Effects of anthocyanins on cardiovascular risk factors and inflammation in pre-hypertensive men: a double-blind randomized placebo-controlled crossover study.

High intake of fruits and vegetables is associated with reduced cardiovascular risk. A number of fruits and vegetables are rich in anthocyanins, which constitute a subgroup of the flavonoids. Anthocyanins have demonstrated anti-inflammatory and anti-oxidative properties, and anthocyanin-rich interventions have indicated beneficial effects on blood pressure and other cardiovascular risk factors. We assessed whether a purified anthocyanin supplement improves cardiovascular metabolic risk factors and markers of inflammation and oxidative stress in prehypertensive participants, and whether plasma polyphenols are increased 1-3 h following intake. In all, 31 men between 35-51 years with screening blood pressure >140/90 mm Hg without anti-hypertensive or lipid-lowering medication, were randomized in a double-blinded crossover study to placebo versus 640 mg anthocyanins daily. Treatment durations were 4 weeks with a 4-week washout. High-density lipoprotein (HDL)-cholesterol and blood glucose were significantly higher after anthocyanin versus placebo treatment (P=0.043 and P=0.024, respectively). No effects were observed on inflammation or oxidative stress in vivo, except for von Willebrand factor, which was higher in the anthocyanin period (P=0.007). Several plasma polyphenols increased significantly 1-3 h following anthocyanin intake. The present study strengthens the evidence that anthocyanins may increase HDL-cholesterol levels, and this is demonstrated for the first time in prehypertensive and non-dyslipidemic men. However, no other beneficial effects in the short term were found on pathophysiological markers of cardiovascular disease.

Changes in electrocardiographic left ventricular hypertrophy and risk of major cardiovascular events in isolated systolic hypertension: the LIFE study.

The predictive value of changes in the severity of electrocardiographic left ventricular hypertrophy (ECG-LVH) during antihypertensive therapy remains unclear in isolated systolic hypertension (ISH). In a Losartan Intervention For Endpoint reduction in hypertension substudy, we included 1320 patients aged 54-83 years with systolic blood pressure (BP) of 160-200 mm Hg, diastolic BP <90 mm Hg and ECG-LVH by Cornell voltage-duration product and/or Sokolow-Lyon voltage criteria, randomized to losartan- or atenolol-based treatment with a mean follow-up of 4.8 years. The composite end point of cardiovascular death, non-fatal myocardial infarction (MI) or stroke occurred in 179 (13.6%) patients. In Cox regression models controlling for treatment, Framingham risk score, as well as baseline and in-treatment BP, less severe in-treatment ECG-LVH by Cornell product and Sokolow-Lyon voltage was associated with 17 and 25% risk reduction for the composite end point (adjusted hazard ratio (HR) 0.83, 95% confidence interval (95% CI:) 0.75-0.92, P=0.001 per 1050 mm × ms (1 s.d.) lower Cornell product; and HR 0.75, 95% CI: 0.65-0.87, P<0.001 per 10.5 mm (1 s.d.) lower Sokolow-Lyon voltage). In parallel analyses, lower Cornell product and Sokolow-Lyon voltage were associated with lower risks of cardiovascular mortality and MI, and lower Sokolow-Lyon voltage with lower risk of stroke. Lower Cornell product and Sokolow-Lyon voltage during antihypertensive therapy are associated with lower likelihoods of cardiovascular events in patients with ISH.

Markers of collagen synthesis is related to blood pressure and vascular hypertrophy: a LIFE substudy.

Cardiac fibrosis and high levels of circulating collagen markers has been associated with left ventricular (LV) hypertrophy. However, the relationship to vascular hypertrophy and blood pressure (BP) load is unclear. In 204 patients with essential hypertension and electrocardiographic LV hypertrophy, we measured sitting BP, serum collagen type I carboxy-terminal telopeptide (ICTP) reflecting degradation, procollagen type I carboxy-terminal propeptide (PICP) reflecting synthesis and LV mass by echocardiography after 2 weeks of placebo treatment and after 1 year of antihypertensive treatment with a losartan- or an atenolol-based regimen. Furthermore, we measured intima-media thickness of the common carotid arteries (IMT), minimal forearm vascular resistance (MFVR) by plethysmography and ambulatory 24-h BP in around half of the patients. At baseline, PICP/ICTP was positively related to IMT (r=0.24, P<0.05), MFVR(men) (r=0.35, P<0.01), 24-h systolic BP (r=0.24, P<0.05) and 24-h diastolic BP (r=0.22, P<0.05), but not to LV mass. After 1 year of treatment with reduction in systolic BP (175+/-15 vs 151+/-17 mmHg, P<0.001) and diastolic BP (99+/-8 vs 88+/-9 mmHg, P<0.001), ICTP was unchanged (3.7+/-1.4 vs 3.8+/-1.4 microg/l, NS) while PICP (121+/-39 vs 102+/-29 microg/l, P<0.001) decreased. The reduction in PICP/ICTP was related to the reduction in sitting diastolic BP (r=0.31, P<0.01) and regression of IMT (r=0.37, P<0.05) in patients receiving atenolol and to reduction in heart rate in patients receiving losartan (r=0.30, P<0.01). In conclusion, collagen markers reflecting net synthesis of type I collagen were positively related to vascular hypertrophy and BP load, suggesting that collagen synthesis in the vascular wall is increased in relation to high haemodynamic load in a reversible manner.

Alcohol consumption and cardiovascular risk in hypertensives with left ventricular hypertrophy: the LIFE study.

The Losartan Intervention For End point reduction in hypertension (LIFE) study showed superiority of losartan over atenolol for reduction of composite risk of cardiovascular death, stroke, and myocardial infarction in hypertensives with left ventricular hypertrophy. We compared hazard ratios (HR) in 4287 and 685 participants who reported intakes of 1-7 and >8 drinks/week at baseline, respectively, with those in 4216 abstainers, adjusting for gender, age, smoking, exercise, and race. Within categories, clinical baseline characteristics, numbers randomized to losartan and atenolol, and blood pressure (BP) lowering were similar on the drug regimens. Overall BP control (<140/90 mmHg) at end of follow-up was similar in the categories. Composite end point rate was lower with 1-7 (24/1000 years; HR 0.87, P<0.05) and >8 drinks/week (26/1000 years; HR 0.80, NS) than in abstainers (27/1000 years). Myocardial infarction risk was reduced in both drinking categories (HR 0.76, P<0.05 and HR 0.29, P<0.001, respectively), while stroke risk tended to increase with >8 drinks/week (HR 1.21, NS). Composite risk was significantly reduced with losartan compared to atenolol only in abstainers (HR 0.81 95% confidence interval, CI (0.68, 0.96), P<0.05), while benefits for stroke risk reduction were similar among participants consuming 1-7 drinks/week (HR 0.73, P<0.05) and abstainers (HR 0.72, P<0.01). Despite different treatment benefits, alcohol-treatment interactions were nonsignificant. In conclusion, moderate alcohol consumption does not change the marked stroke risk reduction with losartan compared to atenolol in high-risk hypertensives. Alcohol reduces the risk of myocardial infarction, while the risk of stroke tends to increase with high intake.

Supine and exercise systolic blood pressure predict cardiovascular death in middle-aged men.

AIM AND METHODS: The outcome of 1999 apparently healthy men, aged 40-59 years, initially investigated in the period 1972-1975, has previously been ascertained at 7 and 16 year follow-ups. This has now been repeated after 21 years, to determine whether seated systolic blood pressure (BP) during a bicycle ergometer exercise test adds prognostic information on cardiovascular (CV) mortality beyond that of systolic BP measured after 5 min of supine rest. RESULTS: After 21 years, 41 979 years of observation, 470 patients had died, 255 from CV causes. Supine systolic BP [2 SD increase: relative risk (RR) 1.6, 95% confidence interval (CI) 1.3-2.0, P < 0.0001], 6 min exercise systolic BP (2 SD increase: RR 1.6, 95% CI 1.3-2.0, P < 0.0001) on the starting workload of 600 kpm/min (approximately 100 W, 5880 J/min) and maximal systolic BP (2 SD increase: RR 1.5, 95% CI 1.2-1.9, P = 0.0005) during work were all related to CV mortality when adjusting for a large number of variables measured in the present study including age, exercise capacity, heart rates, smoking habits, glucose tolerance and serum cholesterol. When including other systolic BPs in the continuous multivariate analysis, supine systolic BP (2 SD increase: RR 1.4, 95% CI 1.04-1.9, P = 0.029) and 6 min systolic BP at 600 kpm/min (2 SD increase: RR 1.4, 95% CI 1.06-1.9, P = 0.017) were independent predictors of CV death but not maximal systolic BP during exercise (2 SD increase: RR 1.0, 95% CI 0.7-1.2, P = 0.95). CONCLUSION: These results are different from the mortality data at 16 years, when the independent predictive effect of supine systolic BP was cancelled out by 6 min exercise systolic BP at 600 kpm/min. Twenty-one years of follow-up of 1999 apparently healthy men disclose independently predictive information on CV death, of both supine systolic BP and 6 min exercise systolic BP taken at an early moderate workload. The influence of maximal exercise systolic BP on CV death is however cancelled out by the two other systolic BPs.

Polymorphisms in candidate genes for blood pressure regulation in young men with normal or elevated screening blood pressure.

We have previously shown correlations between cardiovascular risk factors such as blood pressure (BP), sympathetic nervous system activity, lipids and insulin resistance in young men with elevated screening BP. In the present study we aimed to: (1) compare the genotype distribution and allele frequencies of 11 polymorphisms in seven candidate genes for BP regulation in healthy 21-year-old Caucasian men, between 18 men with normal and 67 men with high screening BP, and (2) evaluate the effect of these polymorphisms in candidate genes on casual BP, BP responses to mental stress or catecholamines and metabolic parameters including insulin sensitivity. There were no differences in genotype distributions or allele frequencies between the subjects with normal and those with high screening BP. Insulin sensitivity was significantly higher in GG homozygotes in the G-261A polymorphism at the alpha 2A-adrenergic receptor (alpha(2A)AR) locus compared to GA heterozygotes (p = 0.007). Subjects who were homozygous both GG in the G-261A polymorphism at the alpha(2A)AR locus and GlyGly in the Arg16Gly polymorphism at the beta2-adrenergic (beta2AR) receptor loci had significantly higher insulin sensitivity and lower catecholamine levels during mental stress than subjects with other genotypes. Subjects who were II homozygous at the angiotensin converting enzyme (ACE) locus and AA homozygous at the angiotensin type I receptor (AT1R) locus had lower BP and a better lipid profile than the rest of the group. Thus, in this explorative study, we report an association between insulin sensitivity and a polymorphism at the alpha(2A)AR locus. We suggest the presence of gene-gene interactions in the renin-angiotensin system and the sympathetic nervous system.

Blood viscosity, plasma adrenaline and fasting insulin in hypertensive patients with left ventricular hypertrophy. ICARUS, a LIFE Substudy. Insulin CARotids US Scandinavica.

We have seen relationships between whole blood viscosity (WBV) and components of the metabolic cardiovascular syndrome in borderline hypertensive young men and suggested that sympathetic nervous system (SNS) activity may be a mediator. In the present study we aimed to test this hypothesis in established hypertension and to investigate the relationship between WBV and cardiac dimensions. Unmedicated patients (n = 42) with stage II-III hypertension and electrocardiographic left ventricular hypertrophy (LVH) underwent hyperinsulinemic isoglycemic glucose clamp to assess glucose disposal rate (GDR) and echocardiographic studies. WBV, plasma catecholamines and insulin were measured in arterialized venous blood. WBV at high shear rate correlated with baseline plasma adrenaline (r = 0.33, p = 0.04) and fasting insulin (r = 0.34, p = 0.04) while there was a negative trend for GDR (r = -0.21, p = 0.2). WBV at low shear rate correlated with plasma adrenaline (r = 0.49, p = 0.002) and resting heart rate (r = 0.36, p = 0.02). WBV was higher in smokers than in non-smokers (p = 0.02) and in males than in females (p = 0.02). Fasting insulin independently explained 12% of the variation in WBV at high shear, while baseline adrenaline independently explained 17% of the variation in WBV at low shear. Systolic blood pressure explained 31% of the variation in LV mass index. Thus, we demonstrate positive relationships between blood viscosity versus plasma adrenaline and fasting insulin in hypertensive patients with LVH. We suggest that adrenergic activity may increase hematocrit and viscosity and hence reduce insulin sensitivity.

Predictors of 7-year changes in exercise blood pressure: effects of smoking, physical fitness and pulmonary function.

BACKGROUND: The health status of 1999 apparently healthy men, aged 40-59 years, was ascertained after 16 years. We found that their systolic blood pressure during an ergometer exercise test added prognostic information beyond that from their blood pressure at rest concerning total cardiovascular mortality and mortality from myocardial infarction. OBJECTIVE: To determine predictors of the change in systolic blood pressure at rest during 7 years and of the change in the prognostically important peak exercise systolic blood pressure at 600 kilopondmetres/min during 7 years. METHODS: Predictors of the changes in blood pressures were investigated in 1393 middle-aged men who had been healthy without drug treatment for chronic disease or hypertension for 7 years. Twelve potential independent predictors were investigated. RESULTS: Previous blood pressures, age and body mass index were independent predictors and could explain 18% of the change in systolic blood pressure at rest over 7 years. For systolic blood pressure at 600 kilopondmetres/min also smoking was associated with a rise whereas a high body mass index, physical fitness and forced expiratory volume in 1 s (all P< 0.001) were associated with lower blood pressure, explaining 19% of the variability. CONCLUSIONS: Beyond a relatively strong tracking of blood pressures and the expected effect of age, smoking is associated with a 7-year rise in exercise systolic blood pressure whereas relatively higher body mass, physical fitness and pulmonary function are associated with lower exercise systolic blood pressure after 7 years in middle-aged healthy men.

Relationship between hemorheological factors and insulin sensitivity in normotensive and hypertensive premenopausal women.

The present study aimed at testing a possible relationship between hemorheologic factors such as hematocrit and whole blood viscosity, and insulin sensitivity in premenopausal, hypertensive (HT), and normotensive (NT) women. Fourteen HT and 12 NT women were studied with the hyperinsulinemic euglycemic glucose clamp technique. Insulin sensitivity was similar in NT and HT (8.7 +/- 0.8 v 7.6 +/- 0.8 arbitrary units). Whole blood viscosity did not differ between the two groups at any shear rate (shear rate 5.2 sec-1: 7.5 +/- 0.4 in NT and 8.0 +/- 0.3 in HT, P = NS). Statistically significant negative correlations were observed between the insulin sensitivity index and calculated whole blood viscosity at both high (r = -0.49, P < .01) and low shear rates (r = -0.50, P < .01, n = 26). Insulin sensitivity index was also negatively correlated to body mass index in the combined groups (r = -0.40, P = .04), and to both systolic and diastolic blood pressure (r = -0.44, P = .02 and r = -0.38, P = .05, respectively). In multiple regression analysis, whole blood viscosity, body mass index, systolic, and diastolic blood pressure accounted for 39% of the variation in insulin sensitivity index, but only whole blood viscosity was an independent explanatory variable for the insulin sensitivity index. These results suggest hemorheologic, and therefore indirectly hemodynamic factors as correlates to insulin sensitivity.

Quality of life on enalapril after acute myocardial infarction.

Quality of life was assessed 4-6 months after an acute myocardial infarction in a randomized double-blind study of enalapril versus placebo. Quality of life was evaluated using the Nottingham Health Profile (NHP), the Physical Symptoms Distress Index (PSDI), the Work Performance Scale (WPS) and the Life Satisfaction Index (LSI). The study comprised 36 women (aged 46-85 years, mean 68) and 96 males (aged 39-81 years, mean 62). Quality of life did not differ significantly between patients treated with enalapril versus placebo. The scores were (enalapril vs placebo, mean +/- SE): average NHP 15.4 +/- 2.3 vs 17.1 +/- 2.3; PSDI 9.5 +/- 1.0 vs 10.8 +/- 0.9; WPS 19.8 +/- 2.0 vs 19.4 +/- 1.4; LSI 24.1 +/- 1.0 vs 22.5 +/- 1.4. Men reported a better quality of life than women on most assessments, and non-smokers and ex-smokers better than smokers. Patients with moderate or severe angina pectoris had a worse quality of life measured by PSDI and NHP than patients with minimal or no angina pectoris. Patients with congestive heart failure had a higher PSDI than those without (13.6 +/- 1.7 vs 9.4 +/- 0.7, P < 0.05), while no significant differences were observed in the NHP scores. In conclusion, quality of life was similar in enalapril and placebo-treated patients after an acute myocardial infarction. However, it was reduced in patients with angina pectoris or heart failure and in those who continued smoking.

Exercise blood pressure predicts cardiovascular mortality in middle-aged men.

The outcome of 1999 apparently healthy men aged 40 to 59 years investigated from 1972 through 1975 was ascertained after 16 years to determine whether systolic blood pressure measured with subjects in the sitting position during a bicycle ergometer exercise test adds prognostic information on cardiovascular mortality beyond that of casual blood pressure measured after 5 minutes of supine rest. During a total follow-up of 31,984 patient years, 278 patients died, 150 from cardiovascular causes. Casual blood pressure and pulse pressure as well as peak exercise systolic blood pressure during 6 minutes on the starting workload of 600 kpm/min (approximately 100 W, 5880 J/min) were all related to cardiovascular mortality. The relative risk (RR) of dying from cardiovascular causes associated with an increment of 48.5 mmHg (= 2 SD) in systolic blood pressure at 600 kilopondmeter (kpm)/min was significant (RR = 1.5, 95% confidence interval [CI] = 1.1-2.3, P = .040) even when adjusting for a large number of variables measured in the present study, including age, exercise capacity, smoking habits, and casual blood pressures. The influence of blood pressure at 600 kpm/min was so strong that the predictive value of resting casual blood pressures became nonsignificant when these were analyzed as continuous variables also including exercise blood pressure as a covariate. However, the maximal systolic blood pressure during the exercise test was unrelated to cardiovascular mortality.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of ovarian stimulation on blood pressure and plasma catecholamine levels.

Effects of ovarian stimulation for in vitro fertilization on blood pressure and plasma catecholamine levels were studied in 10 women. The examinations were carried out before hormonal treatment with human menopausal gonadotropin (day three of the menstrual cycle, mean serum oestradiol concentration 0.2 nmol l-1, and on the day after ovulation induction with human chorionic gonadotropin (cycle days 10-12, mean serum oestradiol concentration 7.4 nmol l-1). Systolic and diastolic blood pressures (mean +/- SD) decreased 6.7 +/- 8.6 mm Hg, p = 0.049, and 5.3 +/- 4.7 mm Hg, p = 0.009, respectively), and venous plasma noradrenaline increased (42 +/- 44 pg ml-1, p = 0.02) during ovarian stimulation. No significant change was observed in either arterial noradrenaline, arterial adrenaline or venous adrenaline. After stimulation a positive correlation was observed between systolic blood pressure and arterial adrenaline (r = 0.73, p = 0.027), and between systolic blood pressure and the arterial-venous difference for adrenaline (r = 0.81, p = 0.007). The increased venous noradrenaline levels may be a reflex-mediated activation of the sympathetic nervous tone due to a decrease in blood pressure, or may indicate reduced neuronal re-uptake of released noradrenaline. The mechanisms behind the strong correlation between adrenaline and blood pressure are unclear, but may be induced by the supraphysiological oestradiol levels. Thus, adrenaline seems to be more important for blood pressure control in this particular setting.

Progesterone reduces sympathetic tone without changing blood pressure or fluid balance in men.

There is scant information on the effects of progesterone on circulation. Changes in catecholamine levels, blood pressure and transcapillary fluid balance were measured in 12 men before and during administration of natural progesterone (Utrogestan). Before administration, systolic blood pressure was significantly correlated with venous adrenaline (r = 0.67, p = 0.01). There was a significant decrease (p = 0.004) in venous noradrenaline during progesterone administration, and systolic blood pressure was significantly correlated with the arteriovenous difference for noradrenaline (r = 0.66, p = 0.02). Serum progesterone, which attained levels similar to those found in women during the luteal phase, did not significantly alter blood pressure, body weight or intra- to extravascular fluid shift. It is concluded that progesterone may have a direct action by increasing the uptake of noradrenaline from the synaptic cleft or by decreasing the nerve firing rate. Interestingly, the pretreatment finding of a significant correlation between blood pressure and adrenaline was less evident during progesterone administration.

Mild essential hypertension in nonobese premenopausal women is characterized by low renin.

The pathophysiological mechanisms in hypertension may differ in men and women. Plasma renin activity was measured in 27 premenopausal, never-treated hypertensive women (blood pressure 141 +/- 2/93 +/- 1 mm Hg) and in 18 age-matched normotensive women (blood pressure 113 +/- 2/71 +/- 2 mm Hg). All subjects were unaware of their blood pressure status. The hypertensive women had on average lower plasma renin activity (0.21 +/- 0.03 nmol/L/h) than their normotensive controls (0.42 +/- 0.07 nmol/L/h, P less than .01). Serum estradiol was also lower in the hypertensive women (0.57 +/- 0.06 v 0.81 +/- 0.09 nmol/L, P less than .05). No difference in epinephrine, norepinephrine, atrial natriuretic peptide, or vasopressin was found between the groups. Plasma renin activity was positively correlated to plasma norepinephrine in the hypertensive women only (r = 0.41, P less than .05). Since low renin hypertension is associated with less cardiovascular complications, this may offer an explanation for the better prognosis of hypertension in women.

Platelet function during antihypertensive treatment with quinapril, a novel angiotensin converting enzyme inhibitor.

The effect of various antihypertensive medications on platelet function is of increasing interest. Conflicting effects of captopril on platelet function are reported and the impact of angiotensin converting enzyme (ACE) inhibitors not containing a sulfhydryl group such as enalapril, lisinopril, and quinapril on platelet function remains unstudied. Therefore, the aim of the present study was to examine the effect of antihypertensive treatment with quinapril, a novel ACE inhibitor not containing a sulfhydryl group, on platelet function. Ten white men (age range of 32-61 years) with untreated mild-to-moderate essential hypertension (supine diastolic blood pressure greater than 95 mm Hg) were treated with 4 weeks each of placebo and quinapril in a double-blind, randomized, crossover design. Quinapril (20 mg twice a day) significantly lowered systolic (p less than 0.01) and diastolic blood pressure (p less than 0.01) without any significant effect on heart rate or plasma catecholamines. No significant change was noted for in vitro platelet aggregation induced by epinephrine, ADP, or collagen. Plasma concentrations of the platelet release factors beta-thromboglobulin and platelet factor 4 did not change, nor did the platelet content of norepinephrine, platelet weight (mg/10 ml of blood), circulating platelet count, or platelet size. Thus, as assessed by a broad spectrum of platelet parameters, we found that antihypertensive treatment with quinapril has no significant effect on platelet function in patients with mild-to-moderate essential hypertension. These "platelet-neutral" properties of quinapril suggest that quinapril, both from a thromboembolic and a hemostatic point of view, may be a rather safe agent for treatment of hypertension.

Increased erythrocyte magnesium in never treated essential hypertension.

In the present study we aimed at evaluating the intracellular concentrations of magnesium, potassium and sodium in 50-year-old, otherwise healthy white men with never treated, essential hypertension (n = 12) and in normotensive control subjects (n = 12) matched for age, sex, race, height, weight and smoking habits. Intraerythrocyte magnesium was significantly increased in the hypertensive group (P less than .001) and correlated positively and significantly to blood pressure in the total group (P less than .01). The intracellular potassium to sodium ratio tended to be lower in the hypertensive group (P less than .05). Thus, the present study supports increased intracellular magnesium probably unrelated to intracellular potassium-sodium imbalance in never treated, essential hypertension.

Increased erythrocyte magnesium content in essential hypertension.

The present study aimed at testing the hypothesis of decreased erythrocyte magnesium content and magnesium deficiency in essential hypertension. Atomic absorption was used to measure the erythrocyte content of total magnesium in 50-year-old otherwise healthy white males with essential hypertension (n = 12, blood pressure (mean +/- SE) 155 +/- 4/109 +/- 2 mmHg) that had never been treated and in normotensive control subjects (n = 12, blood pressure 128 +/- 2/88 +/- 1 mmHg) matched for age, sex, race, height, weight and smoking habits. The erythrocyte magnesium content was significantly increased in the hypertensive group (2.266 +/- 0.063 vs 1.903 +/- 0.069 mmol/l erythrocytes, p less than 0.001). No significant difference between the groups was detected for serum concentration or the 24-h urinary excretion of magnesium. In conclusion, the present study indicates increased rather than decreased erythrocyte content of magnesium in 50-year-old white males with 'never-treated', essential hypertension. Magnesium deficiency is, therefore, unlikely in this subset of critically selected and matched hypertensive patients.

Effects of adrenaline infusion on platelet number, volume and release reaction.

At the end of a diagnostic right heart catheterization ten patients received an intravenous infusion of l-adrenaline which gradually increased the arterial plasma adrenaline concentration from resting physiological values to high values as seen during myocardial infarction, pheochromocytoma and hypoglycemia. Blood was sampled from the brachial artery, femoral vein and hepatic vein. During the adrenaline infusion venous beta-thromboglobulin concentrations increased 23% from 61 +/- 5 to 80 +/- 7 micrograms/l (mean +/- SE), arterial platelet counts 20% from 212 +/- 17 to 253 +/- 25 X 10(9)/l and arterial platelet volume 4% from 7.25 +/- 0.20 to 7.56 +/- 0.21 femtoliter. All changes were significant at the 5% level. Thus, acute increments of arterial plasma adrenaline significantly stimulated the blood platelet parameters studied.