Effect of chronic ACE inhibition on the diagnostic value of renography for renovascular hypertension: a preliminary report. Vascular compliance and mean circulatory filling pressure in trout: effects of ACE inhibition. Molecular mechanism for the relative binding affinity to the intestinal peptide carrier. Comparison of three ACE-inhibitors: enalapril, enalaprilat, and lisinopril. Rx drugs

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Nephrol Dial Transplant. 1995;10(2):263-5.
Effect of chronic ACE inhibition on the diagnostic value of renography for renovascular hypertension: a preliminary report.

Visscher CA, de Zeeuw D, Huisman RM.

Department of Medicine, Groningen Institute for Drug Studies (GIDS), University Hospital, The Netherlands.

We compared the effects of acute and chronic ACE inhibition (ACEi) on the 123I-hippurate in the stenotic kidney of two 2-kidney, 1-clip hypertensive dogs. In the period after clip implantation poststenotic renograms without ACEi of both dogs were normal. Acute ACEi always resulted in delayed hippurate handling. Chronic ACEi, however, induced abnormal poststenotic renograms in only 36% of the cases. Withdrawal of chronic ACEi restored the phenomenon of acute ACE-induced delayed hippurate handling within 5 months in both dogs. These data indicate that chronic ACEi or recent ACEi medication reduces the effectiveness of ACEi renography in diagnosing hypertension due to a moderate renal-artery stenosis. This phenomenon may explain why the sensitivity of ACEi renography in human studies varies more than in animal studies.

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Am J Physiol. 1995 May;268(5 Pt 2):H1814-20.
Vascular compliance and mean circulatory filling pressure in trout: effects of ACE inhibition.

Zhang Y, Jenkinson E, Olson KR.

Department of Biological Sciences, University of Notre Dame, Indiana, USA.

Mean circulatory filling pressure (MCFP), whole body vascular compliance (C), and unstressed blood volume (USV) are important indexes of cardiovascular function in mammals, but they have not been measured in fish. In the present experiments, dorsal aortic (PDA) and sinus venosus (PSV) pressures were measured in unanesthetized trout before and during electrical cardiac fibrillation, while blood volume (BV) was manipulated between 50 and 150% of normal. Measurements were repeated after angiotensin-converting enzyme (ACE) inhibition with lisinopril. Cardiac fibrillation (zero-flow condition) rapidly (approximately 5 s) dropped PDA and increased PSV (equals MCFP). MCFP in normovolemic trout (4.8 +/- 0.3 mmHg) varied directly with BV. C determined from in vivo capacitance curves was similar to that obtained gravimetrically, in vitro (3.4 and 3.5 ml.mmHg-1.kg body wt-1, respectively). USV was 13.3 ml/kg body wt (approximately 45% of BV). ACE inhibition reduced PDA in unfibrillated trout at all BV and reduced PDA in fibrillated fish at BV > or = 80%. ACE inhibition did not affect PSV, MCFP, C, or USV. The systemic arteriovenous pressure gradient at zero flow (delta PF0) was greatest at 100% BV (8.2 +/- 0.5 mmHg) and was reduced by ACE inhibition at 80-120% BV. These results show that key indexes of venous function are readily measured in fish and that the trout venous system is not an effector of angiotensin-mediated regulation of arterial blood pressure. Thus angiotensin acts solely on arterial resistance vessels. Furthermore, the drop in delta PF0 during ACE inhibition is due to a decrease in arteriolar resistance.

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Biochim Biophys Acta. 1995 May 24;1236(1):31-8.
Molecular mechanism for the relative binding affinity to the intestinal peptide carrier. Comparison of three ACE-inhibitors: enalapril, enalaprilat, and lisinopril.

Swaan PW, Stehouwer MC, Tukker JJ.

Department of Pharmaceutics, Utrecht Institute of Pharmaceutical Sciences (UIPS), University of Utrecht, The Netherlands.

The affinity of three substrates for the intestinal peptide carrier is explained based on their three-dimensional (3D) structural data. The kinetic transport parameters of three ACE-inhibitors, enalapril, enalaprilat, and lisinopril, have been determined in an in vivo system using rat intestine. The observed kinetic transport parameters (+/- asymptotic standard error) of enalapril are: 0.81 (+/- 0.23) mM, 0.58 (+/- 0.37) mumol/h per cm2, and 0.56 (+/- 0.04) cm/h for the half-maximal transport concentration (KT), the maximal transport flux (Jmax) and the passive permeability constant (Pm). Enalaprilat was transported by passive diffusional with a Pm of 0.51 (+/- 0.04) cm/h. For lisinopril the kinetic transport parameters were 0.38 (+/- 0.19) mM, 0.12 (+/- 0.07) mumol/h per cm2, and 0.18 (+/- 0.02) cm/h for KT, Jmax, and Pm, respectively. The affinity of the ACE-inhibitors for the intestinal peptide carrier has been evaluated based on their ability to inhibit the transport rate of cephalexin. The inhibition constants (Ki) of enalapril, enalaprilat and lisinopril were 0.15, 0.28 and 0.39 mM, respectively. 3D structural analysis of lisinopril using molecular modelling techniques reveals that intramolecular hydrogen bond formation is responsible for decreased carrier affinity.

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