they are secreted in excess (particularly endothelin-1);
their receptor density increases or their affinity changes; or
- (iv)the compensatory dilator mechanisms which include the release of either
ANP (Fukuda et al. 1988),
EDRF and prostacyclin (de Nucci et al.1988) fail, or diminish, then systemic vascular resistance may increase, because endothelin (endothelin-1) has a potent and sustained vasoconstrictor effect (Table 17.1).
KeywordsVasoconstrictor Effect Hypertensive State Constrictor Effect Affinity Change Binding Site Density
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