Drugs online research references
Clin Exp Pharmacol Physiol. 1987 Mar;14(3):155-8.
Blockade of angiotensin converting enzyme in circumventricular organs of the brain after oral lisinopril administration demonstrated by quantitative in vitro autoradiography.
Sakaguchi K, Chai SY, Jackson B, Johnston CI, Mendelsohn FA.
Department of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Victoria.
1. To elucidate the central effect of lisinopril, a new angiotensin converting enzyme (ACE) inhibitor, ACE localization and levels were followed in the brain of Sprague-Dawley rats by quantitative in vitro autoradiography after administration of the drug. 2. Following acute lisinopril (10 mg/kg p.o.) treatment, serum ACE activity was acutely reduced, but returned to normal by 24 h. 3. Levels of ACE in most parts of the brain, including the basal ganglia and choroid plexus of all ventricles were not affected by lisinopril. Lisinopril inhibited brain ACE in the subfornical organ and organum vasculosum of the lamina terminalis, circumventricular organs, where the blood brain barrier is deficient. These regions are rich in ACE and angiotensin II receptors, and are known targets for angiotensin II-induced effects on fluid, electrolyte and blood pressure homeostasis. 4. These observations indicate that quantitative in vitro autoradiography is a powerful method to study the access of drugs to the central nervous system. 5. This study shows that blood brain barrier plays an important role in limiting the penetration of lisinopril into the central nervous system. The circumventricular organs may be important targets for ACE inhibitors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2822304&dopt=Abstract
word match zestril online literature
Clin Exp Pharmacol Physiol. 1987 Apr;14(4):343-7.
Pharmacokinetics of angiotensin converting enzyme inhibition in tissues following oral lisinopril: studies in the rat using quantitative radioinhibitor binding.
Jackson B, Cubela R, Sakaguchi K, Johnston CI.
University of Melbourne, Department of Medicine, Austin Hospital, Heidelberg, Victoria, Australia.
1. The pharmacokinetics of angiotensin converting enzyme (ACE) inhibition in plasma and tissues were measured in the rat following 10 mg/kg lisinopril given by oral gavage. 2. Specific binding of 125I-351A to ACE was measured in plasma, and homogenates of lung, aorta, kidney, testis, epididymis and brain, and used as an index of ACE activity. 3. Plasma ACE binding of 125I-351A was reduced to 5% of that in untreated rats 2 h after treatment, and returned to normal by 48 h. Kidney ACE showed a similar time course. Angiotensin converting enzyme from lung, aorta and brain was inhibited at a slower rate, and to a lesser degree. No significant inhibition of ACE was detected in epididymis or testis. 4. Individual tissues in the rat had differences in time course and degree of ACE inhibition after a single dose of lisinopril.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2822313&dopt=Abstract
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Gen Pharmacol. 1987;18(6):577-87.
Increase in vasoactive intestinal polypeptides (VIP) by the angiotensin converting enzyme (ACE) inhibitor lisinopril in congestive heart failure. Relation to haemodynamic and hormonal changes.
Woie L, Dickstein K, Kaada B.
Department of Medicine, Rogaland Central Hospital, Stavanger, Norway.
1. The effects of the angiotensin-converting enzyme (ACE) inhibitor lisinopril on plasma vasoactive intestinal polypeptides (VIP) and plasma noradrenaline, adrenaline and dopamine were studied in 12 patients with congestive heart failure over two consecutive 48-hr periods. The first day in each period served as a treatment day and the second as a control day. 2. A parallel monitoring was made of various hormonal parameters related to the renin-angiotensin-aldosterone system, and a right-heart catheter was used to monitor haemodynamics at rest. 3. Potent inhibition of the renin-system (as demonstrated by decreases in angiotensin converting enzyme (ACE) activity, angiotensin II and plasma aldosterone) together with improved haemodynamics (decreases in mean right atrial pressure, mean pulmonary arterial pressure, mean pulmonary capillary wedge pressure and mean systemic arterial pressure) were recorded. 4. Plasma VIP was significantly increased by a mean of 20.3% (P less than 0.01) on the lisinopril treatment days compared with the control days, whereas circulating catecholamines showed no significant pattern of change. 5. It is postulated that the potent vasodilatory neuromodulator VIP is implicated in the ACE inhibitor effects. 6. The ACE is a non-specific peptidase that previously has been implicated in the potentiation of other vasoactive endogenous systems (kinins and enkephalins).
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2822521&dopt=Abstract
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