Drugs online research references
J Cardiovasc Pharmacol. 1989 Aug;14(2):248-52.
Cilazapril and enalapril inhibit local angiotensin I conversion in human veins but lack direct venodilating properties.
Eichler HG, Blochl-Daum B, Kyrle PA, Gasic S.
Medizinische Universitatsklinik, Vienna University Hospital, Austria.
We studied the angiotensin-converting enzyme (ACE)-dependent and ACE-independent (direct) effects of two ACE inhibitors, cilazaprilat and enalaprilat, in 12 healthy human subjects. The dorsal hand vein compliance technique was used because venous constriction and relaxation, independent of reflex responses and systemic ACE inhibition, can be measured by local infusions of very small amounts of drugs. Angiotensin I (dose range 6-1,550 ng/min) was infused alone or coinfused with cilazaprilat or enalaprilat (dose range 7.8-3,900 ng/min). In separate experiments, cilazaprilat or enalaprilat (dose range 3.9-31 micrograms/min), or prostaglandin I2 (PGI2, dose range 0.13-32 ng/min) was infused into veins that had been submaximally preconstricted with phenylephrine. Angiotensin I caused a marked venoconstriction limited by rapid tachyphylaxis. At doses greater than 78 ng/min, cilazaprilat and enalaprilat completely inhibited angiotensin I-induced venoconstriction. This inhibition was reversible after 14-31 min, suggesting an inhibition of ACE associated with the vein wall. Infusions of cilazaprilat or enalaprilat had no effect on the diameter of the vein at rest or after submaximal preconstriction with phenylephrine. In contrast, exogenous PGI2 was a potent venodilator in our system. We conclude that cilazaprilat and enalaprilat are inhibitors of ACE associated with the vein wall, but there is no evidence for either drug of direct, ACE-independent, prostaglandin-mediated vasodilation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2476598&dopt=Abstract
J Hypertens Suppl. 1987 Jul;5(2):S53-8.
Effect of a renin-system inhibitor on blood-vessel adaptation in spontaneously hypertensive rats.
Gould AB, Goodman SA.
Department of Medicine, Hahnemann University, Philadelphia, PA 19102.
We tested the hypothesis that a metabolic error may be the triggering mechanism which leads to blood-vessel hypertrophy and hypertension. Young spontaneously hypertensive rats (SHR) were fed a moderately high salt diet to exacerbate the purported metabolic error. Haematocrit values and rubidium transport were measured as evidence of renal ATP deficiency and blood-vessel adaptation. The renin system was inhibited in two groups of SHR by giving them enalapril to determine whether angiotensin II was involved in blood-vessel adaptation. Spontaneously hypertensive rats fed the moderately high salt diet had higher haematocrit values than normotensive rats fed the same diet or SHR fed Purina rat food, suggesting a renal ATP deficiency. Spontaneously hypertensive rats had higher Na+,K+-ATPase activity in thoracic aorta after 60 min incubation than a similar group given enalapril (P less than 0.001), suggesting blood-vessel adaptation. Possibly, angiotensin II within the vasa vasorum stimulates hypertrophy which, according to the Folkow hypothesis, leads to higher blood pressure, but may concomitantly increase the respiratory chain units which provide ATP for renal function and ion transport.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2821207&dopt=Abstract
Ren Fail. 1998 May;20(3):481-91.
Preventive effect of ACE inhibitor on interstitial myofibroblast formation and matrix deposition in a nephrotic model.
Mizuno S, Horikawa Y, Okamoto M, Kurosawa T.
Institute of Experimental Animal Sciences, Osaka University Medical School, Suita, Japan.
The nephrotic mouse (ICGN strain) is a useful model for progressive nephrotic syndrome (NS). In the present study, we demonstrated the preventive effects of enalapril, an angiotensin converting enzyme (ACE) inhibitor, on the progression of renal dysfunction and tubulo-interstitial fibrosis in the NS mice. Administration of enalapril (5 mg/dL in drinking water) to the 4-week-old NS mice for a 4-week-period did not improve their nephrotic symptoms such as albuminuria and hypoalbuminemia, but significantly suppressed the increases in blood urea nitrogen and serum creatinine levels. Renal histopathology demonstrated that the administration of the ACE inhibitor significantly attenuated the progression of the tubular and interstitial lesions (tubular dilatation, luminal cast accumulation and interstitial expansion) rather than the glomerular sclerotic changes. The suppression of the increase in blood urea nitrogen level by enalapril depended on the attenuated tubular injury rather than on the unchanged glomerular matrix deposition. Immunohistochemical examination revealed that the administration of the ACE inhibitor suppressed the formation of myofibroblasts, identified by the alpha-smooth muscle actin-positive cells, in the interstitial spaces. Consequently, interstitial matrix deposition was significantly reduced in the NS mice treated with enalapril. From the results obtained with the spontaneous nephrotic model, we emphasize a possibility that ACE inhibitor may be effective for attenuating progression of renal dysfunction and fibrosis in human NS, even if the ACE inhibitor fails to improve nephrotic symptoms such as albuminuria and hypoalbuminemia.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9606736&dopt=Abstract
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