Key result
Endothelin-1 elicited significantly greater increases in coronary perfusion resistance in hypertensive rat hearts compared to normotensive hearts, mediated by both ETA and ETB receptors.
Why the study?
Does endothelin-1 stimulation alter coronary perfusion resistance differently in hypertensive versus normotensive rat hearts, and what is the role of ETA and ETB receptors?
Population
Isolated hearts of spontaneously hypertensive rat (SHR) and normotensive Wistar-Kyoto (WKY) rat
Comparison
Endothelin-1 infusion with or without ETA… vs Normotensive Wistar-Kyoto (WKY) rat hearts
Design
Preclinical
Authors
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Augmented ET-1 coronary vasoconstriction in SHR leaves open whether ETA/ETB blockade improves coronary flow in hypertension; human trials required.
Does endothelin-1 stimulation alter coronary perfusion resistance differently in hypertensive versus normotensive rat hearts, and what is the role of ETA and ETB receptors?
The augmented vasoconstrictor response of coronary arteries to ET-1 in hypertensive hearts is mediated by both ETA and ETB receptors, potentially contributing to impaired coronary circulation in hypertension.
Miki et al. (1998) studied Hypertension. Endothelin-1 (ET-1) with or without ETA (FR139317) and ETB (BQ788) receptor antagonists vs. Normotensive Wistar-Kyoto (WKY) rat hearts was evaluated on Coronary perfusion resistance (CPR). Endothelin-1 elicited significantly greater increases in coronary perfusion resistance in hypertensive rat hearts compared to normotensive hearts, mediated by both ETA and ETB receptors.
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