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A study was conducted to test whether the production of endothelin-1 in hearts is changed by prolonged exercise in rats. The left ventricle and lungs were homogenized with a Polytron homogenizer for 60 seconds. Reverse transcription polymerase chain reaction was then carried out to determine the expression of prepro-endothelin-1 mRNA. Results indicated that the production of endothelin-1 was significantly increased in the heart by exercise without alterations in endothelin-converting enzyme and receptor expression.

Uterine smooth muscle preparations from pregnant humans were analyzed to determine the alterations in endothelin-1 (ET-1)-induced contraction, ET receptors and receptor subtypes due to pregnancy. Analysis of human uterine membrane preparations from gravid humans indicated the presence of increased ET-1-induced uterine contractions that was attenuated by ETA receptor antagonist. ET-1-induced contractions were also mediated by increased ETA receptors and reduced ETB receptors in pregnant human uterus.

The ET(sub A)- and ET(sub B)-receptor systems are greatly accelerated in the failing heart of rats with chronic heart failure (CHF). This was the main finding in a study that sought to determine the details of the ET system in the failing heart of rats with CHF due to myocardial infarction. Details observed include the markedly higher mRNA level of preproET-1 and the peptide level of ET-1 in the failing heart of rats with CHF than control rats, as well as the equivalent level of ECE-1 mRNA in the two groups. The upregulation of ACE mRNA in the failing heart was also observed