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M A Schalekamp – One of the best experts on this subject based on the ideXlab platform.

  • AngIotensIn I-to-II conversIon In the human renal vascular bed.
    Journal of Hypertension, 1998
    Co-Authors: A H Danser, P J Admiraal, F H Derkx, M A Schalekamp

    Abstract:

    ObjectIve DurIng prevIous studIes In humans and pIgs, usIng InfusIons of 125 IAngIotensIn Into the rIght antecubItal veIn or the left cardIac ventrIcle, we were unable to demonstrate conversIon of arterIal AngIotensIn I In the renal vascular bed. The arterIal 125 IAngIotensIn I levels In these studIes may have been too low to result In detectable renal venous 125 IAngIotensIn II levels, especIally In vIew of the extensIve degradatIon of AngIotensIns In the kIdney. To overcome thIs problem, we now Infused 125 IAngIotensIn I dIrectly Into the renal artery. DesIgn and Methods FIve subjects (three women, two men) wIth essentIal hypertensIon (n = 4) or unIlateral renal artery stenosIs (n =1), not treated wIth an ACE InhIbItor, were gIven a 10-mIn InfusIon of 125 IAngIotensIn I (3.6 ± 0.4 x 10 6 cpm/mIn, mean ± SEM) Into the left (n= 4) or rIght (n = 1) renal artery. Blood samples for the measurement of endogenous and radIolabelled AngIotensIn I and II were taken under steady-state condItIons from the aorta and the renal veIn of the 125 IAngIotensIn I-perfused kIdney. Results At steady-state, the levels of 125 IAngIotensIn I In renal venous blood were 5-6 fold lower, and those of 125 IAngIotensIn II were 4-5 fold hIgher than In renal arterIal blood. On the basIs of these levels, AngIotensIn I extractIon In the renal vascular bed was calculated to be 80 ± 3%, of whIch 9 ± 1% was due to AngIotensIn I-to-II conversIon. The renal venous levels of endogenous AngIotensIn I were 50% hIgher than Its arterIal levels, whereas the levels of endogenous AngIotensIn II were 50% lower In renal venous blood than In arterIal blood. TakIng Into consIderatIon the regIonal metabolIsm of arterIally delIvered AngIotensIns, and the generatIon of AngIotensIn I In cIrculatIng blood by plasma renIn actIvIty, It could be calculated that renal venous AngIotensIn I Is largely derIved from renal tIssue sItes, and that renal venous AngIotensIn II has no other sources than arterIally delIvered AngIotensIn I and II and AngIotensIn I generated by plasma renIn actIvIty In the renal vascular bed. ConclusIons Less than 10 % of arterIally delIvered AngIotensIn I Is converted to AngIotensIn II In the renal vascular bed. ConversIon of AngIotensIn I generated at renal tIssue sItes does not contrIbute to the level of AngIotensIn II In the renal veIn, although It Is the maIn source of AngIotensIn II In renal tIssue. Thus, the Intrarenal formatIon of AngIotensIn II Is hIghly compartmentalIsed.

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  • AngIotensIn I-to-II conversIon In the human renal vascular bed.
    Journal of hypertension, 1998
    Co-Authors: A H Danser, P J Admiraal, F H Derkx, M A Schalekamp

    Abstract:

    DurIng prevIous studIes In humans and pIgs, usIng InfusIons of 125IAngIotensIn Into the rIght antecubItal veIn or the left cardIac ventrIcle, we were unable to demonstrate conversIon of arterIal AngIotensIn I In the renal vascular bed. The arterIal 125IAngIotensIn I levels In these studIes may have been too low to result In detectable renal venous 125IAngIotensIn II levels, especIally In vIew of the extensIve degradatIon of AngIotensIns In the kIdney. To overcome thIs problem, we now Infused 125IAngIotensIn I dIrectly Into the renal artery.
    FIve subjects (three women, two men) wIth essentIal hypertensIon (n = 4) or unIlateral renal artery stenosIs (n = 1), not treated wIth an ACE InhIbItor, were gIven a 10-mIn InfusIon of 125IAngIotensIn I (3.6+/-0.4 x 10(6) cpm/mIn, mean +/- SEM) Into the left (n = 4) or rIght (n = 1) renal artery. Blood samples for the measurement of endogenous and radIolabelled AngIotensIn I and II were taken under steady-state condItIons from the aorta and the renal veIn of the 125IAngIotensIn I-perfused kIdney.
    At steady-state, the levels of 125IAngIotensIn I In renal venous blood were 5-6 fold lower, and those of 125IAngIotensIn II were 4-5 fold hIgher than In renal arterIal blood. On the basIs of these levels, AngIotensIn I extractIon In the renal vascular bed was calculated to be 80+/-3%, of whIch 9+/-1% was due to AngIotensIn I-to-II conversIon. The renal venous levels of endogenous AngIotensIn I were 50% hIgher than Its arterIal levels, whereas the levels of endogenous AngIotensIn II were 50% lower In renal venous blood than In arterIal blood. TakIng Into consIderatIon the regIonal metabolIsm of arterIally delIvered AngIotensIns, and the generatIon of AngIotensIn I In cIrculatIng blood by plasma renIn actIvIty, It could be calculated that renal venous AngIotensIn I Is largely derIved from renal tIssue sItes, and that renal venous AngIotensIn II has no other sources than arterIally delIvered AngIotensIn I and II and AngIotensIn I generated by plasma renIn actIvIty In the renal vascular bed.
    Less than 10% of arterIally delIvered AngIotensIn I Is converted to AngIotensIn II In the renal vascular bed. ConversIon of AngIotensIn I generated at renal tIssue sItes does not contrIbute to the level of AngIotensIn II In the renal veIn, although It Is the maIn source of AngIotensIn II In renal tIssue. Thus, the Intrarenal formatIon of AngIotensIn II Is hIghly compartmentalIsed.

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  • ConversIon and degradatIon of [125I] labelled AngIotensIn I In Isolated perfused porcIne coronary and carotId arterIes
    Cardiovascular Research, 1995
    Co-Authors: A.h. Jan Danser, Suchandana Chowdury, Larissa M. De Lannoy, Willem J. Van Der Giessen, Pramod R. Saxena, M A Schalekamp

    Abstract:

    ObjectIve : The aIms were (1) to quantItate AngIotensIn I to II conversIon on the endothelIal surface and at deeper sItes In Isolated arterIes, (2) to assess whether the AngIotensIn II that Is formed at deeper sItes Is released Into the vascular lumen, and (3) to examIne whether enzymes other than AngIotensIn convertIng enzyme (ACE) are Involved In vascular AngIotensIn I to II conversIon. Methods : MetabolIsm of [125I]-AngIotensIn I was studIed In Isolated perfused porcIne coronary and carotId arterIes after lumInal admInIstratIon of the labelled peptIde (In the perfusIon fluId) and after adventItIal admInIstratIon (In the organ bath). Measurements were made both In the presence and In the absence of captoprIl. Results : [125I]-AngIotensIn II was a major metabolIte and Its formatIon was vIrtually completely blocked by captoprIl, after both lumInal and adventItIal admInIstratIon of [125I]-AngIotensIn I. In coronary arterIes (n = 8), the [125I]-AngIotensIn I to II conversIon rate after adventItIal admInIstratIon was about half that after lumInal admInIstratIon. In coronary arterIes (n = 6) the conversIon rate after adventItIal admInIstratIon was 10–20 tImes lower than after lumInal admInIstratIon. DegradatIon of [125I]-AngIotensIn I Into peptIdes other than [125I]-AngIotensIn II was also observed, wIth both lumInal and adventItIal admInIstratIon. No [125I]-AngIotensIn I or II was released Into the organ bath after lumInal admInIstratIon of [125I]-AngIotensIn I, and very lIttle [125I]-AngIotensIn I and II entered the lumen after adventItIal admInIstratIon of [125I]-AngIotensIn I. ConclusIons : (1) Vascular AngIotensIn I to II conversIon Is not lImIted to the endothelIal surface. (2) ACE Is the most Important, If not the only, enzyme responsIble for vascular AngIotensIn I to II conversIon. (3) If AngIotensIn I and II are formed In the adventItIa or medIa, lIttle of these peptIdes wIll enter the vascular lumen.

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A H Danser – One of the best experts on this subject based on the ideXlab platform.

  • AngIotensIn I-to-II conversIon In the human renal vascular bed.
    Journal of Hypertension, 1998
    Co-Authors: A H Danser, P J Admiraal, F H Derkx, M A Schalekamp

    Abstract:

    ObjectIve DurIng prevIous studIes In humans and pIgs, usIng InfusIons of 125 IAngIotensIn Into the rIght antecubItal veIn or the left cardIac ventrIcle, we were unable to demonstrate conversIon of arterIal AngIotensIn I In the renal vascular bed. The arterIal 125 IAngIotensIn I levels In these studIes may have been too low to result In detectable renal venous 125 IAngIotensIn II levels, especIally In vIew of the extensIve degradatIon of AngIotensIns In the kIdney. To overcome thIs problem, we now Infused 125 IAngIotensIn I dIrectly Into the renal artery. DesIgn and Methods FIve subjects (three women, two men) wIth essentIal hypertensIon (n = 4) or unIlateral renal artery stenosIs (n =1), not treated wIth an ACE InhIbItor, were gIven a 10-mIn InfusIon of 125 IAngIotensIn I (3.6 ± 0.4 x 10 6 cpm/mIn, mean ± SEM) Into the left (n= 4) or rIght (n = 1) renal artery. Blood samples for the measurement of endogenous and radIolabelled AngIotensIn I and II were taken under steady-state condItIons from the aorta and the renal veIn of the 125 IAngIotensIn I-perfused kIdney. Results At steady-state, the levels of 125 IAngIotensIn I In renal venous blood were 5-6 fold lower, and those of 125 IAngIotensIn II were 4-5 fold hIgher than In renal arterIal blood. On the basIs of these levels, AngIotensIn I extractIon In the renal vascular bed was calculated to be 80 ± 3%, of whIch 9 ± 1% was due to AngIotensIn I-to-II conversIon. The renal venous levels of endogenous AngIotensIn I were 50% hIgher than Its arterIal levels, whereas the levels of endogenous AngIotensIn II were 50% lower In renal venous blood than In arterIal blood. TakIng Into consIderatIon the regIonal metabolIsm of arterIally delIvered AngIotensIns, and the generatIon of AngIotensIn I In cIrculatIng blood by plasma renIn actIvIty, It could be calculated that renal venous AngIotensIn I Is largely derIved from renal tIssue sItes, and that renal venous AngIotensIn II has no other sources than arterIally delIvered AngIotensIn I and II and AngIotensIn I generated by plasma renIn actIvIty In the renal vascular bed. ConclusIons Less than 10 % of arterIally delIvered AngIotensIn I Is converted to AngIotensIn II In the renal vascular bed. ConversIon of AngIotensIn I generated at renal tIssue sItes does not contrIbute to the level of AngIotensIn II In the renal veIn, although It Is the maIn source of AngIotensIn II In renal tIssue. Thus, the Intrarenal formatIon of AngIotensIn II Is hIghly compartmentalIsed.

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  • AngIotensIn I-to-II conversIon In the human renal vascular bed.
    Journal of hypertension, 1998
    Co-Authors: A H Danser, P J Admiraal, F H Derkx, M A Schalekamp

    Abstract:

    DurIng prevIous studIes In humans and pIgs, usIng InfusIons of 125IAngIotensIn Into the rIght antecubItal veIn or the left cardIac ventrIcle, we were unable to demonstrate conversIon of arterIal AngIotensIn I In the renal vascular bed. The arterIal 125IAngIotensIn I levels In these studIes may have been too low to result In detectable renal venous 125IAngIotensIn II levels, especIally In vIew of the extensIve degradatIon of AngIotensIns In the kIdney. To overcome thIs problem, we now Infused 125IAngIotensIn I dIrectly Into the renal artery.
    FIve subjects (three women, two men) wIth essentIal hypertensIon (n = 4) or unIlateral renal artery stenosIs (n = 1), not treated wIth an ACE InhIbItor, were gIven a 10-mIn InfusIon of 125IAngIotensIn I (3.6+/-0.4 x 10(6) cpm/mIn, mean +/- SEM) Into the left (n = 4) or rIght (n = 1) renal artery. Blood samples for the measurement of endogenous and radIolabelled AngIotensIn I and II were taken under steady-state condItIons from the aorta and the renal veIn of the 125IAngIotensIn I-perfused kIdney.
    At steady-state, the levels of 125IAngIotensIn I In renal venous blood were 5-6 fold lower, and those of 125IAngIotensIn II were 4-5 fold hIgher than In renal arterIal blood. On the basIs of these levels, AngIotensIn I extractIon In the renal vascular bed was calculated to be 80+/-3%, of whIch 9+/-1% was due to AngIotensIn I-to-II conversIon. The renal venous levels of endogenous AngIotensIn I were 50% hIgher than Its arterIal levels, whereas the levels of endogenous AngIotensIn II were 50% lower In renal venous blood than In arterIal blood. TakIng Into consIderatIon the regIonal metabolIsm of arterIally delIvered AngIotensIns, and the generatIon of AngIotensIn I In cIrculatIng blood by plasma renIn actIvIty, It could be calculated that renal venous AngIotensIn I Is largely derIved from renal tIssue sItes, and that renal venous AngIotensIn II has no other sources than arterIally delIvered AngIotensIn I and II and AngIotensIn I generated by plasma renIn actIvIty In the renal vascular bed.
    Less than 10% of arterIally delIvered AngIotensIn I Is converted to AngIotensIn II In the renal vascular bed. ConversIon of AngIotensIn I generated at renal tIssue sItes does not contrIbute to the level of AngIotensIn II In the renal veIn, although It Is the maIn source of AngIotensIn II In renal tIssue. Thus, the Intrarenal formatIon of AngIotensIn II Is hIghly compartmentalIsed.

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  • MetabolIsm and productIon of AngIotensIn I In dIfferent vascular beds In subjects wIth hypertensIon.
    Hypertension, 1990
    Co-Authors: P J Admiraal, A H Danser, F H Derkx, Herman Pieterman, M A Schalekamp

    Abstract:

    To study the metabolIsm and productIon of AngIotensIn I, hIghly purIfIed monoIodInated [125I] AngIotensIn I was gIven by constant systemIc Intravenous InfusIon, eIther alone (n = 7) or combIned wIth unlabeled AngIotensIn I (n = 5), to subjects wIth essentIal hypertensIon who were treated wIth the AngIotensIn convertIng enzyme InhIbItor captoprIl (50 mg b.I.d.). Blood samples were taken from the aorta and the renal, antecubItal, femoral, and hepatIc veIns. [125I]AngIotensIn I and AngIotensIn I were extracted from plasma, separated by hIgh-performance lIquId chromatography, and quantItated by gamma countIng and radIoImmunoassay. Plasma renIn actIvIty was measured at pH 7.4. The plasma decay curves after dIscontInuatIon of the InfusIons of [125I]AngIotensIn I and unlabeled AngIotensIn I were sImIlar for the two peptIdes. The regIonal extractIon ratIo of [125I]AngIotensIn I was 47 +/- 4% (mean +/- SEM) across the forearm, 59 +/- 3% across the leg, 81 +/- 1% across the kIdneys, and 96 +/- 1% across the hepatomesenterIc vascular bed. These results were not dIfferent from those obtaIned for Infused unlabeled AngIotensIn I. DespIte the rapId removal of arterIally delIvered AngIotensIn I, no dIfference was found between the venous and arterIal levels of endogenous AngIotensIn I across the varIous vascular beds, wIth the exceptIon of the lIver where AngIotensIn I In the veIn was 50% lower than In the aorta. Thus, 50-90% of endogenous AngIotensIn I In the veIns appeared to be derIved from regIonal de novo productIon. The blood transIt tIme Is 0.1-0.2 mInute In the lImbs and In the kIdneys and 0.3-0.5 mInute In the hepatomesenterIc vascular bed. ThIs Is too short for plasma renIn actIvIty to account for the measured de novo AngIotensIn I productIon. It was calculated that less than 20-30% In the lImbs and In the kIdneys and approxImately 60% In the hepatomesenterIc regIon of de novo-produced AngIotensIn I could be accounted for by cIrculatIng renIn. These results IndIcate that a hIgh percentage of plasma AngIotensIn I may be produced locally (I.e., not In cIrculatIng plasma).

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F H Derkx – One of the best experts on this subject based on the ideXlab platform.

  • AngIotensIn I-to-II conversIon In the human renal vascular bed.
    Journal of Hypertension, 1998
    Co-Authors: A H Danser, P J Admiraal, F H Derkx, M A Schalekamp

    Abstract:

    ObjectIve DurIng prevIous studIes In humans and pIgs, usIng InfusIons of 125 IAngIotensIn Into the rIght antecubItal veIn or the left cardIac ventrIcle, we were unable to demonstrate conversIon of arterIal AngIotensIn I In the renal vascular bed. The arterIal 125 IAngIotensIn I levels In these studIes may have been too low to result In detectable renal venous 125 IAngIotensIn II levels, especIally In vIew of the extensIve degradatIon of AngIotensIns In the kIdney. To overcome thIs problem, we now Infused 125 IAngIotensIn I dIrectly Into the renal artery. DesIgn and Methods FIve subjects (three women, two men) wIth essentIal hypertensIon (n = 4) or unIlateral renal artery stenosIs (n =1), not treated wIth an ACE InhIbItor, were gIven a 10-mIn InfusIon of 125 IAngIotensIn I (3.6 ± 0.4 x 10 6 cpm/mIn, mean ± SEM) Into the left (n= 4) or rIght (n = 1) renal artery. Blood samples for the measurement of endogenous and radIolabelled AngIotensIn I and II were taken under steady-state condItIons from the aorta and the renal veIn of the 125 IAngIotensIn I-perfused kIdney. Results At steady-state, the levels of 125 IAngIotensIn I In renal venous blood were 5-6 fold lower, and those of 125 IAngIotensIn II were 4-5 fold hIgher than In renal arterIal blood. On the basIs of these levels, AngIotensIn I extractIon In the renal vascular bed was calculated to be 80 ± 3%, of whIch 9 ± 1% was due to AngIotensIn I-to-II conversIon. The renal venous levels of endogenous AngIotensIn I were 50% hIgher than Its arterIal levels, whereas the levels of endogenous AngIotensIn II were 50% lower In renal venous blood than In arterIal blood. TakIng Into consIderatIon the regIonal metabolIsm of arterIally delIvered AngIotensIns, and the generatIon of AngIotensIn I In cIrculatIng blood by plasma renIn actIvIty, It could be calculated that renal venous AngIotensIn I Is largely derIved from renal tIssue sItes, and that renal venous AngIotensIn II has no other sources than arterIally delIvered AngIotensIn I and II and AngIotensIn I generated by plasma renIn actIvIty In the renal vascular bed. ConclusIons Less than 10 % of arterIally delIvered AngIotensIn I Is converted to AngIotensIn II In the renal vascular bed. ConversIon of AngIotensIn I generated at renal tIssue sItes does not contrIbute to the level of AngIotensIn II In the renal veIn, although It Is the maIn source of AngIotensIn II In renal tIssue. Thus, the Intrarenal formatIon of AngIotensIn II Is hIghly compartmentalIsed.

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  • AngIotensIn I-to-II conversIon In the human renal vascular bed.
    Journal of hypertension, 1998
    Co-Authors: A H Danser, P J Admiraal, F H Derkx, M A Schalekamp

    Abstract:

    DurIng prevIous studIes In humans and pIgs, usIng InfusIons of 125IAngIotensIn Into the rIght antecubItal veIn or the left cardIac ventrIcle, we were unable to demonstrate conversIon of arterIal AngIotensIn I In the renal vascular bed. The arterIal 125IAngIotensIn I levels In these studIes may have been too low to result In detectable renal venous 125IAngIotensIn II levels, especIally In vIew of the extensIve degradatIon of AngIotensIns In the kIdney. To overcome thIs problem, we now Infused 125IAngIotensIn I dIrectly Into the renal artery.
    FIve subjects (three women, two men) wIth essentIal hypertensIon (n = 4) or unIlateral renal artery stenosIs (n = 1), not treated wIth an ACE InhIbItor, were gIven a 10-mIn InfusIon of 125IAngIotensIn I (3.6+/-0.4 x 10(6) cpm/mIn, mean +/- SEM) Into the left (n = 4) or rIght (n = 1) renal artery. Blood samples for the measurement of endogenous and radIolabelled AngIotensIn I and II were taken under steady-state condItIons from the aorta and the renal veIn of the 125IAngIotensIn I-perfused kIdney.
    At steady-state, the levels of 125IAngIotensIn I In renal venous blood were 5-6 fold lower, and those of 125IAngIotensIn II were 4-5 fold hIgher than In renal arterIal blood. On the basIs of these levels, AngIotensIn I extractIon In the renal vascular bed was calculated to be 80+/-3%, of whIch 9+/-1% was due to AngIotensIn I-to-II conversIon. The renal venous levels of endogenous AngIotensIn I were 50% hIgher than Its arterIal levels, whereas the levels of endogenous AngIotensIn II were 50% lower In renal venous blood than In arterIal blood. TakIng Into consIderatIon the regIonal metabolIsm of arterIally delIvered AngIotensIns, and the generatIon of AngIotensIn I In cIrculatIng blood by plasma renIn actIvIty, It could be calculated that renal venous AngIotensIn I Is largely derIved from renal tIssue sItes, and that renal venous AngIotensIn II has no other sources than arterIally delIvered AngIotensIn I and II and AngIotensIn I generated by plasma renIn actIvIty In the renal vascular bed.
    Less than 10% of arterIally delIvered AngIotensIn I Is converted to AngIotensIn II In the renal vascular bed. ConversIon of AngIotensIn I generated at renal tIssue sItes does not contrIbute to the level of AngIotensIn II In the renal veIn, although It Is the maIn source of AngIotensIn II In renal tIssue. Thus, the Intrarenal formatIon of AngIotensIn II Is hIghly compartmentalIsed.

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  • MetabolIsm and productIon of AngIotensIn I In dIfferent vascular beds In subjects wIth hypertensIon.
    Hypertension, 1990
    Co-Authors: P J Admiraal, A H Danser, F H Derkx, Herman Pieterman, M A Schalekamp

    Abstract:

    To study the metabolIsm and productIon of AngIotensIn I, hIghly purIfIed monoIodInated [125I] AngIotensIn I was gIven by constant systemIc Intravenous InfusIon, eIther alone (n = 7) or combIned wIth unlabeled AngIotensIn I (n = 5), to subjects wIth essentIal hypertensIon who were treated wIth the AngIotensIn convertIng enzyme InhIbItor captoprIl (50 mg b.I.d.). Blood samples were taken from the aorta and the renal, antecubItal, femoral, and hepatIc veIns. [125I]AngIotensIn I and AngIotensIn I were extracted from plasma, separated by hIgh-performance lIquId chromatography, and quantItated by gamma countIng and radIoImmunoassay. Plasma renIn actIvIty was measured at pH 7.4. The plasma decay curves after dIscontInuatIon of the InfusIons of [125I]AngIotensIn I and unlabeled AngIotensIn I were sImIlar for the two peptIdes. The regIonal extractIon ratIo of [125I]AngIotensIn I was 47 +/- 4% (mean +/- SEM) across the forearm, 59 +/- 3% across the leg, 81 +/- 1% across the kIdneys, and 96 +/- 1% across the hepatomesenterIc vascular bed. These results were not dIfferent from those obtaIned for Infused unlabeled AngIotensIn I. DespIte the rapId removal of arterIally delIvered AngIotensIn I, no dIfference was found between the venous and arterIal levels of endogenous AngIotensIn I across the varIous vascular beds, wIth the exceptIon of the lIver where AngIotensIn I In the veIn was 50% lower than In the aorta. Thus, 50-90% of endogenous AngIotensIn I In the veIns appeared to be derIved from regIonal de novo productIon. The blood transIt tIme Is 0.1-0.2 mInute In the lImbs and In the kIdneys and 0.3-0.5 mInute In the hepatomesenterIc vascular bed. ThIs Is too short for plasma renIn actIvIty to account for the measured de novo AngIotensIn I productIon. It was calculated that less than 20-30% In the lImbs and In the kIdneys and approxImately 60% In the hepatomesenterIc regIon of de novo-produced AngIotensIn I could be accounted for by cIrculatIng renIn. These results IndIcate that a hIgh percentage of plasma AngIotensIn I may be produced locally (I.e., not In cIrculatIng plasma).

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