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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After explaining the role of estrogens in normal human physiology with a discussion of fertilization which mentions cytogenetical research, the history of estrogen synthesis, forms of estrogen, and the roles estrogens play in female physiology after birth are discussed. The observation that estrus in an animal was mediated by a chemical agent was made in 1922. In 1927, studies showed that urine of pregnant women contained estrogenic substances, and in 1929, estrone, an oxidation product of estradiol, was isolated from this source. The natural oxidation products of estradiol include, besides estrone, estriol, equilin, and equilenin, these last 3 being very weak estrogens. Conjugated estrogens consist chiefly of sodium estrone sulfate. In 1938, diethylstilbestrol, a nonsteroidal estrogen, was synthesized. A discussion of the estrogens activities when administered orally or parenterally follows; nonsteroidal estrogens are thought to have good oral action as do esterified estrogens. Estrogenic effects on female physiology include secondary sexual characteristics, menstrual cycle, and ovulation. Other estrogen functions mentioned were antidiuretic action, retardation of atherosclerosis, increased calcium deposition in bone, and epiphyseal closure acceleration after initial stimulation. The rationale for and problems with patient package inserts are discussed.
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PMID:Estrogens: their function, uses and hazards. Part 1. 62 25

The contraction of smooth muscle cells in response to the effect of catecholamines and potassium chloride was studied in experiments on isolated ring segments of the rabbit aorta under normal conditions and in experimental cholesterol atherosclerosis at its early developmental stages. It was found that at the early stages of atherosclerosis development the character of the contractile reactions was marked by changes which may be considered from the standpoint of disorder in the ion mechanisms of the interrelationships of sodium and calcium both on the membrane and within the smooth muscle cell, and from the standpoint of increased reactivity of chemically sensitive calcium channels of the membrane. The cause of these changes may be the accumulation of cholesterol, lipoproteins and acid mucopolysaccharides in the vascular wall at the early stages of atherosclerosis development.
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PMID:[Physiological properties of the blood vessel smooth muscles in experimental atherosclerosis]. 67 57

When rats were fed a diet containing 0.3% clofibrate or a derivative of this drug, BM 15075, serum cholesterol was lowered within 3-7 days by 26-38%. Both drugs diminished the activity of hydroxymethylglutaryl CoA reductase, the regulatory enzyme of hepatic cholesterol biosynthesis, in rat liver microsomes by about 60% under the same conditions. The decrease in the activity of the enzyme obviously is due to changes in the amount of enzyme protein. Under in vitro conditions microsomal hydroxymethylglutaryl CoA reductase was inhibited competitively by (1.35 mM) clofibric acid (sodium salt) and by BM 15075 (1 mM) with respect to its substrate. These results give evidence that these drugs can affect both, the rate of synthesis and the substrate affinity of hydroxymethylglutaryl CoA reductase.
Atherosclerosis 1978 Jun
PMID:Mode of action of the lipid-lowering agents, clofibrate and BM 15075, on cholesterol biosynthesis in rat liver. 67 16

In 6 healthy adults the effect of essential oil of garlic on platelet aggregation was studied in vitro with an aggreganometer. The blood was collected in a siliconized centrifuge tube containing sodium citrate. The aggregating agents used were ADP, epinephrine and collagen. In each subject aggregation was studied 3 times: (i) initial fasting control; (ii) immediately after (i) but with essential oil of garlic drawn into the syringe together with the sodium citrate; (iii) 5 days after feeding 0.5 mg of essential oil of garlic daily. Addition of essential oil of garlic inhibited in-vitro platelet aggregation induced by ADP, epinephrine or collagen; the effect was dose-related. Oral administration of garlic also decreased platelet aggregation. Thus, garlic seems to inhibit some aspects of thrombus formation.
Atherosclerosis 1978 Aug
PMID:Effect of garlic on human platelet aggregation in vitro. 70 92

Blood of normal rabbits and those on atherogenic cholesterol diet was incubated with 2--14C-acetate of sodium. After incubation cholesterol and its precursors -- squalene and lanosterin -- were found and identified in the non-saponified fractions of leukocytes and platelets. The maximum specific activity was revealed in cholesterol, next in turn were lanosterin and squalene of leukocytes both in the normal rabbits and in those with atherosclerosis. In platelets the label was mainly accumulated in lanosterin.
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PMID:[Cholesterol biosynthesis in the blood of rabbits with experimental atherosclerosis]. 72 10

Thoracic aortae of normal rabbits were perfused with pancreatic elastase in vitro at 37 degrees C and 70 mm Hg pressure in the presence or absence of elastin ligands previously shown to stimulate or inhibit the enzymatic degradation of elastin. Perfusion with elastase results in an average of 3.6 lamellae degraded, whereas addition of sodium linoleate before and during the perfusion with elastase increases this value to 7.9 (P less than 0.001). Conversely, perfusion with the cationic detergent, dodecyltrimethylammonium chloride, completely prevents the degradation of elastic lamellae by elastase. These effects do not reflect alterations of the intrinsic catalytic activity of elastase, but apparently indicate the formation of complexes between the elastin ligands and arterial elastic lamellae, as is consistent with prior studies indicating such interactions between fatty acids or detergents and purified elastin. These studies suggest that agents such as fatty acids may significantly alter the metabolic susceptibility of elastin in vivo and possibly contribute to the degradation of elastic lamellae seen in arteries with advanced atherosclerosis.
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PMID:A possible role for elastin ligands in the proteolytic degradation of arterial elastic lamellae in the rabbit. 75 37

The smooth muscle cell plays an important role in the process of atherogenesis, proliferating in the arterial intima and becoming filled with lipid during the course of the disease. In these experiments the effect of insulin and glucose on sterol synthesis in cultured rat arterial smooth muscle cells was studied. Arterial smooth muscle cells were cultured from pieces of intima and inner media of young rat aortas. The cells were grown in Petri dishes in culture medium with foetal calf serum and when confluent were exposed to insulin or glucose for 24 hours. Insulin in concentrations of 10 micromicron-100 millimicron per ml stimulated the incorporation of sodium [2-(14)C]acetate into non-saponifiable lipids and digitonin precipitable sterols. However, insulin had no effect on the incorporation of labelled mevalonate into cell sterols. Increasing concentrations of glucose in the medium up to 140 mM had had no effect on the incorporation of isotope into sterols, but higher concentrations of glucose caused cell damage and sterol synthesis was markedly depressed. These results may have relevance to the development of atherosclerosis in diabetes and obesity.
Atherosclerosis 1977 Jul
PMID:The effect of insulin and glucose on sterol synthesis in cultured rat arterial smooth muscle cells. 90 24

Effects of (4S)-1-methyl-3-[(2S)-2-[N-((1S)-1-ethoxycarbonyl-3-phenylpropyl)amino]- propionyl]-2-oxoimidazolidine-4-carboxylic acid hydrochloride (TA-6366) on morphological change and mechanical property related to sodium ion permeability in the aorta of spontaneously hypertensive rats (SHRs) were examined, as compared with those of enalapril and captopril. Ten-week oral administration of TA-6366 (1 and 5 mg/kg/d) from 4 weeks of age impeded aortic media-thickening together with a rise in blood pressure in SHRs. Concomitantly, aorta weights in both groups were markedly decreased. The higher dose of TA-6366 almost fully suppressed the accelerated tension development induced by K(+)-free medium and decreased total sodium ion content in the aorta. These vascular effects of TA-6366 was more prominent than those of enalapril and captopril at 5 mg/kg/d. The difference in potencies on the above vascular parameters between TA-6366 and these drugs seemed to be mainly related to the difference in their antihypertensive activities. These results suggest that TA-6366 has preventive effects against progression of vascular diseases, particularly atherosclerosis, accompanied with hypertension.
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PMID:Effects of long-term administration of (4S)-1-methyl-3-[(2S)-2-[N-((1S)-1-ethoxycarbonyl-3- phenylpropyl)amino]propionyl]-2-oxoimidazolidine-4-carboxylic acid hydrochloride (TA-6366), a new angiotensin I converting enzyme (ACE) inhibitor, from the pre-hypertensive stage on morphological change and mechanical property related to sodium ion permeability in aorta of spontaneously hypertensive rats (SHRs). 128 1

We studied the effects of native (N) and oxidized (Ox) low density lipoproteins (LDLs) on adenosine 3',5'-cyclic monophosphate (cAMP)-mediated and on guanosine 3',5'-cyclic monophosphate (cGMP)-mediated dilator mechanisms in isolated, perfused human mammary and rabbit femoral arteries. Dilations were induced in preconstricted, deendothelialized segments by either forskolin (Fo) or sodium nitroprusside (SNP) (intraluminal or adventitial application). Lipoproteins (0.5 mg/ml) were administered to the segments from the intraluminal side. N-LDL had no effect on Fo-induced dilation and caused a weak attenuation of SNP-induced dilation only when SNP was also administered into the intraluminal perfusate. In contrast, Ox-LDL inhibited both Fo- and SNP-induced dilation, independent of the route of dilator application. The effects of Ox-LDL were specific for dilation mediated by cyclic nucleotides. Dilation elicited by the Ca2+ antagonist nitrendipine was inhibited neither by N-LDL nor by Ox-LDL. Determination of basal and stimulated (SNP, Fo) cGMP and cAMP content in rabbit femoral segments after preincubation with N-LDL and Ox-LDL revealed a significant decrease of stimulated vascular cGMP and cAMP content by Ox-LDL, whereas N-LDL had no effect. These data indicate that Ox-LDL selectively inhibits vascular smooth muscle relaxation elicited by increases in cyclic nucleotides. This inhibition might contribute to the attenuation of vasodilation in hypercholesterolemia and atherosclerosis.
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PMID:Inhibition of cyclic AMP- and cyclic GMP-mediated dilations in isolated arteries by oxidized low density lipoproteins. 131 46

Oxidation of low density lipoprotein (LDL) has been shown to occur in the artery wall of atherosclerotic lesions in both animal models and human arteries. The oxidant(s) responsible for initiating this process are under intensive investigation and 15-lipoxygenase has been suggested in this context. Another possibility is that nitric oxide and superoxide, generated by cells present in the artery wall, react together to form peroxynitrite which decomposes to form the highly reactive hydroxyl radical. In the present study we have modelled the simultaneous generation of superoxide and nitric oxide by using the sydnonimine, SIN-1 and have investigated its effects on LDL. SIN-1 liberates both superoxide and nitric oxide during autooxidation resulting in the formation of hydroxyl radicals. We have demonstrated that superoxide generated by SIN-1 is not available to take part in a dismutation reaction since it reacts preferentially with nitric oxide. It follows, therefore, that during the autooxidation of SIN-1 little or no superoxide, or perhydroxyl radical will be available to initiate lipid peroxidation. We have shown that SIN-1 is capable of initiating the peroxidation of LDL and also converts the lipoprotein to a more negatively charged form. The SIN-1-dependent peroxidation of LDL is completely inhibited by superoxide dismutase which scavenges superoxide. Neither sodium nitroprusside or S-nitroso-N-acetyl penicillamine, which only produce nitric oxide, are able to modify LDL. These results are consistent with the hypothesis that a product of superoxide and nitric oxide could oxidize lipoproteins in the artery wall and so contribute to the pathogenesis of atherosclerosis in vivo.
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PMID:The simultaneous generation of superoxide and nitric oxide can initiate lipid peroxidation in human low density lipoprotein. 133 19


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