Drugs online research references
Cardiovasc Res. 1995 Apr;29(4):543-8.
Prevention of angiotensin II induced myocyte necrosis and coronary vascular damage by lisinopril and losartan in the rat.
Kabour A, Henegar JR, Devineni VR, Janicki JS.
Department of Internal Medicine, University of Missouri, Columbia 65212, USA.
OBJECTIVE: The aims were to determine: (1) if angiotensin converting enzyme (ACE) inhibition and angiotensin II receptor blockade can prevent angiotensin II induced coronary vascular damage; (2) if the cardioprotective properties of ACE inhibition are dose dependent; and (3) if the cardioprotective properties of ACE inhibition are independent of its ability to prevent the conversion of angiotensin I to angiotensin II. METHODS: Control rats and rats with either renovascular hypertension or continuous angiotensin II infusion (150 ng.min-1) for 14 d were subdivided into nine groups as follows: unoperated and untreated controls (n = 5); untreated renovascular hypertension (n = 8); untreated angiotensin II (n = 9); a renovascular hypertension group receiving one of the following doses of lisinopril 20 (n = 8), 2.5 (n = 4), and 0.6 (n = 6) mg.kg-1.d-1; a renovascular hypertension group receiving losartan (7.5 mg.d-1, n = 4); and an angiotensin II group receiving either the high dose of lisinopril (n = 6) or losartan (n = 4). Treatment was started one day before initiation of renovascular hypertension and angiotensin II infusion and continued throughout the study period. The number and size of necrotic areas and numbers of damaged coronary vessels were determined in sections of right and left ventricular tissue. RESULTS: Both coronary vascular injury and myocyte injury induced by angiotensin II were prevented by losartan. In renovascular hypertension, the lowest dose of lisinopril prevented vascular and attenuated myocyte damage but to a lesser degree than the higher doses. The cardioprotective ability of ACE inhibition is primarily the result of its ability to prevent the conversion of angiotensin I to angiotensin II. CONCLUSIONS: Angiotensin II related cardiomyocyte necrosis and coronary vascular damage are angiotensin type 1 receptor mediated and completely preventable with the receptor antagonist losartan. The ability of ACE inhibition to prevent this damage is dose dependent and primarily related to the degree to which the inhibitor can prevent the conversion of angiotensin I to angiotensin II.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7796449&dopt=Abstract
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J Hum Hypertens. 1994 Sep;8 Suppl 1:S21-5.
Insulin-like growth factor I and collagen type III synthesis in patients with essential hypertension and left ventricular hypertrophy.
Diez J, Laviades C.
Department of Internal Medicine, University of Navarra, School of Medicine, Pamplona, Spain.
An excess of circulating insulin-like growth factor I (IGF-I) has been found in patients with essential hypertension and left ventricular hypertrophy (LVH). In addition, an increase in collagen type III synthesis has also been reported in hypertensive patients. Since IGF-I is a positive effector of collagen type III expression, we have investigated whether a relationship exists between circulating IGF-I and collagen type III synthesis in patients with essential hypertension. The relationship between plasma concentrations of IGF-I and an index of tissue synthesis of collagen type III (serum concentrations of procollagen type III aminoterminal peptide [PIIIP]) was investigated in 37 patients with essential hypertension before and after six months of treatment with lisinopril. The control group consisted of 30 age- and sex-matched normotensive subjects without LVH. Baseline concentrations of IGF-I were higher in hypertensive patients than in normotensive controls (285 +/- 25 vs. 240 +/- 15 ng/ml; P < 0.01). Mean IGF-I levels were higher in hypertensive patients with LVH (n = 10, 330 +/- 49 ng/ml) than in those without LVH (n = 27, 252 +/- 25 ng/ml; P < 0.05). Baseline concentrations of PIIIP were higher in hypertensive patients than in normotensive controls (10.07 +/- 0.54 vs. 8.47 +/- 0.77 ng/ml; P < 0.01). Mean PIIIP levels were higher in hypertensives with LVH than in those without LVH (12.20 +/- 0.78 vs. 7.97 +/- 0.55 ng/ml; P < 0.05). There was no correlation between IGF-I and PIIIP at baseline.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7807509&dopt=Abstract
word match zestril online literature
J Hum Hypertens. 1994 Sep;8 Suppl 1:S27-30.
Quality of life in hypertension.
Os I.
Department of Internal Medicine, Ulleval Hospital, University of Oslo, Medical School, Norway.
Mild to moderate hypertension is usually asymptomatic and therefore the impact on quality of life and side-effects of the antihypertensive treatment can have a negative effect on treatment compliance. A number of comparative studies have addressed quality of life issues with various antihypertensive agents, and the results of these studies are summarised in this article with particular reference to ACE inhibitors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7807510&dopt=Abstract
word match zestril online literature
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