Drugs online research references
Eur J Pharmacol. 1994 Apr 1;255(1-3):73-9.
Cardiovascular effects of felodipine are not antagonized by dietary salt.
Mervaala EM, Laakso J, Karppanen H.
Department of Pharmacology and Toxicology, University of Helsinki, Finland.
Increased dietary intake of regular salt (sodium chloride) interferes markedly with the therapeutic effects of angiotensin converting enzyme inhibitors. To study further the interactions between dietary salt intake and antihypertensive drug treatment, we examined the effects of felodipine, a dihydropyridine derivative Ca2+ channel antagonist with natriuretic properties, on blood pressure and the development of left ventricular hypertrophy in the stroke-prone spontaneously hypertensive rats during different levels of sodium chloride in the diet. We also compared the influence of regular salt on the cardiovascular effects of felodipine with that of a novel K(+)-, Mg(2+)- and l-lysine-enriched and Na(+)-reduced salt alternative, which in previous studies markedly improved the therapeutic effects of enalapril and ramipril. During the 28-day experiment regular salt produced a marked rise in blood pressure and induced left ventricular hypertrophy, while the salt alternative neither induced any rise of blood pressure nor caused cardiac hypertrophy. Felodipine had an enhanced antihypertensive effect during the increased intake of sodium chloride, and lowered the blood pressure to the same normotensive level as it did during the control and the salt alternative diets. Felodipine also completely blocked the development of the sodium chloride-induced cardiac hypertrophy. The heart rate of the felodipine-treated animals was significantly increased during the first two study weeks but thereafter it did not differ from that of the controls. Hence, unlike regular salt, the novel Na(+)-reduced, K(+)-, Mg(2+)-, and l-lysine-enriched salt alternative did not raise blood pressure and produced little if any left ventricular hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8026556&dopt=Abstract
Kidney Int. 1988 Apr;33(4):804-11.
Myocardial interstitial fibrosis in experimental uremia--implications for cardiac compliance.
Mall G, Rambausek M, Neumeister A, Kollmar S, Vetterlein F, Ritz E.
Department Pathology, University of Heidelberg, Republic of Germany.
Experimental uremia is known to cause cardiac hypertrophy. In the present study we examined the effect of uremia with or without concomitant treatment of hypertension by the converting enzyme Ramipril (125 micrograms/day) on micromorphometric indices of cardiac interstitium at the light microscopical and ultrastructural level. In male SD rats, 21 days of uremia caused an increase of total heart weight (1040 +/- 73 mg wet wt vs. 871 +/- 81 in controls, P less than 0.05) with an increase of both right and left ventricular weight. This was accompanied by reduction of capillary cross-sectional area despite unchanged capillary length. The volume density (cm3/cm3) of cardiomyocytes was unchanged (0.881 +/- 0.01 vs. 0.871 +/- 0.016 in controls), but volume density of interstitial tissue (excluding capillary lumen) was significantly increased (0.042 +/- 0.011 cm3 interstitial tissue/cm3 total heart tissue vs. 0.019 +/- 0.007 in controls). This was associated with signs of activation of interstitial cells, that is, increased volume of interstitial cell nuclei and interstitial cell cytoplasm. Concomitantly, a significant increase of volume density of non-cellular interstitial ground substance was found which was not normalized by antihypertensive treatment using Ramipril. After three months of uremia, electron microscopy showed collagen fiber deposition in the interstitium. Comparable interstitial fibrosis was not observed in hearts of rats with renovascular (one clip-two kidney) hypertension. It is concluded that uremia increases myocardial interstitial ground substance by mechanisms independent of hypertension. The data may be relevant for recent findings of diastolic heart malfunction secondary to impaired compliance in uremic patients.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2968479&dopt=Abstract
J Cardiovasc Pharmacol. 1991;18 Suppl 2:S110-5.
Preservation of endothelial function by ramipril in rabbits on a long-term atherogenic diet.
Becker RH, Wiemer G, Linz W.
Hoechst AG, Frankfurt/Main, Germany.
Hypertension and hypercholesterolemia predispose to atherosclerosis. Ramipril, known to lower blood pressure, was used to study the effect of converting-enzyme inhibition on impairment of endothelium-derived relaxation and changes in basal cGMP content in rabbits fed an atherogenic diet (0.25% cholesterol). The generation of cGMP in the presence of bradykinin and ramiprilat was studied in vitro in aortic segments from normal untreated rabbits as well as in bovine endothelial cells. The ability to relax in response to acetylcholine was almost abolished in aortic segments from the vehicle-treated rabbits fed the atherogenic diet for 4 months. The basal cGMP content was substantially reduced. Aortic segments from rabbits concomitantly treated with ramipril (0.3 and 3.0 mg/kg/day) for 3 months showed well-preserved relaxation and matching basal cGMP content compared to normal controls. The relaxation was not significantly greater in aortic segments from ramipril-treated rabbits fed the standard diet, but the cGMP content was more than doubled. In vitro studies in aortic segments and in endothelial cells showed that both the ramiprilat and bradykinin concentrations dependently stimulated cGMP formation, which serves as a biochemical marker of nitric oxide or EDRF release. Thus, the observed endothelial protection against hypercholesterolemia by ramipril may be the result of continuously increased cGMP formation due to preserved EDRF release. This is presumably produced by enhanced bradykinin activity through inhibition of degradation by converting-enzyme inhibition with ramipril.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1725017&dopt=Abstract
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