin-1 (ET-1) was evaluated on Regional vascular resistances and mean arterial blood pressure. Intravenously administered endothelin-1 caused dose-dependent increases in mean arterial blood pressure and regional vascular resistances in pigs, with the kidney being most sensitive.
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