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The abdominal aorta of 20 pregnant rabbits was surgically constricted below the renal arteries on the 21st day of pregnancy, producing a stricture that decreased the blood flow by 60%. Four pregnant rabbits underwent sham operation and served as control. The pressor response to angiotensin II (A-II) was assessed by measuring the systolic blood pressure in the ear of rabbits. We intravenously administered 20 mg/kg of OKY-046, a thromboxane A2 (TXA2) synthetase inhibitor (OKY group: n = 13) or saline (n = 7) daily from the 23rd day of pregnancy until the day of delivery. After stricture of the abdominal aorta, the "effective pressor dose" (EPD:nanograms of A-II/kg/min necessary to cause a 20 mmHg rise in systolic pressure) was significantly lower in the saline group than in the control group. On the 27th and 29th day of pregnancy, the EPD in the OKY group was significantly higher than that in the control group. The plasma thromboxane B2 (TXB2) level in the OKY group was significantly lower than that in the saline group on the 27th day. The fetal birth weight in the saline group was significantly lower than that in the control group. These finding suggest that OKY-046 restores the vascular refractoriness induced by A II and suppresses TXA2 synthesis in pregnant rabbits with aortic constriction.

The release of prostacyclin by endothelial cells (EC) in culture was studied after exposure to two toxic stimuli (UV light or dimethylsulfoxide-soluble smoke particles (DSP)) or to medium conditioned by smooth muscle cells (SMC), basically or after injury to the SMC. An activity stimulating the release of prostacyclin was found together with growth inhibiting activity from arterial SMC, but dissociated from growth stimulating activity. The prostacyclin stimulating activity was increased when SMC were exposed to UV light, while DSP caused a decrease. EC directly exposed to UV light or DSP generally released more prostacyclin than controls. One exception was very low concentrations of DSP. UV light induced a burst of release in contrast to DSP where a continuous release after a two hours lag period was seen. It is concluded that EC will increase the release of prostacyclin in response to injury but the release pattern will depend on the kind and doses of the stimulus. SMC release prostacyclin stimulating activity for EC, which can be modified by exposure to toxic stimuli. The results might have applications for atherogenesis.

Vascular responsiveness to angiotensin II in pregnant rats with a normal or a low calcium diet were examined. From day 6 of pregnancy, Wistar rats were separated into two groups. One group was fed a normal diet containing 1.2% calcium (control group) and the other group was fed a low calcium diet containing 0.02% calcium (low Ca group). Using a tail cuff method, the systolic blood pressure in the low Ca group was found to be significantly higher than that in the control group on day 18 of pregnancy. On days 12 and 18 of pregnancy using the hindquarters perfusion technique, the vascular response to bolus angiotensin II (30, 100, 300, and 1000 ng/kg of rat body weight) in the low Ca group increased significantly more than that in the control group. However, the pressor response to norepinephrine and the depressor response to acetylcholine did not differ between the low Ca group and the control group. Urinary sodium excretion in the low Ca group was lower than that in the control group on days 12 and 18 of pregnancy, and decreased toward term, whereas urinary phosphorus excretion in the low Ca group was higher than that in the control group on days 12 and 18 of pregnancy. These data indicate that low calcium intake during pregnancy increases sensitivity to the pressor effects of angiotensin II and increases systolic blood pressure in normotensive pregnant rats.

This study examined the effect of oral heparin on systolic blood pressure, platelet cytosolic free calcium, aortic calcium uptake and renal vascular changes in Dahl salt-sensitive (DS) rats on low (0.4% NaCl) and high (8% NaCl) salt diet. Twenty-four male DS rats, age 8 weeks, were divided into four groups of 6 animals each. Groups I and II were on low salt diet and groups III and IV on the high salt diet. Additionally, groups I and III were placed on 100% H2O and groups II and IV on sodium heparin 0.5 mg/ml in H2O as their drinking water for a period of 6 weeks. At 14 weeks, systolic blood pressure, platelet cytosolic free calcium and aortic calcium uptake were significantly higher in rats on high salt diet and water compared with rats from all other groups. Oral heparin treatment prevented the increase in systolic blood pressure, platelet cytosolic free calcium and aortic calcium uptake in rats on high salt diet. Heparin also prevented or attenuated the onset of adverse renal vascular changes observed in Dahl salt-sensitive rats on high salt diet. Oral heparin treatment did not cause abnormal hematological, biochemical or pathological changes in rats.

Accumulation of cholesterol in the tunica intima of arteries is a feature of atherosclerotic development. Recently, the demonstration of oxidized LDL in atherosclerotic lesions considerably strengthened the possibility of its role in the atherogenesis in vivo. However, the mechanism of lipid accumulation in monocyte-derived macrophages has not yet been clarified. It has been reported that the complement system may be related to atherosclerosis. In this report, complement receptors in the atherosclerotic lesions obtained from autopsy sample were investigated. Initially C3b receptors were detected using sheep erythrocytes bearing human C3b (EAC1423b cells). EAC1423b cells adherent to only aortic sections showing intimal thickening, but not to intact artery. Second, immunostaining of consecutive aortic sections was performed. Apo B and C5b-9 complex were stained using the indirect immunoperoxidase method, and macrophage, C3b receptor (CR1) and C3bi receptor (CR3) were stained using monoclonal antibody in the alkaliphosphatase anti-alkaliphosphatase method. In the intact artery of 3 month old patient, antigen- specific staining were not observed. In intimal thickening and atheroma of older patients, consecutive sections suggested that complement receptor-expressing cells were macrophages. Staining for apo B antigen existed at extracellular site in the intima, and C5b-9 complex was observed in intima and partially in the media. The above data showed that macrophage complement receptors were expressed in the atherosclerotic lesions when the complement system was activated. We conclude that these data suggest that the complement system and complement receptors may be related to the uptake of LDL by macrophages.

The present study examined contractile responses to norepinephrine in isolated aortae from 4-, 8-, and 12-week duration of streptozocin-induced diabetic rats. The pD2 value and the maximum contractile responses were significantly increased in 8-week and 12-week diabetic aortae, respectively, compared to the age-matched control aortae. Moreover, the bethanechol-induced relaxation of 12-week diabetic aortae preconstricted with norepinephrine was also significantly different from the age-matched control aortae. On the other hand, the KCl-, phenylephrine-induced contraction in 4-, 8-, and 12-week diabetic and age-matched control aortae were similar. Presumably the duration of diabetes altered the sensitivity and responsiveness of aortae to norepinephrine. The possibility of the enhanced norepinephrine response in diabetic aortae was discussed.

Clonidine as a partial agonist of alpha adrenoceptor in Wistar rat aorta has been documented. It was however observed that the effect of clonidine on the isolated rat aorta of Sprague Dawley rats was slightly different. The concentration effect curve induced by clonidine was on the right of that induced by phenylephrine, with EC50 of 1.5 x 10(-7) M and 3.5 x 10(-4) M for the phenylephrine- and clonidine-induced responses, respectively; but the maximal contraction induced by clonidine was similar to that of phenylephrine. In the presence of clonidine, the concentration effect curve of phenylephrine was shifted to the right. Both the phenylephrine- and clonidine-induced contraction were inhibited by prazosin, and the EC50 values for prazosin in phenylephrine- and clonidine-induced contraction were 1.0 x 10(-8) M and 1.8 x 10(-6) M, respectively. Yohimbine in concentration sufficient to antagonize almost completely the effect of phenylephrine was found to slightly prevent the effects of clonidine. Further increase of clonidine above 2 x 10(-3) M, the concentration sufficient to induce the maximal contraction, however induced depression of the clonidine-induced contraction, and this phenomenon was concentration dependent. Possible explanation of this phenomenon was discussed.

The formation of type I collagen fibrils by vascular human endothelial cells in culture was demonstrated by the indirect immunofluorescence method. The fibrillar structure was formed on the cell surface on the third day after subcultivation and had grown like a knitting ball of 0-3 microns in diameter and 0-200 microns in length on the seventh day. The fibril formation was stimulated by the addition of basic fibroblast growth factor, but completely blocked by the presence of beta-aminopropionitrile. The fibrils were eliminated by the treatment with clostridial collagenase or with 0.5% Triton X-100. The pathophysiological significance of type I collagen fibril formation by vascular endothelial cells in vascular diseases is also discussed.

We studied the effects of administering probucol on the catabolism of low density lipoprotein (LDL) in guinea pigs. Probucol administration significantly lowered the levels of total and LDL-cholesterol in animals given either normal chow or the high cholesterol (1% W/W) diet. High-density lipoprotein cholesterol was decreased significantly in the animals fed cholesterol, but not normal chow diet. Triglyceride levels were unaffected in both groups. No significant changes were observed in the LDL receptor-dependent and LDL receptor-independent catabolism of native LDL and LDL obtained from a probucol-treated patient. However, when the LDL isolated from a probucol-treated patient was injected, the fractional catabolic rate was significantly lower than that of injected native LDL. This study indicates that probucol lowered the plasma LDL cholesterol level neither by an increased catabolism of LDL via an LDL receptor nor an LDL receptor-independent pathway.

Proteoglycan (PG), isolated and purified from bovine aorta (intima-media), consisted of 68.6% chondroitin 4/6-sulfate (CS 4/6-S), 30% dermatan sulfate (DS), 1.4% heparan sulfate (HS), and a trace of hyaluronic acid (HA). PG did not affect platelet aggregation induced by ADP, collagen, and epinephrine, but inhibited that induced by thrombin. Of the standard GAGs investigated, hyaluronic acid (HA) and CS-4/6-S slightly inhibited only thrombin-induced platelet aggregation. However, PG and standard GAGs did not affect the thrombin induced aggregation of washed platelets. The effect of PG after papain digestion on thrombin-induced platelet aggregation was less potent than that before. It is suggested by the results of this study that PG in the aorta inactivates plasma thrombin, probably by inhibiting thrombin activators or potentiating substances which inactivate thrombin and that these effect of PG would be mainly due to PG-DS and partly due to PG-HS.