Although endothelin (ET)-1 is one of the strongest known vasoconstrictors in most
species, we and others have previously found that it is only weakly effective in the mouse
aorta. The aim of this study was to further investigate vasoactive effects of ET-1 in
vascular beds generally known to be particularly sensitive to ET-1, such as the renal
artery. Experiments were performed to determine the vasoconstrictor responses in the
thoracic aorta, and in the carotid, femoral, and renal arteries. Isolated vascular rings
of C57BL/6 adult male mice (35–40 weeks of age) were exposed to ET-1 (0.01–300
nM) in the presence of the nitric oxide synthase inhibitor
l-NAME (0.3 mM) to exclude effects of nitric oxide. Vessels from
different vascular beds demonstrated distinct patterns in potency of the contractions to
ET-1 and the dynamics of the responses. The maximal contraction to ET-1 was strong and
significantly greater in the femoral (105 ± 7% KCl) and renal artery (62 ± 7% KCl) than in
the carotid artery or the aorta (P < 0.05). The dynamics of the
contractile response to ET-1 varied between the different vessels: the renal artery showed
a rapid vasoconstriction, followed by a near complete loss of tension, whereas in the
aorta, carotid, and femoral artery, vasoconstriction was more sustained. In conclusion,
the data demonstrate that mouse femoral and renal arteries exhibit strong contractions in
response to ET-1 compared with aorta and carotid artery, and that contractile dynamics
differ markedly between arterial vascular beds. These findings may be important for
studying the effects of endothelin in mouse models of human disease.
