Heart rate and the cardiovascular risk.
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Adolescent↗
Biomedical subjects
S Julius
Publications and source records attributed to S Julius.
Relationship of tachycardia with high blood pressure and metabolic abnormalities: a study with mixture analysis in three populations.
Faster resting heart rate has been shown to be associated with a higher risk of developing hypertension and a greater incidence of cardiovascular morbidity and mortality. The aim of this study was to investigate the distribution of heart rate and its relationship with blood pressure and other cardiovascular risk factors in three populations. One European general population (Belgian study), one North American general population (Tecumseh study), and one European hypertensive population (HARVEST trial) were studied. Within each population, mixture analysis was used to investigate whether a mixture of two normal distributions explained the variance in heart rate better than a single distribution. In the men of all populations, mixture analysis identified a larger subpopulation of subjects with normal heart rate and a smaller one with fast heart rate. The subgroups with tachycardia had higher blood pressure and lipid levels than those with normal heart rate. In the populations in which they were measured, fasting insulin and postload glucose were also higher in the men with faster heart rate. A subgroup with tachycardia could also be singled out among the women from Tecumseh, but no relation between heart rate and blood pressure could be found. These findings show that in Western societies, high heart rate pertains to a distinct subgroup of subjects, who are more frequently men and exhibit the characteristic features of the insulin resistance syndrome. Sympathetic overactivity is likely to be the mechanism underlying this clinical condition.
Adolescent↗
Trends in left ventricular function over three years in the Tecumseh Study.
The relationship between blood pressure and left ventricular diastolic function was examined in participants of the Tecumseh Blood Pressure study. When subjects were divided into three blood pressure groups according to blood pressure levels 3 years apart, it was found that subjects who were had sustained "hypertension" at both time points (SH) had a decreased early/late diastolic filling rate (E/A ratio) compared to subjects who were hypertensive at only one of the timepoints (OH) and those who were consistently normotensive (NN) (1.71 +/- 0.02 NN vs 1.55 +/- 0.05 OH, (p < 0.0001) vs 1.56 +/- 0.07 SH, (p < 0.04)). This relative order was maintained when the second estimation of diastolic filling was performed 3 years later, but the E/A ratio had decreased significantly in all groups (1.54 +/- 0.01 NN vs 1.45 +/- 0.03 OH (p < 0.01) vs 1.37 +/- 0.06 SH (p < 0.006)), consistent with an age-related reduction in diastolic filling. Heart rates were significantly higher in the hypertensive groups initially (63.5 NN vs 66.2 OH (p < 0.03) vs SH 67.3 (p < 0.01)) and increased in all groups over time, with the largest increase in the SH group (64.9 +/- 0.04 NN vs 67.8 +/- 1.02 OH (p < 0.0001) vs 70.9 +/- 1.6 SH (p < 0.01)). Stroke volume index changed in all groups over time, with the increase greatest in the NN group and least in the SH groups the reverse of this pattern was seen for changes in heart rate. All subjects gained weight over the 3 years of the study so that these unexpected changes in stroke volume index and heart rate could be a consequence of a weight gain-related increase in the sympathetic tone, although we have no direct evidence that this is the case. Should this be so, the smaller increase in stroke volume in conjunction with the larger increase in the heart rate in the sustained hypertensive group may reflect the effects of mild blood pressure elevation in producing a reduction in left ventricular diastolic function associated with a decrease in the inotropic responsiveness of the heart to enhanced sympathetic tone.
Adolescent↗
Coronary disease in hypertension: a new mosaic.
HYPERTENSION-ASSOCIATED ABNORMALITIES THAT PROMOTE CORONARY DISEASE: Although antihypertensive treatment has been effective in reducing premature cardiovascular mortality, the effect on various organ-specific morbid events has been unequal; the effect is much more impressive on stroke reduction than on reduction of coronary events. A student of pathophysiology would have anticipated such an outcome since blood pressure elevation is only one of multiple abnormalities in hypertension. Even in its mildest form hypertension is associated with the metabolic syndrome of dyslipidemia/insulin resistance which is conducive to early atherosclerosis. A large proportion of patients also have increased sympathetic and decreased parasympathetic tone, a constellation conducive to arrhythmias and, ultimately, to sudden death. An elevated hematocrit is also found in a substantial proportion of male patients and excessive platelet aggregability has also been described in hypertension. These hematologic abnormalities are conducive to coronary thrombosis. Angiotensin II and norepinephrine, two of the most potent trophic hormones, are frequently elevated in hypertension. The effect of these hormones on the cardiac and vascular structure further increases the predilection for negative outcomes. Left ventricular hypertrophy is a potent risk factor of coronary mortality, congestive heart failure and sudden death. Vascular hypertrophy reduces the coronary reserve and at the level of skeletal muscles contributes to the evolution of the metabolic syndrome. ORGAN-SPECIFIC HYPERTENSION TREATMENT: Because of these abnormalities we are entering a new era of treatment in hypertension. Whereas an effective fall in blood pressure remains the main goal of treatment, differential effects of various antihypertensive agents on organ-specific morbidity are being actively explored. If this research proves that certain drugs have a specific advantage in defined subgroups of patients, clinical practice will change. It is reasonable to expect that in the next century we will witness a further improvement in the impact of antihypertensive treatment on public health.
Coronary Disease↗
The Losartan Intervention For Endpoint reduction (LIFE) in Hypertension study: rationale, design, and methods. The LIFE Study Group.
The treatment of hypertension mainly with diuretics and beta blockers reduces cardiovascular mortality and morbidity, largely due to a decreased incidence of stroke, whereas the beneficial effects of antihypertensive therapy on the occurrence of coronary events have been less than expected from epidemiological studies. Furthermore, treated hypertensive patients still have a higher cardiovascular complication rate, compared with matched normotensives. This is particularly evident in patients with left ventricular hypertrophy (LVH), a major independent risk indicator for cardiovascular disease. In addition to elevating blood pressure, angiotensin II (A-II) exerts an important influence on cardiac structure and function, stimulating cell proliferation and growth. Thus, to further reduce morbidity and mortality when treating hypertensive patients, it may be important to effectively block the effects of A-II. This can be achieved directly at the A-II receptor level by losartan, the first of a new class of antihypertensive agents. It therefore seems pertinent to investigate whether selective A-II receptor blockade with losartan not only lowers blood pressure but also reduces LVH more effectively than current therapy, and thus improves prognosis. The Losartan Intervention For Endpoint reduction (LIFE) in Hypertension study is a double-blind, prospective, parallel group study designed to compare the effects of losartan with those of the beta-blocker atenolol on the reduction of cardiovascular morbidity and mortality in approximately 8,300 hypertensive patients (initial sitting diastolic blood pressure 95 to 115 mm Hg or systolic blood pressure 160 to 200 mm Hg) with electrocardiographically documented LVH. The study, which will continue for at least 4 years and until 1,040 patients experience one primary endpoint, has been designed with a statistical power that will detect a difference of at least 15% between groups in the incidence of combined cardiovascular morbidity and mortality. It is also the first prospective study with adequate power to link reversal of LVH to reduction in major cardiovascular events. The rationale of the study, which will involve more than 800 clinical centers in Scandinavia, the United Kingdom, and the United States, is discussed, and the major features of its design and general organization are described. On April 30, 1997, when inclusion was stopped, 9,218 patients had been randomized.
Adrenergic beta-Antagonists↗
Association of tachycardia with morbidity and mortality: pathophysiological considerations.
An increased rate of cardiovascular and all-cause mortality has been documented in subjects with tachycardia. Hypertensive subjects with tachycardia often also exhibit overweight, higher haematocrit, plasma insulin, cholesterol, and triglyceride levels whereas high density lipoprotein (HDL) is decreased. Sympathetic overactivity seems to be responsible both for the increase in heart rate and blood pressure (BP), and for metabolic abnormalities. Excessive stimulation of beta-adrenergic receptors in the skeletal muscles can cause insulin resistance and chronic beta-adrenergic stimulation which leads to a greater proportion of fast twitch insulin-resistant fibres. Also alpha-adrenergic stimulation can cause insulin resistance through vasoconstriction and the consequent decrease in the delivery of glucose and insulin to the muscles. Experimental studies in monkeys have shown that tachycardia can also produce atherosclerotic lesions via haemodynamic disturbances, by elevating the pulsatile nature of the arterial blood flow. Conversely, a reduction of heart rate could retard the development of vascular lesions. If tachycardia in hypertension is a marker of an abnormality of the autonomic control of circulation, a centrally acting antihypertensive agent which decreases the sympathetic outflow should be preferred. Drugs with agonistic properties of the I1-imidazoline receptors of the rostral ventrolateral medulla appear particularly suitable in this respect.
Animals↗
The Hypertension Optimal Treatment (HOT) Study in the United States.
The international Hypertension Optimal Treatment Study has yet to be completed but preliminary analysis of data has revealed trends that suggest that physicians in the United States treat hypertension much more aggressively than their foreign colleagues. At the onset of the study, the previously-treated US patients had blood pressures that were substantially lower than those of patients in other participating countries. However, after the washout period, the blood pressures of the US patients became the same as those of their foreign counterparts. This suggests that physicians in the United States aim for target blood pressures that are lower than those generally achieved in other countries. After participants of the HOT study were treated for 6 months, the blood pressure levels achieved in US patients were lower than those achieved in their foreign counterparts. Furthermore, US physicians moved their patients more quickly up the step care protocol, suggesting that they were much more aggressive in adding new drugs to treatment regimen than were physicians from other participating countries. These findings strongly suggest that United States physicians treat hypertension much more aggressively, and the fact that mortality trends in US hypertensive patients have decreased over the past decade lends further support for this consensus.
Humans↗
Sympathetic overactivity in hypertension. A moving target.
Considerable progress has been made in our understanding of the role of the nervous system in human hypertension. The evidence for a widespread autonomic abnormality in the early phases of hypertension is overwhelming and excessive sympathetic activity is consistently present in such patients since their childhood. The enhanced sympathetic tone in hypertension is associated with the metabolic syndrome of insulin resistance and dyslipidemia. Multiple mechanisms by which sympathetic overactivity could cause both hypertension and the metabolic syndrome have been documented. Furthermore, the excessive sympathetic tone is conducive to coronary heart disease through its association with high hematocrit values and with excessive platelet aggregability. Surprisingly, the myth that patients with neurogenic hypertension have a benign prognosis continues to persist. Much of the misunderstanding stems from the idea that patients with neurogenic hypertension, commonly called "white coat" or borderline hypertension, do not develop established hypertension. There is no support for such an assessment; in fact, patients with neurogenic hypertension are at a high risk of future accelerated hypertension. Another misunderstanding relates to differences in hemodynamics between neurogenic and established hypertension. It is true that patients with neurogenic hypertension initially show an increase of cardiac output. However, this later evolves into a classic picture of established high resistance hypertension. The hemodynamic transition is secondary to a decrease in cardiac responsiveness and an increase in vascular responsiveness over the course of hypertension. With passage of time, vascular reactivity increases, yet sympathetic tone tends to decrease. This can be explained by the "blood pressure seeking behavior of the central nervous system." In hypertension, the central nervous system appears to seek a higher blood pressure level and, as the vasculature becomes hyperresponsive, less sympathetic tone is needed to maintain the elevated blood pressure. This decrease of sympathetic tone in later phases of hypertension should not be viewed as a normalization, since sympathetic tone in relationship to vascular hyperresponsiveness remains excessive and the central nervous system maintains a crucial role in sustaining high blood pressure in hypertension.
Animals↗
Angiotensin mediates forearm glucose uptake by hemodynamic rather than direct effects.
Insulin sensitivity may be improved with the angiotensin-converting enzyme inhibitor captopril, suggesting that inhibition of angiotensin II (Ang II) improves insulin resistance. However, the administration of systemic Ang II has also been associated with an improvement in rather than worsening of glucose utilization. Since both stimulating and antagonizing the renin-angiotensin system improve glucose uptake and both angiotensin-converting enzyme inhibitors and intravenous Ang II elicit skeletal muscle vasodilation, it is conceivable that hemodynamic factors rather than a direct effect of either Ang II or angiotensin-converting enzyme inhibitors on skeletal muscle metabolism modulate the increase in glucose utilization. The direct effects of Ang II on glucose extraction in intact human skeletal muscle have not been previously described. We investigated the effects of local infusion of Ang II on glucose uptake in the forearm of 20 healthy subjects. With the use of the isolated insulin-perfused forearm model, local plasma insulin values were raised to 100 mU/mL over fasting values and maintained there for a 90-minute infusion period. After the first 60 minutes of insulin alone, Ang II was infused into the brachial artery for the last 30 minutes. Intra-arterial Ang II infusion caused a 38% decrease in forearm blood flow (P <.05) and 59% increase in the arteriovenous glucose gradients (P <.05) to maintain a steady glucose utilization (a decrease of 4%, P=NS). Thus, local Ang II infusion does not impair insulin-stimulated glucose utilization. Furthermore, glucose extraction increases to compensate for the decrease in forearm blood flow (as the Fick principle would predict for freely diffusible substances). We conclude that the described increase in glucose utilization from systemic infusion of Ang II and during angiotensin-converting enzyme inhibitor treatment is mediated by hemodynamic factors rather than a direct effect of Ang II on skeletal muscle metabolism.
Adult↗
Effects of increased arterial epinephrine on insulin, glucose and phosphate.
The relationship between sympathetic nervous system activity and glucose and insulin metabolism is not fully understood. In the present study we therefore investigated the effect of raising arterial plasma epinephrine within the lower pathophysiological concentration range on insulin, glucose and phosphate in blood. Arterial plasma epinephrine was raised over 60 min by a stepwise increasing intravenous infusion in healthy men aged 20-40 years (n = 40). Compared with infusion of saline, epinephrine caused a small but significant rise in serum insulin of 10 +/- 26 pmol/L (p = 0.016), more than 70% increase in serum glucose (p < 0.0001) and a decrease in serum phosphate (p < 0.0001). The changes in serum insulin during epinephrine infusion correlated negatively with the changes in arterial plasma epinephrine (r = -0.46, p = 0.003) and the changes in serum phosphate correlated negatively with the changes in serum glucose (r = -0.42, p = 0.007). Thus, arterial plasma epinephrine raised within the lower pathophysiological concentration range over a rather short period of time (60 min) has pronounced effects on insulin, glucose and phosphate in blood. These results suggest that epinephrine when infused acutely may suppress the insulin response to raised glucose, and that the acute hypophosphatemic effect of epinephrine is related to the glucose production. Thus, when epinephrine is released into the circulation during various forms of daily stress, e.g. mental stress, it may significantly affect insulin and glucose metabolism.
Adult↗
Sympathetic nervous system as a coronary risk factor in hypertension.
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Coronary Disease↗
Effect of circulating epinephrine on platelet function and hematocrit.
We investigated the effect of raising arterial plasma epinephrine within the lower pathophysiological concentration range on various indicators of blood platelet function and hematocrit. Epinephrine was raised over 60 minutes by a stepwise increasing intravenous infusion in 40 healthy men aged 20 to 40 years. Platelet count increased progressively with increasing arterial epinephrine to a maximal change of 69 +/- 6 x 10(9)/L in EDTA-anticoagulated blood and a maximal change of 42 +/- 6 x 10(9)/L in acid-citrate-dextrose (ACD)-anticoagulated blood, and the weight of circulating platelets increased by 29% (P < .001). Platelet size increased significantly in EDTA and decreased in ACD, and the difference between EDTA and ACD was significant (P < .0001) for both count and size, suggesting that epinephrine not only recruits platelets into the circulation but also induces some microaggregation in vivo or adhesion ex vivo. Aggregation of platelets in vitro induced by epinephrine decreased (P < .003 for delta optical density and P = .038 for maximal optical density) after epinephrine infusion compared with saline but did not change when stimulated with ADP or collagen. These findings suggest a selective downregulation of the epinephrine-activating mechanisms concomitant with a rise in the platelet content of epinephrine by 81% (P < .001) and no change in the platelet sodium-proton membrane exchange. The release of granular content (beta-thromboglobulin and platelet factor 4) to the circulation in response to epinephrine was not significant. Thus, under acute conditions it seems that the platelets may protect themselves against inappropriate overstimulation by epinephrine. The importance of platelet epinephrine uptake is still unknown, but sodium-proton exchange does not seem to be involved in regulating the effects of circulating epinephrine on platelet function. Epinephrine has a pronounced effect on raising hematocrit (maximal change of 1.74 +/- 0.13 x 10(-2), P < .0001).
Adult↗
The role of the autonomic nervous system in hypertension.
The role of the autonomic nervous system in the genesis and maintenance of hypertension is becoming clearer with time. Early research suggested that increased vascular resistance in hypertension was not dependent on excess autonomic tone and thus it was presumed that the autonomic nervous system had little to do with hypertension. More recent studies have demonstrated that the initial hemodynamic abnormality in hyperkinetic borderline hypertension is "normal" vascular resistance, with an elevated cardiac optput and heart rate, associated with markers of increased sympathetic and decreased parasympathetic tone of central origin. Over time there is a transition to the high peripheral resistance and normal cardiac output hemodynamic state characteristic of established hypertension, which is due to the development of adaptive structural changes in the peripheral resistance vessels and heart. The autonomic abnormality in hypertension and subsequent vascular and cardiac changes may explain some of association between hypertension and risk factors for coronary heart disease. The autonomic imbalance found in hypertension may not be a chance occurrence and we postulate that it is due to the inheritance of the genes responsible for a more pronounced defense reaction, which in earlier times may have conferred a survival advantage but now permit the negative impact of this trait to become evident.
Adult↗
Abnormalities of autonomic nervous control in human hypertension.
The pathophysiology of various stages of hypertension is different. In early hyperkinetic borderline hypertension, the sympathetic drive to the heart and blood vessels is increased while the parasympathetic cardiac inhibition is decreased. The elevated cardiac output, vascular resistance, and blood pressure at that stage can be fully normalized by autonomic blockade. As hypertension advances, a hyperkinetic circulation is less evident, since beta-adrenergic responsiveness and cardiac compliance tend to decrease. Simultaneously hypertrophy of the resistance vessels increases the baseline vascular resistance and the vessels' responsiveness to constrictive stimuli. Eventually a picture of a normal cardiac output/high vascular resistance typical for established essential hypertension emerges. As the blood vessels become hyperreactive, the same degree of vasoconstriction/blood pressure elevation can be achieved with less sympathetic tone. In that phase the sympathetic overactivity is less evident, as the brain resets itself to maintain the same blood pressure elevation with a small amount of sympathetic discharge. While sympathetic overactivity may be less evident in established hypertension, it remains an important pathophysiologic factor, not only for the maintenance of blood pressure, but also for a number of other abnormalities in hypertension. Hypertension is intimately associated with higher levels of pressure-unrelated risk for development of atherosclerosis: dyslipidemia, overweight, and hyperinsulinemia. Furthermore, a number of factors in hypertension favor a poorer outcome from coronary heart disease. These pressure-independent factors increase the risk of coronary thrombosis, arrhythmic deaths, and coronary spasms. Sympathetic overreactivity appears to be crucially implicated in the evolution of this added coronary risk in hypertension. Understanding the pathophysiology of coronary risk and its relationship to sympathetic overreactivity in hypertension is helpful in seeking further improvements in clinical practice. At present antihypertensive treatment is less efficacious in reducing coronary events in hypertension than would be expected. Judicious use of appropriate drugs promises to further improve the efficacy of antihypertensive treatment in those patients who, in addition to high blood pressure, also have other associated risk factors.
Aging↗
The effect of hypertensive episodes and cardiac hypertrophy on the canine cardiac baroreflex.
1. Left ventricular (LV) hypertrophy has been implicated in the reduction of baroreflex sensitivity present in hypertension. The aim of the current study was to investigate the mean arterial pressure-heart rate reflex (MAP-HR) in a model which induced left ventricular hypertrophy but no sustained blood pressure elevation. 2. Five mongrel dogs were exposed to transient blood pressure elevation of between 20 and 30 mmHg, through hindlimb compression using a pneumatic pressure suit, for 7 h per day, 6 days per week for 6 weeks. Resting blood pressure was not altered by the 6 week hindlimb compression intervention. 3. Echocardiographically determined LV mass (mean +/- s.e.m.) was 116.0 +/- 7.4 g prior to hindlimb compression (baseline) and elevated to 125.4 +/- 8.1 g (P = 0.003) after 6 weeks of compression. A reduction in the early (E) to late (A) transmitral diastolic flow ratio (E/A) from 1.80 +/- 0.06 at baseline to 1.54 +/- 0.09 (P = 0.037) after the 6 week intervention suggested that cardiac compliance was reduced. 4. The maximum gain of the MAP-HR reflex, studied using the 'steady-state' drug technique, when blood pressure was normal, showed a trend for reduction from 3.85 +/- 0.43 beats/min per mmHg at baseline to 3.10 +/- 0.45 beats/min per mmHg (P = 0.067) after 6 weeks of compression. This gain reduction became significant after beta-adrenoceptor blockade with propranolol (3.13 +/- 0.55 vs 2.32 +/- 0.25 beats/min per mmHg; P = 0.039). Covariant analysis showed a significant inverse correlation between LV mass and maximum gain (r = 0.96; P < 0.001) during the 6 week compression period.(ABSTRACT TRUNCATED AT 250 WORDS)
Analysis of Variance↗
Sex-specific determinants of increased left ventricular mass in the Tecumseh Blood Pressure Study.
BACKGROUND: Left ventricular hypertrophy (LVH) defined by either ECG or echocardiographic criteria is a risk factor for cardiovascular morbidity and mortality. A number of determinants of LVH have been described in previous studies, principally male sex, hypertension, obesity, and aortic valvular stenosis. We examined the distribution of LV mass (LVM) in a population of 18- to 42-year-old normotensive men and women who were free of valvular heart disease to establish sex-specific normal values for LVM index (LVMI) and to determine the correlates of LVMI. METHODS AND RESULTS: LVM was derived from measurements obtained by M-mode echocardiography. Average LVMI is significantly greater in men (102.9 +/- 0.7 g/m2) than women (88.2 +/- 0.7 g/m2). By defining LVH as an LVMI greater than the 90th percentile, we developed sex-specific criteria for LVH: men, > 125.4 g/m2; women, > 110 g/m2. We found that LVH in men is associated with indices of enhanced sympathetic nervous system reactivity and with elevated fasting insulin and triglyceride levels, which may be caused by insulin resistance. In women, LVH was associated with higher body weight and obesity. CONCLUSIONS: Before the onset of hypertension, increased LVMI appears to have different determinants in men and women. We suggest that early LVH in young men is a manifestation of hyperkinetic borderline hypertension, a state previously shown to be associated with increased sympathetic nervous system activity and insulin resistance. The hyperkinetic state is less prevalent in young women, in whom increased adiposity seems to be the predominant factor associated with LVH.
Adult↗
Vasoconstriction with norepinephrine causes less forearm insulin resistance than a reflex sympathetic vasoconstriction.
We used the insulin-perfused human forearm model to assess the effects of vasoconstriction induced with norepinephrine on the extraction of glucose in the forearm in two groups of healthy young volunteers. The norepinephrine findings were compared with a previously studied group in which vasoconstriction has been caused by reflex activation of the sympathetic nervous system. The aim of the study was to determine the relative importance of hemodynamic and receptor-mediated mechanisms of insulin resistance. Plasma insulin, arterial and venous glucose samples, and forearm blood flow were measured at 10-minute intervals during a 30-minute baseline, a 60-minute intra-arterial insulin infusion, and during 30 minutes of insulin infusion plus vasoconstriction. Group 1 (n = 14) had physiological vasoconstriction induced by inflation of bilateral thigh cuffs to 40 mm Hg to cause pooling of blood in the lower extremities and reflex vasoconstriction in the forearm; group 2 (n = 8) had intra-arterial infusion of norepinephrine to achieve the same degree of vasoconstriction as seen with inflation of thigh cuffs in group 1. Subjects in group 3 (n = 7) had infusion of intra-arterial norepinephrine to achieve a twofold increase in physiological vasoconstriction. With a physiological decrease in forearm blood flow (group 1), there was a 19% decrease in forearm blood flow resulting in a 23% reduction in glucose uptake in the forearm (P < .03). The same degree of reduction in forearm blood flow with a predominantly alpha-adrenergic agonist, norepinephrine (group 2), causes much less insulin resistance (a decrease in utilization of 13%) (P < .04).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Sympathetic nervous system involvement in essential hypertension: increased platelet noradrenaline coincides with decreased beta-adrenoreceptor responsiveness.
Platelet catecholamine content may reflect integrated plasma catecholamine concentrations over time. The present study aimed at examining sympathetic nervous system (SNS) involvement in essential hypertension by assessing platelet noradrenaline (NA) and typically beta-adrenoreceptor mediated responses to adrenaline (A) infusion as indices of sympathetic tone. Healthy white men were recruited by public advertising and screening (mean +/- SD): Hypertensives (n = 13, sitting blood pressure [BP] 153 +/- 13/106 +/- 7 mmHg, age 34 +/- 5 years, weight 83 +/- 10 kg) were compared to normotensives (n = 13, sitting BP 114 +/- 9/75 +/- 9 mmHg, age 30 +/- 6 years [n.s.], weight 82 +/- 9 kg [n.s.]). Loss of platelet granular contents (including NA) prior to analysis was minimized by studying young subjects (age range 20-40 years, minimal atherosclerosis), using arterial blood sampling, and processing blood immediately. These procedures resulted in plasma beta-thromboglobulin and platelet factor 4 levels which were not significantly different between groups. Sympathetic activation resulting from stress was minimized by not labelling subjects as either hypertensive or normotensive. Mean arterial platelet NA content was significantly higher in hypertensives (64 +/- 31 pg/mg of platelet weight) compared to normotensives (43 +/- 20 pg/mg, p < 0.05) both at baseline and following 35% expansion of the circulating platelet pool by A infusion (p < 0.05) and correlated with arterial NA in the hypertensives (r = 0.79, p < 0.002) but not in the normotensives (r = 0.04, n.s.). Similar increases in platelet and plasma A during infusion in both groups suggest unchanged platelet uptake capacity and plasma clearance in the hypertensive group.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗