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Kidney Int. 1993 Dec;44(6):1266-72.
Captopril inhibits the 72 kDa and 92 kDa matrix metalloproteinases.

Sorbi D, Fadly M, Hicks R, Alexander S, Arbeit L.

Department of Medicine, SUNY at Stony Brook.

Gelatinases are metalloproteinases in the kidney which can cleave type IV collagen as well as gelatin. We partially purified the 72 kDa and 92 kDa gelatinases. The gelatinolytic activity was measured by zymography and a quantitative biotin-avidin assay. By zymography, captopril in concentrations of 20 mM and 40 mM added to the incubation buffer reduced the gelatinolytic activity in a dose-dependent manner. The addition of zinc in a concentration of 50 to 100 microM reversed most of the inhibitory effect of captopril. By the biotin-avidin assay, captopril in a concentration of 30 to 50 nM reduced half of either the 72 kDa or 92 kDa gelatinolytic activity. Zinc in a concentration of 50 microM completely reversed the inhibitory effect of 1 microM captopril on both gelatinases. Lisinopril, a non-sulfhydryl ACE inhibitor, similarly inhibited the gelatinases, but a 100-fold higher concentration of the drug was needed. These findings suggest that captopril reversibly inhibits the 72 kDa and 92 kDa metalloproteinases by interacting with the zinc ion at their active sites. This inhibitory effect is observed with captopril levels comparable to the concentrations needed to inhibit the angiotensin converting enzyme in vivo and may at least partially explain some of the renoprotective effects seen with this drug.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8301928&dopt=Abstract




Clin Exp Pharmacol Physiol. 1992 Aug;19(8):547-53.
Circulating angiotensin II levels under repeated administration of lisinopril in normal subjects.

Kawamura M, Imanashi M, Matsushima Y, Ito K, Hiramori K.

Second Department of Internal Medicine, Iwate Medical University, Japan.

1. To examine the effect of chronic administration of angiotensin I-converting enzyme (ACE) inhibitor on circulating angiotensin II (AII) concentration, 20 mg of lisinopril was administered once daily for 7 consecutive days to eight healthy volunteers. 2. Plasma ACE activity was inhibited to less than approximately 30% of the pretreatment level during the repeated administration. 3. Mean arterial pressure (MAP) was slightly but significantly reduced during the administration period. Plasma AII concentration measured by an established method using high performance liquid chromatography combined with a radioimmunoassay, however, was maintained at approximately the pretreatment level when it was measured at 24 h intervals after each administration of lisinopril. 4. With the gradual recovery of ACE activity following discontinuation of administration, the plasma AII concentration correlated with AI concentration (r = 0.46), and also with the product of AI and ACE activity (AI x ACE; r = 0.80), corresponding to the formula obtained from the kinetics of ACE activity. No correlation was observed between MAP and AII levels throughout the study period. 5. We conclude that in normal subjects repeatedly administered with ACE inhibitor, the AII level in the circulation is still determined by an elevated level of AI and any remaining ACE activity, thus maintaining AII at pretreatment levels. We confirmed that it is not necessary to achieve a decrease in plasma AII concentration through the chronic administration of ACE inhibitor in order to effectively lower blood pressure.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1326422&dopt=Abstract




Am J Emerg Med. 1992 Jul;10(4):321-2.
Angioedema associated with lisinopril.

Rees RS, Bergman J, Ramirez-Alexander R.

Department of Medicine, Department of Veterans Affairs Medical Center, New York, NY 10010.

Angioedema has been reported to occur in association with all angiotensin-converting enzyme inhibitors used in the United States. We reviewed nine cases of angioedema associated with lisinopril use seen in the emergency department at our hospital among 1,970 patients that had been prescribed lisinopril from March 1989 to May 1990. Cases were considered as probably (six cases) or possibly (three cases) drug related, depending on the temporal relationship of the initiation of therapy and the onset of angioedema. All of the cases had edema of the lips, buccal mucosa, and or face. None presented with laryngeal edema or stridor. The angioedema resolved within 1 to 2 days with diphenhydramine treatment and discontinuation of lisinopril. Our data suggest that the incidence of angioedema associated with lisinopril is greater than that associated with captopril or enalapril.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1319709&dopt=Abstract












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