| pubmed-article:1826412 | pubmed:abstractText | The cardiovascular effects of endothelin-1 (ET-1) in trout were examined in unanesthetized fish, perfused tissues, and isolated vascular rings. In vivo, a bolus of 500 ng/kg body wt ET-1 transiently lowered arterial (postgill) blood pressure (BP) by nearly 30%; 1,500 ng/kg body wt produced a triphasic, pressor-depressor-pressor, response. Continuous infusion of 0.1, 1, 10, and 30 ng.kg-1.min-1 progressively lowered BP but did not affect heart rate (HR), urine flow, or electrolyte excretion. In the in situ perfused heart ET-1 (10(-11) to 10(-8) M) had no effect on HR or power output. ET-1 produced dose-dependent increases in vascular resistance in the perfused gill, renal-skeletal muscle, and splanchnic circulations, and increased tension, independent of endothelium, in vascular rings from celiacomesenteric (CA) and coronary arteries and anterior cardinal veins (CV). Ventral aortas were refractory to ET-1. In vitro, ET-1 effects were slow in onset and long lasting. External calcium was required for maximal ET-1 responses in gill and CA. ET-1 effects on CA but not CV were partially inhibited by calcium channel blockers, diltiazem, and D 600, and by the guanylate cyclase activators, atrial natriuretic factor, and sodium nitroprusside. [3H]water flux across the perfused gill was stimulated by ET-1 through what appeared to be a vascular-independent mechanism. These experiments show that the trout vasculature is exquisitely sensitive to ET-1, and they suggest that the physiological expression of this peptide has been highly conserved during the course of vertebrate evolution. | lld:pubmed |
