Angiotensin-converting enzyme (ACE) cleaves angiotensin I to generate the active vasoconstrictor angiotensin II. The pulmonary vascular bed is rich in ACE activity1 and it was believed that the lung is the exclusive site of generation of angiotensin II. However, potent ACE activity has subsequently been demonstrated in other vascular beds.2 Indeed, the fractional conversion of angiotensin I to angiotensin n across the human forearm (approximately 40%)3 is similar to that across the lung. ACE is present on endothelial cells and may regulate local vascular responses to angiotensin I. Locally generated angiotensin II could function as a paracrine rather than an endocrine mechanism. This is a flexible and potentially important means of regulating regional blood flow since local generation could vary in different vascular beds, whereas systemic tissues are all exposed to the same circulating concentration of angiotensin II. Messenger ribonucleic acid for renin is present in the heart,4 and local generation of angiotensin n in the coronary circulation could be of considerable functional importance. This study investigates effects of locally infused angiotensin I and II, with and without an ACE inhibitor, on canine coronary blood flow in vivo.