Why the study?
Does endothelin induce different vasoconstrictor responses in microvessels and macrovessels of hypertensive rats compared to normotensive controls?
Does endothelin induce different vasoconstrictor responses in microvessels and macrovessels of hypertensive rats compared to normotensive controls?
Endothelin induces greater reactivity in the microvessels, but not macrovessels, of hypertensive rats compared to controls, suggesting altered microvascular sensitivity or endothelial dysfunction in hypertension.
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Should not change practice; extends animal data on microvascular endothelin reactivity in hypertension.
The response to endothelin, a novel 21-amino acid peptide, is investigated in isolated aortas with and without endothelium and in mesenteric microvessels in vivo-in situ, in Goldblatt II (GII) and deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Median effective concentrations and maximal responses to endothelin did not differ in aortas with endothelium isolated from GII, DOCA-salt hypertensive, and control rats. After removal of the endothelium, the potentiation of the aorta responses to endothelin was of the same magnitude in hypertensive and control rats. A closed-circuit television system was used to observe the microvascular bed of the exteriorized mesentery of anesthetized GII, DOCA-salt hypertensive, and control rats. The time necessary to induce a vasoconstrictor response was determined after the topical application of endothelin. Vessel diameters at rest and after endothelin application were also estimated. At the microcirculatory level, a greater reactivity to endothelin was observed in both hypertensive rat groups, whereas higher sensitivity to endothelin was recorded in the GII hypertensive microvessel preparations alone. It is suggested that the increased response to endothelin observed in hypertensive rats might be due to abnormal sensitivity or reactivity of the microvessels of these rats reflecting an alteration of the contractile sequence possibly at the plasma membrane level, or due to both. Endothelial dysfunction at the microcirculatory level, however, cannot be dismissed.
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Carvalho et al. (1990) studied this question.
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