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Twenty patients with mild to moderate hypertension took part in this study consisting of a two-week placebo treatment period, followed by treatment with an extended-release calcium channel blocker, felodipine-ER (5 to 20 mg once daily) for 12 weeks. The study evaluated the effects of felodipine-ER on blood pressure, platelet function and rheological properties in hypertension. Felodipine-ER significantly reduced systolic and diastolic blood pressure without changing heart rate. There was a significant decrease in adenosine diphosphate-induced platelet aggregation and platelet intracellular calcium concentration, but no significant change in plasma thromboxane B2 (TXB2), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and platelet cyclic 3'5'-adenosine monophosphate concentrations. Adverse effects on biochemical and rheological properties were not found. In conclusion, felodipine-ER is an effective and metabolically safe antihypertensive drug. It reduces platelet aggregability and intracellular free calcium concentration without altering the production of TXB2 and 6-keto-PGF1 alpha.

Captopril 12.5 mg twice daily was initially administered given to a woman with chronic renal failure and hypertension. Three weeks later, she developed chills, high fever and sore throat. Hemogram showed severe neutropenia; the white cell count showed 600/cu mm; bone marrow aspirate and biopsy revealed a paucity of myeloid series. Antineutrophil antibody was not detected in the serum. The neutrophil counts returned to normal after captopril was discontinued two weeks later. We recommend that the peripheral white blood cell count in patients whom captopril is prescribed must be carefully monitored in the first three months, particularly in those with impaired renal function.

To determine the value of transesophageal echocardiography in the assessment of prosthetic cardiac valves, 11 patients with clinically suspected cardiac prosthetic valve dysfunction were studied by transesophageal two-dimensional imaging, as well as by color Doppler flow mapping. Among these 11 patients, there were 10 with biological tissue valves and 3 with metallic valves (1 Bjork-Shiley, 2 St. Jude). Nine patients had replacement of mitral valves alone. The remaining two had received both mitral and aortic prostheses. The degree of mitral regurgitation was graded by transesophageal color Doppler according to the area of the regurgitant jet visualized. The degree of aortic regurgitation was graded by the jet height/left ventricular outflow height ratio method. All transesophageal studies were performed without complication and all were well tolerated. The pathological morphology of the cardiac prosthesis was clearly visualized by transesophageal two-dimensional imaging and subsequently proven at surgery. Of those tested, one patient was found to have a torn leaflet, one had a dislodged leaflet, one patient had paravalvular leakage, four had cusp vegetations, and five patients had prosthetic degeneration for other reasons. Mitral regurgitation was graded as absent in one patient, mild in two patients, moderate in two patients, and severe in six patients. Aortic regurgitation was graded as severe in both patients with aortic prostheses. We conclude that in patients with clinically suspected cardiac prosthetic dysfunction, transesophageal two-dimensional imaging combined with color Doppler can provide reliable information that corresponds to surgical findings.

A 77-year-old woman presented with general weakness, dizziness and slow, irregular heart beats. An electrophysiologic study revealed a markedly prolonged sinus node recovery time of up to 5,900 msec, accompanied with dizziness. A permanent pacemaker with an AAIR mode was implanted. An abnormal shadow in the right lower lung field was found on chest x-ray. Selective arteriography revealed a right internal mammary to right pulmonary artery fistula. No significant hemodynamic abnormalities were found. This anomaly is extremely rare. Our patient is the oldest among 20 cases reported in the literature, and is the first one associated with sick sinus syndrome. Most reported cases have involved surgical ligation and excision, due to the risk of rupture of the malformation, endarteritis and congestive heart failure. Our patient refused surgical intervention and has done well during the past year.

In a span of 3 decades, investigation as to whether elevated plasma triglyceride (TG) is associated with increased risk of coronary artery disease (CAD) produced results that have largely been inconsistent. Therefore, these investigations have been relegated to the background when compared to the significance give to cholesterol in the 80's. The first study to report an association between TG and myocardial infarction was in 1959. Since then, many other studies have been done starting from case control studies to prospective studies and then progressing to interventional studies. Many have found TG significant on a univariate but not on a multivariate analysis. Attempts have been made to analyse TG in diabetics, especially those with a normal cholesterol, in ischemic cerebrovascular disease (ICD), and in other disease states where atherosclerosis is involved in their pathogenesis. Of particular interest is that our studies in Taiwan have consistently showed that TG may indeed be an independent risk factor. Our subjects with ICD, CAD, and in different stages of hypertension, all had significant association with elevated TG. Statistical consider, i. e. discrepancy between univariate and a multivariate analysis, large variability of plasma TG distribution, as well as genetic susceptibility of certain individuals are also factors to be considered. No study to date has specifically been designed to evaluate TG lowering effects on primary prevention of CAD. Despite differences of opinion among the various authorities on this subject, I feel that the TG-CAD association should not be ignored and further intervention studies should be done.

The effects of isradipine on ambulatory blood pressure, platelet aggregation, and oxygen free radicals were assessed in 30 patients with hypertension in a non-comparative 16-week study. After 4 weeks of placebo run-in, patients received isradipine at 2.5 mg twice daily for 12 weeks. The average supine systolic/diastolic blood pressure (155 +/- 17/101 +/- 11 mm Hg) was significantly reduced at the end of treatment (144 +/- 13/95 +/- 9 mm Hg; p less than 0.01). The heart rate was not significantly altered. Isradipine had no adverse effects on red or white blood cells or on plasma viscosity. The thromboxane B2 level and epinephrine-induced platelet aggregation were significantly (p less than 0.05) reduced. High-density lipoprotein cholesterol was significantly (p less than 0.01) increased after vs. before treatment; total cholesterol was significantly (p less than 0.05) increased at midstudy, but this was not significant at the end of the study. Other biochemical parameters were unchanged. Studies of neutrophil oxygen free radicals by serum opsonized zymosan and phorbol myristate acetate were not affected by isradipine. In conclusion, isradipine is an effective antihypertensive agent that also has beneficial effects on platelet aggregation and lipids while having no effects on neutrophil oxygen free radicals or most of the biochemical variables tested, making it an ideal agent for hypertension.

Plasma 6-keto-prostaglandin F 1 alpha and thromboxane B2, the metabolites of prostacyclin and thromboxane A2 respectively, were measured in 12 women with pregnancy-induced hypertension, 12 age-matched normotensive pregnant women and 8 non-pregnant women as controls. Pregnancy was divided into 3 stages, namely: 22-27, 28-32 and 33-39 weeks. The concentrations of thromboxane B2 in the plasma of women with pregnancy-induced hypertension was 1.4-1.7 times greater than normotensive pregnant subjects at the same gestational stage, and 2 times higher than controls. Plasma levels of 6-keto-prostaglandin F 1 alpha in normotensive pregnant women was 1.8 times greater than in those with pregnancy-induced hypertension at 28-32 and 33-39 weeks, and was significantly higher than control. The ratio of thromboxane B2 to 6-keto-prostaglandin F 1 alpha was markedly increased in the group of patients with pregnancy-induced hypertension at 28-32 and 33-39 weeks gestation. The ratio of the two metabolites in normotensive patients at each stage of gestation was similar to the control group. The ratio of circulating aggregated platelets in subjects with pregnancy-induced hypertension was significantly lower than in normotensive pregnant subjects at 33-39 weeks, implying increased turnover of platelets in pregnancy-induced hypertension. There was no significant difference in count of platelets, adenosine diphosphate threshold concentration and variables of platelet aggregation induced by adenosine diphosphate among the 3 groups.(ABSTRACT TRUNCATED AT 250 WORDS)

The responses of aortas to various vasoactive agents were compared in streptozotocin-induced diabetic male rats and age-matched normal controls. There was a shift of the dose-response curve of norepinephrine (NE) to the right from streptozotocin-induced diabetic rats of 8 weeks duration as compared that of to normal rats. The median effective concentration (EC50) of NE in diabetic aortas to NE was significantly increased from 10(-7.5) M to 10(-7.2) M, while the maximum response of diabetic aortas to NE was not different from that of normal controls. In addition, the EC50 and maximum contractile response to KCl were also not different between the two groups. Meanwhile, the contractions induced by angiotensins I and II, were also significantly attenuated in diabetic aortas. The endothelium-dependent relaxation produced by carbachol in aortic rings which is precontracted with NE was significantly lower in diabetic preparations than that in age-matched control animals. The EC50 of carbachol in diabetic and normal aortas to carbachol were 2.8 x 10(-6) M vs 1.2 x 10(-6) M respectively. These results suggest that deterioration of endothelium might exist in diabetic rats.

Several studies have shown that antihypertensive drugs therapy could reduce morbidity and mortality of hypertension related complication such as stroke, congestive heart failure and renal failure, but there was no significant reduction of coronary heart disease. The benefit of the treatment on morbidity and mortality may be counterbalanced by adversed metabolic effects of long-term therapy. The purpose of this study is to evaluate the blood pressure-lowering and adverse metabolic effects of chlorothiazide and propranolol monotherapy. A double-blind, cross-over design clinical trial was performed for 42 cases (22 males and 20 females) with the mean age of 52 (from 30 to 59 years old). After 2 weeks run-in period, the patients were assigned to group A and B with age and sex stratification. Chlorothiazide and propranolol were given for 12 weeks in alternative with 2 weeks placebo washout period. Our studies have shown that, chlorothiazide and propranolol could reduce both systolic and diastolic blood pressure significantly. But they also associated with adverse metabolic effects. Serum uric acid and triglyceride increased and decreased the concentration of high density lipoprotein cholesterol (HDL-C). Those changes could counterbalance the benefit of blood pressure-lowering effect of antihypertension. Carefully monitoring the adverse metabolic effects closely is necessary in therapy with these drugs.

There is considerable evidence from previous studies that platelets play an important role in the development and progression of atherosclerosis in hypertension, more so in relation to the stage of hypertension. Seventy one hypertensive patients (WHO stage I: 39, stage II: 23, stage III: 9) aged 19-84 (mean age: 56, 59 and 62 respectively for each stage) and 37 normal controls (aged 22-72 with a mean age of 52) were involved in this study. Hematocrit, beta-thromboglobulin (beta-TG), platelet factor 4 (PF4), beta-TG/PF4 ratio, total cholesterol (TC), low density lipoprotein-C, and triglycerides were higher in the hypertensive group while platelet count, circulating platelet aggregates, and high density lipoprotein-C were higher in the normotensive group. Among the hypertensives, stage III patients showed the highest beta-TG, PF4, beta-TG/PF4 ratio, triglycerides, and stage I with the least elevation. There were no significant differences noted in the ADP or epinephrine-induced platelet aggregation in both the normal and hypertensive patients. Other parameters such as heart rate, serum sodium, potassium, renal and liver function tests, plasma renin activity, aldosterone, fibrinogen thromboxane B2 and 6-Keto-PGF1 alpha, showed no significant differences in both groups. This study clearly showed that beta-TG/PF4 ratio and triglycerides are closely related to the stage of hypertension and are good indicators of in vivo platelet activation in hypertensives which may account for the acceleration of hypertensive vascular complications secondary to atherogenesis.

Purulent pericarditis is a life-threatening disease associated with a variety of microorganisms. The case presented herein has unusual manifestations of contrast echoes on two-dimensional echocardiography. To our knowledge, this is the first reported case of pericarditis caused by gas-forming group D Streptococcus and Klebsiella pneumoniae with pyopericardium, resulting in contrast echoes on the two-dimensional echocardiographic image.

Transesophageal echocardiography has been increasingly used in addition to the transthoracic approach. It not only allows an unobstructed window for viewing the left atrium, but also provides high-quality imaging to improve diagnosis of prosthetic valve dysfunction. To determine the value of transesophageal echocardiography in detection of dysfunctioning mitral prosthetic regurgitation, 11 patients clinically suspected of dysfunctioning mitral prosthesis were studies by transthoracic, transesophageal echocardiography and was documented by a left ventricular angiography. There were 7 biological tissue valves and 4 metallic Bjork-Shiley valves. Compared with a left ventricular angiography, the transthoracic approach to 8 patients made an underestimation of the grade of regurgitation. The angiographic grading confirmed the transesophageal approach in all patients except one who was graded as mild regurgitation by left ventricular angiography, moderate regurgitation by transesophageal echocardiography, but no regurgitation by transthoracic echocardiography. Our results indicated that in patients with suspected mitral prosthetic dysfunction, a transesophageal echocardiography is more sensitive than a transthoracic echocardiography in detecting mitral regurgitation.

Tiapamil, a new calcium antagonist, was evaluated for its antihypertensive and metabolic effects in a long-term (58 weeks) drug trial in 20 adult outpatient mild to moderately hypertensive subjects. Baseline systolic and diastolic blood pressure dropped after initiation of treatment and was significantly reduced after 4 weeks of treatment, further improving until the termination of the study. There was no impairment of renal and hepatic functions. Electrolytes, plasma aldosterone, plasma renin activity, as well as plasma lipids were not significantly altered during the course of therapy. Fasting blood sugar determinations and oral glucose tolerance test showed significant reductions from the baseline level as a result of the drug treatment. In conclusion, tiapamil is a metabolically safe and effective antihypertensive drug for long-term use.

The effects of angiotensin II (ANG II) alone and in combination with other agonists on platelet aggregation, thromboxane B2 (TxB2) synthesis and cytosolic [Ca2+]i were investigated. Angiotensin II (10(-11)-10(-7) mol/l) alone had no direct effect on aggregation, TxB2 production or [Ca2+]i after short- (< 2 min) or long-term (30 min) incubation. In contrast, low concentrations of ANG II (10(-11) mol/l) enhanced adrenaline-induced platelet aggregation but high concentrations (10(-7) mol/l) had an inhibitory effect. Moreover, ANG II (10(-11)-10(-7) mol/l) augmented platelet responses to the TxA2 mimetic U44069. The facilitatory effect of ANG II on adrenaline-induced platelet aggregation was abolished by pretreatment of platelets with flurbiprofen. Thromboxane B2 synthesis by adrenaline-treated platelets was inhibited by ANG II. The results indicate that ANG II stimulation of agonist-induced platelet activation is due to potentiation of the effects rather than the synthesis of TxA2.

Angiotensin II receptors on platelets were studied in 13 patients with uncomplicated type I diabetes mellitus and in 15 age-matched normal subjects. Receptor density on cells from the diabetic patients was 15% lower than the normal subjects (5.2 +/- 0.8 SD sites/platelet in diabetic patients and 6.4 +/- 0.8 in normals, P less than 0.001), but there were no differences in receptor affinity as measured by Kd (4.9 +/- 1.5 X 10(-10) mol/l in diabetic patients and 5.4 +/- 1.4 X 10(-10) mol/l in normals). Plasma concentrations of renin and angiotensin II were similar in both groups. The reduced density of angiotensin II receptors on platelets from patients with insulin-dependent diabetes may reflect a generalized abnormality of angiotensin II receptor regulation.

The value of maximal treadmill exercise electrocardiogram (TEE) in predicting coronary artery disease was evaluated in a consecutive series of 168 asymptomatic Chinese males, aged 41 to 57 years (mean 53) during annual physical examinations. Their resting electrocardiograms (ECGs) showed no abnormal Q-waves. The end-point of TEE achieved the age-predicted maximal heart rate, and no subjects had classic angina pectoris during or after TEE. Thirty-five subjects had positive electrocardiographic changes defined as reversible horizontal or downsloping ST-segment depression greater than or equal to 1.0 mv which lasted greater than or equal to 0.08 sec. Exercise thallium-201 (T1-201) myocardial imaging was performed on all 35 subjects with positive TEE; 30 subjects (86%) demonstrated normal and 5 abnormal scintigrams. Sixteen of the 30 cases with normal T1-201 scans underwent coronary arteriography, of which 14 showed normal arteriograms and two showed a less than 49% stenosis of the luminal diameter in one major artery. Of the 5 cases with abnormal scintigrams, 4 were found to have greater than 50% stenoses in at least one major artery, and only one case had a less than 49% stenosis of the right coronary artery. We concluded that TEE alone for asymptomatic individuals provided limited value in diagnosing significant coronary artery disease, especially in areas of low prevalence.

1. The antihypertensive and renal effects of cilazapril, a new angiotensin converting enzyme inhibitor, were evaluated in both two-kidney, one-clip Goldblatt hypertensive rats (n = 11) and normotensive rats (n = 6). 2. Intravenous infusion of cilazapril (1 mg/kg followed by 25 micrograms min-1 kg-1) caused significant reductions of blood pressure from 163 +/- 3 to 122 +/- 4 mmHg and from 157 +/- 2 to 113 +/- 3 mmHg in two separate groups of hypertensive rats and from 124 +/- 1 to 105 +/- 2 mmHg in normotensive rats. The hypotensive effect in terms of absolute value of percentage change was greater in hypertensive rats than in normotensive rats (41 +/- 6 vs 20 +/- 3 mmHg or 25 +/- 4% vs 16 +/- 2%, respectively). 3. Cilazapril increased glomerular filtration rate, urine flow, and absolute and fractional excretion rates of sodium and potassium in the non-clipped kidney of hypertensive rats. In contrast, the clipped kidney exhibited a depressed renal function during cilazapril infusion. 4. In normotensive rats, the hypotensive and enhanced renal function responses to cilazapril were much less than those of the non-clipped kidney of hypertensive rats. 5. Superimposed administration of either angiotensin II or angiotensin III during cilazapril infusion completely reversed the blood pressure and bilateral renal responses of cilazapril in both hypertensive and normotensive rats. 6. These results indicate that cilazapril reduces arterial pressure and enhances renal excretion mainly via inhibition of angiotensin II and angiotensin III formation.

Twenty-eight subjects, 16 with old myocardial infarction (OMI) and a control group of 12, received ticlopidine 250 mg/day for 4 weeks. All subjects underwent the standard Bruce protocol exercise test before and after therapy. Blood was collected from a peripheral vein to study platelet function at pre-exercise (rest), peak exercise (end point), and 6 min post-exercise (recovery). Platelet count, platelet aggregatory response, plasma thromboxane B2 (TXB2), and 6-keto-PGF 1 alpha were measured by Coulter counter, aggregometry, and radioimmunoassay, respectively. The platelet count, aggregatory response (induced by ADP, adrenalin, and collagen) and the plasma concentration of TXB2 and 6-keto-PGF 1 alpha were not significantly affected by exercise in the OMI and control groups. Overall, there were no significant changes in exercise duration, heart rate, and blood pressure in both groups before or after ticlopidine treatment, with some minor exceptions. There were no significant changes in the peripheral blood profiles, the bleeding and coagulation times, the blood chemistry data, and the platelet counts between the groups before or after treatment. There was a significant decrease in collagen- and ADP-induced platelet aggregation in both groups after ticlopidine therapy. Prior to treatment, a higher plasma TXB2 concentration was noted in the OMI group during and after exercise; the difference was no longer statistically significant after ticlopidine therapy when both groups were compared. There was a significant reduction in the TXB2 levels in the OMI group after ticlopidine treatment despite exercise. Before therapy, plasma 6-keto-PGF 1 alpha was significantly elevated in the OMI group before or after exercise but was not statistically significant after ticlopidine treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of angiotensin II (ANG II) alone and in combination with other agonists on human platelet aggregation, thromboxane B2 (TxB2) and cytosolic [Ca2+]i were investigated. ANG II (10(-11) - 10(-7) M) alone had no direct effect on aggregation, TxB2 production or [Ca2+]i after short- (less than 2 min) or long-term (30 min) incubation. In contrast, low concentrations of ANG II (10(-11) M) enhanced adrenaline-induced platelet aggregation but high concentrations (10(-7) M) had an inhibitory effect. Moreover, ANG II (10(-11) - 10(-7) M) augmented platelet responses to the TxA2 mimetic, U44069. Pretreatment of platelets with flurbiprofen abolished this facilitatory effect of ANG II on adrenaline- but not on U44069-induced platelet aggregation. These results suggest that ANG II stimulation of agonist-induced platelet activation may be due to potentiation of the effects rather than the synthesis of TxA2.

The effects of changes in dietary intake of sodium and potassium on 125I-angiotensin II binding to platelets were studied in normal subjects. We also defined binding to platelets from patients with essential hypertension and subjects with normal blood pressure. Restriction of sodium intake in normal subjects resulted in a decrease in the number of receptor sites from 6.2 +/- 0.3 sites/cell to 4.1 +/- 0.4 sites/cell (P less than 0.01) but there were no changes in affinity as measured by the Kd. Over a range of sodium intakes from 15 to 200 mmol/day there was a negative correlation between plasma concentration of angiotensin II and receptor site concentration (rs = 0.57, P less than 0.01). Changes in dietary potassium did not affect angiotensin II binding. Angiotensin II binding was also measured in 10 patients with essential hypertension (mean blood pressure [BP] 178/107 mmHg, plasma concentrations of renin [PRC] 12 +/- 2 microU/ml and angiotensin [pANG] II 14 +/- 2 pg/ml) and 10 subjects with normal blood pressure (mean BP 112/74 mmHg, PRC 13 +/- 2 microU/ml, pANG II 13 +/- 2 pg/ml). In the hypertensive patients, binding capacity and affinity (Kd = 5.0 +/- 0.6 X 10(-10) M, 5.7 +/- 0.8 sites/cell) were similar to those in the normotensive subjects (Kd = 4.9 +/- 0.8 X 10(-10) M, 5.4 +/- 0.5 sites/cell). Changes in sensitivity to angiotensin II in essential hypertension may not be determined at receptor level. Angiotensin II receptors in platelets respond to changes in sodium intake like receptors in arterial muscle.

To evaluate the long-term effect of tiapamil, a new calcium antagonist, in hypertension, 20 adult patients suffering from mild to moderate hypertension were entered into a 58-week open study. In 10 patients, blood pressure returned to normal within 1-6 weeks with a daily dose of 600-900 mg tiapamil. In the remaining 10 patients, the blood pressure became normal after 8-28 weeks with a daily dose of 900-1,200 mg tiapamil. The more severe the hypertension, the higher the dose needed and the longer the time required for the blood pressure to return to normal. The overall results at the end of the 58-week treatment showed a significant decrease of the blood pressure to 142 (+/- 9)/88 (+/- 4) mmHg from a before treatment average of 166 (+/- 16)/105 (+/- 7) (p less than 0.001). There was no marked difference in the blood pressure between supine and sitting positions before or after treatment. Side effects were mild and self-limiting, with no patient being dropped from the study. Electrocardiogram (ECG) and laboratory values were not affected during the treatment with the exception of a moderate decrease in the blood glucose. Neither plasma renin activity, nor aldosterone concentration, nor serum cholesterol or triglyceride levels were altered during tiapamil administration. Tiapamil appears to be an effective and well-tolerated drug for use in mild to moderately severe hypertension.

Hypertension complicated by left ventricular hypertrophy is associated with increased morbidity as it leads to left ventricular systolic and diastolic dysfunction. Thus, in the treatment of hypertension, a desirable goal is the regression of left ventricular hypertrophy. Tiapamil, a new calcium antagonist, was evaluated in a 58 week open study to determine its effect on left ventricular mass in relation to its ability to lower blood pressure. Twenty adult patients with mild to moderate hypertension were entered into the study. Blood pressure was significantly reduced from 166 +/- 16/105 +/- 7 mmHg before treatment to 142 +/- 9/88 +/- 4 mmHg after 58 weeks. The posterior and interventricular septal wall thickness and left ventricular systolic dimension did not show any significant change by the end of the trial. On the other hand, left ventricular diastolic dimension, ejection fraction, and left ventricular mass increased significantly (P less than 0.05). Other laboratory parameters were not affected during treatment with the exception of a moderate decrease in the blood glucose. Side effects were mild and self-limiting, and no patients were withdrawn from the study. Although tiapamil appears to be an effective and well-tolerated drug in mild to moderate hypertension, it failed to reduce left ventricular mass.

Platelets were prepared from peripheral venous blood on iso-osmotic density gradients of Percoll, resulting in a good recovery of cells (50-80%) which were relatively free of contaminating blood cells (erythrocyte less than 0.1%, leucocyte less than 1%). At 22 degrees C, specific binding of 125I-labelled angiotensin II (300 pmol/l) was time and temperature dependent, saturable, reversible and linear with cell concentration. Scatchard analysis of saturation curves revealed a single class of binding sites with Kd 1.5 +/- 0.4 X 10(-10) mol/l and total binding capacity 6.3 +/- 1.2 receptors/platelet. Similar values (Kd 2.4 +/- 0.7 X 10(-10) mol/l and binding capacity 6.5 +/- 1.0 receptors/cell) were obtained by displacement analysis. From kinetic studies the forward and reverse rate constants were 3.1 X 10(8) mol min-1 l-1 and 3.6 X 10(-2)/min giving a Kd of 1.2 X 10(-10) mol/l. The relative binding potencies for angiotensin II and analogues were: [Sar1, Thr8]ANG II greater than ANG II greater than ANG III greater than [Sar1, Ala8]ANG II greater than ANG I. Incubation with an extracellular marker (51Cr-labelled EDTA) demonstrated that binding of angiotensin II to platelets was not due to free fluid endocytosis.

In the present study, we changed the fatty acid profile in blood and platelet membranes by dietary manipulation, and examined the effect on platelet aggregation in rats. Fifty-five rats were divided into five groups and fed for 56 days with 1% cholesterol and different types of fatty acid-rich diets: basal, lard, lard + fish oil, soybean oil, and soybean oil + fish oil. a decrease in serum arachidonic acid (20:4, omega-6, AA) and an increase in serum eicosapentaenoic acid (20:5, omega-3, EPA) were found in all experimental dietary groups fed with refined fish oil. Similar changes in the polyunsaturated fatty acids were also found in the platelet membrane phospholipids. Platelet aggregation, quantitated by the slope and height of the aggregation curve induced by different concentrations of ADP in a platelet aggregometer, was inhibited in all groups fed with refined fish oil. This inhibition of platelet aggregation may be related to an increase in the ratio of EPA and AA in the platelet membrane phospholipids after dietary manipulation. The differences in the platelet aggregation and thromboxane B2 (TXB2) concentration between the lard and the lard + fish oil groups were more profound than that between the soybean oil and the soybean oil + fish oil group. However, the malondialdehyde (MDA) concentration revealed no significant differences between the five groups.