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Vasotec (Enalapril)

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Vasotec is an effective strong preparation which is taken in treatment of diabetes symptoms as hypertension diseases, kidney problems, and congestive heart failure. Vasotec can be also helpful for patients after heart attack. Vasotec operates by reducing blood pressure and regulating blood provision to the heart.

Other names for this medication:
Acepril, Acetensil, Alapren, Alicante, Alphapril, Amprace, Analept, Anapril, Angiotec, Antiprex, Atens, Auspril, Bagopril, Bajaten, Baripril, Baypril, Benalapril, Bidinatec, Biocronil, Bitensil, Bql, Calnate, Carlon, Cetampril, Cinbenon, Ciplatec, Clipto, Controlvas, Convertase, Converten, Convertin, Corodil, Corprilor, Corvo, Cosil, Crinoren, Dabonal, Daren, Defluin, Denapril, Dentromin, Dilvas, Dinid, Ditensil, Ditensor, Docenala, Ecaprilat, Ecaprinil, Ednyt, Ekaril, Elpradil, Ena, Ena-puren, Enabeta, Enacard, Enacodan, Enacor, Enadigal, Enadura, Enafril, Enal, Enalabell, Enaladex, Enaladil, Enalafel, Enalagamma, Enalaprili maleas, Enalaprilmaleat, Enalaprilo, Enalaprilum, Enalaprol, Enalart, Enalbal, Enaldun, Enalek, Enalich, Enalin, Enalind, Enalten, Enam, Enap, Enap r, Enaprel, Enapren, Enaprex, Enapril, Enapril-h, Enaprotec, Enarenal, Enaril, Enatec, Enatral, Enazil, Encardil, Enecal, Enetil, Enpril, Envas, Ephicord, Epril, Eril, Eritril, Eupressin, Fabotensil, Feliberal, Fibrosan, Gadopril, Glenamate, Glioten, Gnostocardin, Grifopril, Hasitec, Herten, Hiperpril, Hiperson, Hipertan, Hipertin, Hipoartel, Hipopril, Hypace, Iecatec, Ileveran, Imotoran, Innovace, Innozide, Insup, Intonis, Invoril, Istopril, Jutaxan, Kalpiren, Kaparlon-s, Kinfil, Kintec, Konveril, Korandil, Lapril, Laprilen, Lariludon, Lenaberic, Lenimec, Leovinezal, Lerite, Linatil, Lotrial, Lowtril, M-enalapril, Maxen, Megapress, Meipril, Mepril, Minipril, Myoace, Nacor, Nalabest, Nalapril, Naprilene, Narapril, Neotensin, Norpril, Nuril, Octorax, Ofnifenil, Olinapril, Olivin, Pharmapress, Pharpril, Pms-enalapril, Pralenal, Pres, Presopril, Pressitan, Presuren, Prilace, Prilan, Prilenap, Prilenor, Priltenk, Pulsol, Rablas, Raserpril, Reca, Reminal, Renacardon, Renapril, Renaton, Renil, Renipril, Renistad, Renitec, Reniten, Renivace, Reniveze, Renopent, Revinbace, Selis, Silverit, Spaciol, Stadelant, Stadenace, Sulocten, Supotron, Tenace, Tenaten, Tencas, Tensapril, Tensazol, Tesoren, Ulticadex, Unipril, Vapresan, Vasolapril, Vasopren, Vasopril, Vexopril, Vimapril, Virfen, Vitobel, Xanef, Zacool

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Also known as:  Enalapril.


Vasotec is created by pharmacy specialists to combat not also diabetes symptoms as hypertension diseases, kidney problems, and congestive heart failure but it can be helpful for patients after heart attack.

Target of Vasotec is to control and decrease level of blood pressure.

Vasotec is also known as Enalapril, Renitec, BQL, Benalipril, Amprace, Alphapril, Converten, Enalagamma, Enatec, Envas, Invoril, Xanef.

Vasotec operates by reducing blood pressure and regulating blood provision to the heart.

Vasotec can be used in combination with medicines for heart failure treatment.

Vasotec is ACE (angiotensin-converting enzyme) inhibitor.

Generic name of Vasotec is Enalapril.

Brand name of Vasotec is Vasotec.


You should take it by mouth with water.

It is better to take Vasotec once or twice a day at the same time with meals or without it.

If you want to achieve most effective results do not stop taking Vasotec suddenly.


If you overdose Vasotec and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Vasotec overdosage: fainting, dizziness.


Store at room temperature below 30 degrees C (86 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Vasotec if you are allergic to Vasotec components.

Be very careful with Vasotec if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Vasotec usage in case of having angioedema, throat, heart disease, diabetes, hands, kidney disease, lower legs, lupus, scleroderma.

Be careful with Vasotec usage in case of taking diuretics; aspirin and other nonsteroidal anti-inflammatory medications (NSAIDs) as indomethacin (Indocin); potassium supplements; lithium (such as Eskalith, Lithobid).

Nimotop can be not safety for elderly people.

Avoid dehydration.

Be careful with great care in case you want to undergo an operation (dental or any other).

Do not use potassium supplements or salt substitutes.

If you want to achieve most effective results without any side effects it is better to avoid alcohol.

Do not stop taking Vasotec suddenly.

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Twenty-five patients (aged 18 to 72 years), who recovered after the first bleed from a cerebral aneurysm, were operated on under neuroleptanaesthesia. Isoflurane was added to induce hypotension. It was found that the required hypotension (51 (SEM 1) mmHg) could be obtained and maintained at much lower isoflurane concentrations (less than 1%) after blockade of the angiotensin converting enzyme activity by enalaprilat (2.5 mg i.v.) than without such inhibition. During the hypotension which lasted 78 (SEM 10) min, only minor adjustments of the isoflurane concentration (0.70 (0.04%) were needed. The desired level of hypotension was obtained with preservation of the cardiac output and without tachycardia. No resistance to the blood pressure lowering effect of isoflurane was observed. On recovery from anaesthesia, a small increase of blood pressure above control values was seen in 16 patients and was easily reversed by small doses of clonidine (mean total dose: 220 (61) micrograms). The operative conditions were excellent and the postoperative recovery was uneventful and complete in 23 patients.

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Podocytes were incubated with a medium of mesangial cells co-incubated with aIgA1, which was isolated from IgAN patients, and enalaprilat (10(-5) M), valsartan (10(-5) M) and anti-mouse tumour necrosis factor-alpha antibody (50 ng mL(-1)) separately. Nephrin expression in podocytes was measured by real-time polymerase chain reaction and Western blot analysis.

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Although early studies suggested little role for angiotensin-converting enzyme (ACE) inhibitors in older hypertensive patients, more careful evaluation has confirmed their efficacy and good tolerability. Although the elderly tend to have low plasma renin levels, the fall in blood pressure after ACE inhibitors is at least as great (and in several studies greater) than in younger age groups. Because several ACE inhibitors, including captopril and enalaprilat, are eliminated by the kidneys, there are predictable age-related effects on pharmacokinetics. Reduced renal clearance will contribute, at least in part, to the enhanced intensity and duration of action seen in elderly patients. However, not all the effects of age on the kinetics and dynamics of ACE inhibitors are predictable. Studies with perindopril and benazepril in the elderly confirm the efficacy of this group of drugs but highlight other pharmacokinetic differences. ACE inhibitors are effective in reducing blood pressure and can be considered for wider use in elderly hypertensives.

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Angiotensin converting enzyme (ACE) plays a critical role in the circulating or endocrine renin-angiotensin system (RAS) as well as the local regulation that exists in tissues such as the myocardium and skeletal muscle. Here we report the high-resolution crystal structures of testis ACE (tACE) in complex with the first successfully designed ACE inhibitor captopril and enalaprilat, the Phe-Ala-Pro analogue. We have compared these structures with the recently reported structure of a tACE-lisinopril complex [Natesh et al. (2003) Nature 421, 551-554]. The analyses reveal that all three inhibitors make direct interactions with the catalytic Zn(2+) ion at the active site of the enzyme: the thiol group of captopril and the carboxylate group of enalaprilat and lisinopril. Subtle differences are also observed at other regions of the binding pocket. These are compared with N-domain models and discussed with reference to published biochemical data. The chloride coordination geometries of the three structures are discussed and compared with other ACE analogues. It is anticipated that the molecular details provided by these structures will be used to improve the binding and/or the design of new, more potent domain-specific inhibitors of ACE that could serve as new generation antihypertensive drugs.

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Furosemide-131I-hippuran renography with ACE inhibition is highly predictive in identifying patients with RVH.

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The pharmacodynamic profile of the new angiotensin-converting enzyme (ACE) inhibitor moexipril and its active diacid, moexiprilat, was studied in vitro and in vivo. In vitro, moexiprilat exhibited a higher inhibitory potency than enalaprilat against both plasma ACE and purified ACE from rabbit lung. Upon oral administration of moexipril (10 mg/kg/day) to spontaneously hypertensive rats, plasma angiotensin II concentration decreased to undetectable levels, plasma ACE activity was inhibited by 98% and plasma angiotensin I concentration increased 8.6-fold 1 h after dosing. At 24 h, plasma angiotensin I and angiotensin II concentrations had returned to pretreatment levels, whereas plasma ACE activity was still inhibited by 56%. Four-week oral administration of moexipril (0.1-30 mg/kg/day) to spontaneously hypertensive rats lowered blood pressure and differentially inhibited ACE activity in plasma, lung, aorta, heart and kidney in a dose-dependent fashion. Equidose treatment (10 mg/kg/day) with moexipril and enalapril over 4 weeks led to comparable decreases in blood pressure, inhibition of plasma ACE and reduction of plasma angiotensinogen and to a similar attenuation of the pressor responses to angiotensin I and potentiation of the depressor responses to bradykinin. In contrast, ACE inhibition in aorta, heart and lung was significantly greater with moexipril than with enalapril, whereas in the kidney both drugs inhibited ACE activity to a similar extent. In summary, moexipril is an orally active ACE inhibitor that is comparable to enalapril in potency and duration of antihypertensive activity. The results of the present study demonstrate that 1) the antihypertensive potency of a given ACE inhibitor cannot be predicted from its in vitro characteristics and 2) the degree of blood pressure reduction does not correlate with tissue ACE inhibition.

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We determined whether local bradykinin production modulates cardiac adrenergic activity. Depolarization of guinea pig heart sympathetic nerve endings (synaptosomes) with 1 to 100 mmol/L K+ caused the release of endogenous norepinephrine (10% to 50% above basal level). This release was exocytotic, because it depended on extracellular Ca2+, was inhibited by the N-type Ca(2+)-channel blocker omega-conotoxin and the protein kinase C inhibitor Ro31-8220, and was potentiated by the neuronal uptake-1 inhibitor desipramine. Typical of adrenergic terminals, norepinephrine exocytosis was enhanced by activation of prejunctional angiotensin AT1-receptors and attenuated by adrenergic alpha 2-receptors, adenosine A1-receptors, and histamine H3-receptors. Exogenous bradykinin enhanced norepinephrine exocytosis by 7% to 35% (EC50, 17 nmol/L), without inhibiting uptake 1. B2-receptor, but not B1-receptor, blockade antagonized this effect. The kininase II/angiotensin-converting enzyme inhibitor enalaprilat and the addition of kininogen or kallikrein enhanced norepinephrine exocytosis by approximately equal to 6% to 40% (EC50, 20 nmol/L) and approximately equal to 25% to 60%, respectively. This potentiation was prevented by serine protease inhibitors and was antagonized by B2-receptor blockade. Therefore, norepinephrine exocytosis is augmented when bradykinin synthesis is increased or when its breakdown is inhibited. This is the first report of a local kallikrein-kinin system in adrenergic nerve endings capable of generating enough bradykinin to activate B2-receptors in an autocrine/paracrine fashion and thus enhance norepinephrine exocytosis. This amplification process may operate in disease states, such as myocardial ischemia, associated with severalfold increases in local kinin concentrations.

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The contribution of nonangiotensinergic effects of converting enzyme inhibitors to their hemodynamic effects in patients with chronic heart failure is not clear. A comparison of the effects of renin and converting enzyme inhibition should help to clarify this issue.

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The purpose of this study was to determine whether angiotensin-converting enzyme is present in cultured human bronchial epithelial cells and which types of epithelial cells possess this enzyme. It is well known that serum promotes squamous differentiation of airway epithelial cell culture in vitro. We found that whole-cell homogenates of both basal (serum-untreated) and squamous-differentiated bronchial epithelial cells degraded hippuryl-L-histidyl-L-leucine, a synthetic substrate for angiotensin-converting enzyme. Analysis of RNA expression by reverse transcription-polymerase chain reaction (RT-PCR) showed the presence of mRNA for angiotensin-converting enzyme in both types of cells. In addition, we found that squamous cells secreted the enzyme into the culture medium more than basal cells did. Angiotensin-converting enzyme inhibitors (imidaprilat, enalaprilat) inhibited the enzyme activity in bronchial epithelial cells with an IC50 of 0.9-3.6 nM. Exogenously added bradykinin was degraded to bradykinin-(1-5), an inactive fragment, in the squamous cell cultures. Our data indicate the presence of angiotensin-converting enzyme in cultured human bronchial epithelial cells and also that the enzyme is secreted by squamous differentiated cells.

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The aims of this study were to 1) determine whether renal localization of aliskiren and its antihypertensive and renoprotective effects persist after administration of the drug is stopped and 2) define the renal localization of aliskiren by light microscopy autoradiography. Hypertensive double transgenic rats (dTGR) overexpressing genes for human renin and angiotensinogen were treated with aliskiren (3 mg·kg(-1)·day(-1) sc; osmotic minipumps) or enalapril (18 mg/l in drinking water). After a 2-wk treatment, dTGR were assigned to either continued treatment with aliskiren ("continued"), or to cessation of their respective treatment ("stopped") for a 3-wk washout. One week of treatment with aliskiren and enalapril reduced blood pressure and albuminuria vs. baseline. After cessation of either treatment, blood pressure had returned to pretreatment levels and albuminuria remained relatively low for 1 wk, but rose thereafter similarly in both groups. In contrast, renal mRNA for transforming growth factor-β and renal collagen IV was reduced by aliskiren (continued and stopped groups), but not after cessation of enalapril. Similar patterns were found for collagen IV protein expression. Even 3 wk after stopping aliskiren treatment, renal levels of the drug exceeded its IC50, whereas enalaprilat was not detected. To localize aliskiren accumulation, Wistar rats were treated with [(3)H]-aliskiren for 7 days. Autoradiography demonstrated specific labeling in glomeruli, arterioles, and afferent arterioles as well as in the distal nephron. Labeling could still be observed even after 7 days' washout. These results suggest that the renophilic properties of aliskiren are different from enalapril and could have contributed to the renoprotective mechanism of this renin inhibitor.

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The ACE inhibitors increase bradykinin, an agonist of NO synthase (NOS). Nitric oxide inhibits beta-adrenergic myocardial contractility in patients with heart failure.

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vasotec generic name 2015-03-11

Objectives of this study were to determine if aerosolized bradykinin causes bronchoconstriction in anesthetized, mechanically ventilated rats, Himalaya Trikatu Syrup and if pretreatment with enalaprilat, an inhibitor of angiotensin-converting enzyme (ACE), or phosphoramidon, an inhibitor of endopeptidase 24.11 (EP 24.11), alters the response. We found that aerosolized bradykinin elicited a reproducible bronchoconstrictor response that was significantly amplified by pretreatment with aerosolized enalaprilat or phosphoramidon. Neither inhibitor alone affected airway tone or caused nonspecific airway hyperreactivity. These findings indicate that both ACE and EP 24.11 contribute to bradykinin degradation in rat airways.

vasotec normal dosage 2017-07-25

This study examined the possible contribution of the brain renin-angiotensin system on the sympathetic activation induced by hypoxia in conscious rabbits. Blood pressure (BP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were recorded under conditions of normoxia and hypoxia (10% O2 + 3% CO2) before and after fourth ventricular administration of Feldene Flash Tablet either losartan (10 micrograms in 25 microliters), enalaprilat (500 ng in 25 microliters) or Ringer's (25 microliters). Hypoxia increased the RSNA by 113% and slightly decreased HR without changing BP. It also increased the variability of BP or HR in the 0.2-0.4 Hz frequency domain. Losartan and enalaprilat did not change the resting BP or HR but elevated the RSNA increase seen during hypoxia. Our results suggest that central angiotensin is involved in mediating response to chemoreceptor activation.

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Thirteen subjects with essential hypertension controlled on oral enalapril (20 mg/day) therapy were entered into a protocol to assess serially 24-hour blood pressure, the renin-angiotensin-aldosterone system, angiotensin-converting enzyme activity, and plasma and urine enalaprilat drug levels, following both chronic oral administration of enalapril and its replacement with intravenous enalaprilat. Results indicate that systolic and diastolic blood pressures remain well controlled Aldactone Max Dosage following cessation of oral enalapril and replacement with intravenous enalaprilat. Enalaprilat drug levels, following oral enalapril and intravenous enalaprilat, remained above the therapeutic levels required for angiotensin-converting enzyme inhibition. However, therapeutic enalaprilat levels can probably be achieved with one fourth of the total cumulative dose of enalapril, administered as enalaprilat at 6-hour intervals. Intravenous enalaprilat stimulated plasma renin activity and decreased immunoreactive plasma angiotensin II and plasma aldosterone concentrations. However, immunoreactive plasma angiotensin II concentrations were not suppressed below pretreatment values, suggesting that chronic enalapril/acute enalaprilat therapy controls blood pressure through a nonangiotensin-mediated antihypertension mechanism.

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Low-dose enalaprilat, injection (1 mg/kg) could alleviate organ damage in post-burned rats, Plavix 4 Tab but has little effect on AOSP and AODP.

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The renin-angiotensin-aldosterone system (RAAS) Tricor Cost plays a key role in the pathogenesis of cardiovascular disorders including hypertension and is one of the most important targets for drugs. A whole body physiologically based pharmacokinetic (wb PBPK) model integrating this hormone circulation system and its inhibition can be used to explore the influence of drugs that interfere with this system, and thus to improve the understanding of interactions between drugs and the target system. In this study, we describe the development of a mechanistic RAAS model and exemplify drug action by a simulation of enalapril administration. Enalapril and its metabolite enalaprilat are potent inhibitors of the angiotensin-converting-enzyme (ACE). To this end, a coupled dynamic parent-metabolite PBPK model was developed and linked with the RAAS model that consists of seven coupled PBPK models for aldosterone, ACE, angiotensin 1, angiotensin 2, angiotensin 2 receptor type 1, renin, and prorenin. The results indicate that the model represents the interactions in the RAAS in response to the pharmacokinetics (PK) and pharmacodynamics (PD) of enalapril and enalaprilat in an accurate manner. The full set of RAAS-hormone profiles and interactions are consistently described at pre- and post-administration steady state as well as during their dynamic transition and show a good agreement with literature data. The model allows a simultaneous representation of the parent-metabolite conversion to the active form as well as the effect of the drug on the hormone levels, offering a detailed mechanistic insight into the hormone cascade and its inhibition. This model constitutes a first major step to establish a PBPK-PD-model including the PK and the mode of action (MoA) of a drug acting on a dynamic RAAS that can be further used to link to clinical endpoints such as blood pressure.

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Crystolysis (partial or total) was observed in 16.2% group A; 19.5% of group C; 3.2% of group B and Evecare Himalaya Syrup in 8.8% of group D.

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Hospitalized patients with elevated Diovan Generic Medication blood pressure (BP) in most cases should be treated with intensification of oral regimens, but are often given intravenous (IV) antihypertensives.

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We investigated the processing enzymes involved in the formation of circulating angiotensin-(1-7) after intravenous administration of angiotensin I to conscious spontaneously hypertensive and Wistar-Kyoto rats. Immunoreactive products, including angiotensin I, angiotensin II, and angiotensin-(1-7), were measured in arterial blood by three specific radioimmunoassays. Angiotensin I infusion (2 nmol) induced a rapid increase in immunoreactive angiotensin II and angiotensin-(1-7). Pretreatment with the angiotensin converting enzyme inhibitor enalaprilat (2 mg/kg) eliminated angiotensin II formation and augmented circulating levels of angiotensin I and angiotensin-(1-7) in spontaneously hypertensive and Wistar-Kyoto rats. The elevated levels of angiotensin-(1-7) in enalaprilat-treated rats were blocked by concurrent treatment with the neutral endopeptidase (EC inhibitor SCH 39,370 (15 mg/kg) in both strains. Administration of SCH 39,370 alone decreased angiotensin-(1-7) levels in spontaneously hypertensive rats, whereas angiotensin II levels increased in both strains (p less than 0.01). Comparisons of the metabolism of angiotensin I in the two rat strains showed increased formation of angiotensin-(1-7) in spontaneously hypertensive rats not given any of the enzyme inhibitors. In addition, levels of angiotensin I were higher after administration of SCH 39,370 in hypertensive rats. These novel findings Aggrenox 200 Mg reveal that neutral endopeptidase EC participates in the conversion of angiotensin I to angiotensin-(1-7) and in the metabolism of angiotensin II in the circulation of both spontaneously hypertensive and Wistar-Kyoto rats. Our results suggest that neutral endopeptidase EC is a major enzymatic constituent of the circulating renin-angiotensin system.

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Haemodynamic comparison of three vasodilation regimens [intravenous (i.v.) hydralazine and isosorbide dinitrate (ISDN) combined, i.v. doxazosin, and i.v. enalaprilat] was undertaken in 36 patients with acute left ventricular (LV) failure due to recent myocardial infarction. Each regimen achieved similar reductions in pulmonary artery occluded pressure (PAOP, preload) and systemic arterial pressures (afterload), with increased cardiac and stroke volume (SV) indexes (p less than 0.01). Only the hydralazine and isosorbide combination induced resting tachycardia. Balanced vasodilatation after selective alpha-adrenoceptor blockade (doxazosin) and angiotensin-converting enzyme (ACE) inhibition (enalaprilat) without increase in heart rate (HR) suggests that Myambutol Generic these therapies may have definite haemodynamic advantages over the hydralazine/ISDN combination.

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Primary cultures of human proximal tubular cells (PTC) and renal cortical fibroblasts (CF) were exposed for 24 h to CyA in the presence or absence of enalaprilat. Parameters of tubulo-interstitial nephrotoxicity were then measured including collagen synthesis (proline incorporation), tubular viability and function (thymidine incorporation, lactate dehydrogenase release, and apical sodium-hydrogen exchange), and secretion of insulin-like growth factor I, transforming growth factor beta 1 (TGFbeta1), and platelet-derived growth factor.