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1 Wake Forest University School of Medicine
* To whom correspondence should be addressed. E-mail: atrask{at}wfubmc.edu.
Identification of angiotensin-(1-12) as an intermediate precursor derived directly from angiotensinogen led us to explore whether the heart has the capacity to process angiotensin-(1-12) into the biologically-active angiotensin peptides. The generation of angiotensin I, angiotensin II, and angiotensin-(1-7) from exogenous angiotensin-(1-12) was evaluated in the effluent of isolated perfused hearts mounted on a Langendorff apparatus in three normotensive and two hypertensive strains - the Sprague-Dawley, Lewis, congenic mRen2.Lewis, Wistar-Kyoto, and Spontaneously Hypertensive rats. Hearts were perfused with Krebs solution for 60 minutes before and after the addition of angiotensin-(1-12) (10 nmol/L). Angiotensin-(1-12) caused the rapid appearance of both angiotensin I and angiotensin II in the perfusate that peaked between 30 and 60 minutes of recirculation. Production of angiotensin-(1-7) from exogenous angiotensin-(1-12) rose steadily over the course of the 60-minute experiment. These data directly demonstrate that angiotensin-(1-12) is a substrate for the formation of angiotensin peptides in cardiac tissue. This finding further suggests that this angiotensinogen-derived product is a previously unrecognized important precursor peptide to the renin-angiotensin system cascade.
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