Regulation of platelet alpha2 adrenergic receptors in a population of patients with essential arterial hypertension and in normotensive subjects]

The development of specific binding techniques for the study of adrenergic receptors on circulating human blood cells has allowed a better understanding of the physiological alterations of adrenergic receptors and changes of adrenergic receptors in pathological conditions such as hypertension. Alpha adrenoceptors play an important part in blood pressure regulation at several sites. There are contradictory and conflicting reports on whether alpha receptor mechanisms are altered in essential hypertension. To address further the role of alpha 2 adrenoceptors in human essential hypertension the number and the affinity of alpha 2 adrenergic receptors and plasma catecholamine levels were measured in 20 normotensive and 24 hypertensive subjects. The median number of receptors (Bmax) was 159.10 +/- 14.38 fmol/mg protein for controls versus 179.09 +/- 13.26 fmol/mg protein for hypertensives. The median dissociation constant (KD) of the receptors for 3H-Yohimbine was 1.43 +/- 0.17 nmol/l for controls and 1.85 +/- 0.19 nmol/l for hypertensives patients. There were no differences in catecholamine plasma levels between the two groups. In controls platelet alpha 2 receptor number correlated with age (p less than 0.003) but not with blood pressure values. Our results show that measurement of platelet alpha 2 receptor levels and affinity is unable to differentiate a group of hypertensives from normotensives. Nevertheless, we cannot exclude a possible role of peripheral alpha 2 adrenergic receptors in the pathogenesis of high blood pressure.     

Renal vasculature in essential hypertension: racial differences

In an attempt to explain the greater morbidity from essential hypertension in the black as compared with the white race, we evaluated the intrarenal vasculature of 27 patients with hypertension (19 white and 8 black). All patients had mild-to-moderate hypertension (mean arterial pressure, 110 to 125 mm Hg), normal renal function, and minimal target-organ damage. All patients had selective renal angiograms, which were evaluated for arterial nephrosclerosis. Additionally, renal blood flow was estimated by the clearance of para-aminohippurate. Patient age, blood pressure, and plasma renin activity did not differ between the two races. Black hypertensives had significantly (P less 0.01) more severe nephrosclerosis than the white patients. Renal blood flow was lower (P less than 0.05) in black patients (390 +/- 35 ml/min - m2 body surface area) than white patients (473 +/- 19 ml/min - m2 body surface area). These findings may help to explain racial differences in morbidity and mortality from essential hypertension.     

Cytosolic free calcium concentration in platelets in patients with renovascular hypertension and primary aldosteronism.

To investigate the role of cytosolic free calcium, [Ca2+]i, in secondary hypertension, the levels in platelets from 14 secondary hypertensives (7 renovascular hypertension, 7 primary aldosteronism) were compared with those from 21 essential hypertensives and 15 normotensives by means of the fluorescent indicator, quin-2. The mean BP was significantly higher in both the secondary hypertensives and essential hypertensives (122 +/- 8 and 124 +/- 12 mmHg) than in the normotensives (89 +/- 10 mmHg). Cytosolic free calcium in platelets was significantly higher in the essential hypertensives, but not in the secondary hypertensives, compared with the normotensives (182 +/- 34, 141 +/- 17, 138 +/- 15 nM respectively). There was no significant difference in platelet [Ca2+]i between renovascular hypertension and aldosteronism (142 +/- 19 versus 139 +/- 16 nM). There was no correlation between platelet [Ca2+]i and plasma renin activity, plasma aldosterone concentration or plasma noradrenaline concentration in the three groups. Thus, the increase in platelet [Ca2+]i seen in essential hypertension was not found in patients with secondary hypertension. Our results suggest that the cytosolic calcium handling of secondary hypertensive patients with renal artery stenosis or primary aldosteronism differs from that of essential hypertensives.     

Race and blood pressure status influences cardiovascular responses to challenge.

The influence of race and blood pressure status on cardiovascular responses to three challenges (interview, video game and cold pressor) was investigated in 50 healthy normotensive and 30 unmedicated mild-to-moderate hypertensive black and white men, aged 25-44 years old. Group differences were obtained for two tasks. The interview evoked race and blood pressure status differences: higher heart rate responses were elicited from normotensives compared with hypertensives and larger diastolic blood pressure (DBP) responses were elicited from whites compared with blacks. For the video game, black hypertensives displayed larger DBP responses than white hypertensives and greater systolic blood pressure and DBP responses than black normotensives. The video game heart rate response of white normotensives exceeded that of black normotensives and white hypertensives. These findings suggest that cardiovascular responses to challenge are affected by race and blood pressure status. The blood pressure hyperresponsiveness of black hypertensives compared with black normotensives to a psychological challenge (video game) provides generality to previous research conducted only on whites.     

Relationship of systolic blood pressure with plasma homocysteine: importance of smoking status

BACKGROUND: Elevated plasma homocysteine is a risk factor for cardiovascular disease. Elevations in plasma homocysteine occur in both smokers and hypertensives, but the combined effect of smoking and hypertension on homocysteine is unknown. METHODS: Resting plasma homocysteine levels and blood pressure were determined in 56 normotensives (12 smokers) and 20 essential hypertensives (10 smokers). RESULTS: Plasma homocysteine was significantly higher in all smokers versus all non-smokers (9.46 +/- 0.5 versus 7.9 +/- 0.5 micromol/l, P = 0.041) by two-way ANOVA, and was also significantly higher in all hypertensives versus all normotensives (9.8 +/- 0.6 versus 7.6 +/- 0.4 micromol/l, P = 0.004). There was no interaction between the effects of hypertension and smoking on plasma homocysteine. Hypertensive smokers had significantly higher plasma homocysteine than either normotensive non-smokers (10.65 +/- 0.84 versus 7.05 +/- 0.26 micromol/l), hypertensive non-smokers (7.88 +/- 0.64 micromol/l) or normotensive smokers (8.36 +/- 0.5 micromol/l). In subjects overall, homocysteine levels were correlated (r = 0.306, P = 0.015) with systolic blood pressure but not with diastolic (r = 0.186). This relationship was also significant in smokers, but not non-smokers. Furthermore, subjects in the highest quintile for plasma homocysteine had significantly higher systolic BP than those in the lowest quintile. This effect was not observed when smokers were removed from the analysis. CONCLUSION: Smoking compounds the modest effect of hypertension on plasma homocysteine. The strong relationship between systolic blood pressure and homocysteine that exists only in smokers suggests that smoking-induced homocysteine elevations may raise systolic blood pressure. We speculate that smoking compounds the risk of cardiovascular disease in hypertensives, in part, by elevating homocysteine.     

Enhanced red cell sodium permeability in patients with borderline hypertension

Red cell membrane sodium permeability was studied in 41 untreated patients with essential hypertension (20 borderline hypertensives and 21 established hypertensives) and 21 age matched normotensive subjects by means of the measurement of unidirectional passive influx of 22Na+ into ouabain-treated erythrocytes. The mean value (+/- SD) of 22Na+ influx was greater in the hypertensives than in the normotensives (0.183 +/- 0.047 vs 0.152 +/- 0.047 mmol/l . cells/hr, respectively, p less than 0.02). Among the patients with essential hypertension, the borderline hypertensives demonstrated a higher 22Na+ influx than the established hypertensives (0.207 +/- 0.043 vs 0.160 +/- 0.038 mmol/l . cells/hr, respectively, p less than 0.001), and 22Na+ influx positively correlated with plasma renin activity (r = 0.44, p less than 0.005). In 16 of 20 borderline hypertensives, 5 year blood pressure changes were examined retrospectively, and a positive correlation was observed between mean blood pressure increase and 22Na+ influx value in these subjects (r = 0.64, p less than 0.01). These results suggest that passive sodium influx may be altered in the course of the development of hypertension in relation to the changes in blood pressure level and that enhanced sodium permeability may be a characteristic of the early stage of essential hypertension.     

Disparate effects of mental stress on plasma noradrenaline in young normotensive and hypertensive subjects

The response of blood pressure, heart rate and plasma catecholamines to a mental arithmetic and a cold pressor test was studied in 70 patients with mild essential hypertension and in 41 age- and sex-matched normotensives. Each group consisted of three prospectively stratified age classes: 20-29, 30-39 and 40-55 years. During mental arithmetic, hypertensives showed only a higher increment of systolic blood pressure (+17-19%) than normotensives (+12-15%). Plasma noradrenaline in the youngest normotensives (20-29 years) showed a small but significant decrease (-0.20 +/- 0.07 nmol/l) whereas the youngest hypertensives showed a small but significant increase of plasma noradrenaline (+0.14 +/- 0.04 nmol/l). The difference between both groups was highly significant (P less than 0.001). In the two older age classes there was no difference in plasma noradrenaline response between normo- and hypertensives. During the cold pressor test both the cardiovascular and plasma noradrenaline response were of the same magnitude in normo- and hypertensives. These data reinforce the concept that the increased sympathetic reactivity to mental stress in hypertensives may be restricted to the younger age.     

Racial differences in erythrocyte cation transport

Erythrocyte contents and ouabain-insensitive transport pathways were measured in 120 white and black normotensives and hypertensives. Mean maximal sodium-stimulated lithium-sodium countertransport rate was higher in white hypertensives than in white normotensives, and countertransport was significantly positively correlated with mean arterial pressure in whites. Values similar to those in white normotensives were found in both black normotensives and hypertensives, and countertransport was not significantly correlated with blood pressure in blacks. The rate constant for passive lithium efflux was greater in whites as compared to blacks, and the difference was not related to blood pressure level or sex. Ouabain-insensitive, furosemide-sensitive sodium and potassium effluxes were not found to be altered in hypertension. Furosemide-sensitive sodium efflux rate was lower in blacks but furosemide-sensitive potassium efflux was not similarly depressed. While white subjects demonstrated a close correlation between sodium and potassium effluxes, blacks did not. Further study of these differences in the cellular metabolism of sodium and potassium may provide clues to the pathogenesis of racial dissimilarities in total body sodium handling.     

Homologous radio-immunoassay of human plasma dopamine-beta-hydroxylase: analysis of homospecific activity, circulating plasma pool and intergroup differences based on race, blood pressure and cardiac function

We used a homologous human dopamine-beta-hydroxylase (DBH) radio-immunoassay (RIA) to explore reported differences in plasma DBH enzymatic activity among patient groups stratified for race, blood pressure and cardiac function, as well as to determine plasma immunoreactive DBH protein pool and the relative activity of the enzyme in plasma versus human chromaffin tissue storage vesicles. Plasma DBH activity was lower in patients with congestive heart failure than in control subjects (19.9 +/- 4.0 versus 34.4 +/- 5.9 iu/l, P less than 0.05), paralleled by lower immunoreactive plasma DBH protein concentration (3.50 +/- 0.73 versus 6.34 +/- 1.05 micrograms/ml, P less than 0.05). All subject groups had similar plasma DBH homospecific activity (plasma DBH enzymatic activity/immunoreactive plasma DBH protein), ranging from 5.03 +/- 0.28 to 5.84 +/- 0.44 iu/mg. For the entire subject group, there was a significant relationship between plasma DBH activity and plasma DBH immunoreactive protein (r = 0.89, n = 78, P less than 0.01) from which no subgroup deviated systematically. Black hypertensives had lower plasma DBH activity than white hypertensives (23.0 +/- 5.2 versus 42.9 +/- 4.8 iu/l, P less than 0.01), though their plasma DBH homospecific activities and activity/immunoreactive protein plots were indistinguishable. Total circulating plasma DBH pools were large (from 13.1 +/- 3.7 to 27.5 +/- 4.8 mg).(ABSTRACT TRUNCATED AT 250 WORDS)     

The evaluation of plasma dopamine beta-hydroxylase activity in essential and secondary hypertension

The relation of plasma dopamine beta-hydroxylase (DBH) activity to age was examined in normotensive and hypertensive subjects. Plasma DBH activity was the highest in the group of 25--34 years and gradually decreased with age. Plasma DBH activity was higher in the hypertensives than in the normotensives in all age groups, and the difference was significant between the groups of 45--54 and 55--64 years. Plasma DBH activity was increased in labile hypertension. Plasma DBH activity was higher in the group of essential hypertension with normal renal function than in that with reduced renal function. It was lower in the severe hypertensives than in the mild cases. Plasma DBH activity was also decreased in the hypertensive patients with cerebrovascular disorders. Plasma DBH activity was lower in the hypertensive patients with renal parenchymal diseases than those of essential hypertension with normal renal function. Plasma DBH activity was also decreased in primary aldosteronism, while it was increased in pheochromocytoma. These observations suggest that measurement of plasma DBH activity may be valuable in the differentiation of essential hypertension from the secondary forms of hypertension, and the evaluation of the hypertensive processes. To evaluate plasma DBH activity, it is important to consider its age-related changes.     

A novel platelet-derived renal vasoconstrictor agent in normotensives and essential hypertensives.

Platelet homogenates from 200 ml blood of essential hypertensives (n = 28) and normotensives (n = 13) were deproteinized and separated by gel chromatography. The fractions obtained were then tested for vasopressor activity in the isolated perfused rat kidney. In both normotensives and hypertensives, two vasopressor fractions appeared. There was no difference in vasopressor activity in the first vasoactive fraction between normotensives and hypertensives. In the second vasoactive fraction, the hypertensive patients showed a significant higher activity than the normotensive subjects (increase in perfusion pressure by 35.9 +/- 11.5 vs. 6.8 +/- 5.3 mmHg, p less than 0.01). This vasopressor fraction was not inhibited by saralasin, phentolamine, ketanserin, nitroprusside and daltroban and was effective after pretreatment with indomethacin and reserpine and in enzymatically deendothelialized kidneys. The effect was reduced by nifedipine and unchanged by heating the fraction at 100 degrees C and by incubation with proteinase K. It is concluded that a yet unidentified platelet-derived vasopressor agent may contribute to the enhanced vasoconstriction in essential hypertension.     

White-coat hypertension and sex

OBJECTIVES: To compare, by sex, selected behavioral and biologic characteristics among normotensive, white-coat hypertensive, and essential hypertensive patients, and to assess the similarities and differences in these characteristics between men and women diagnosed as having white-coat hypertension. METHODS: The subjects of this study were 764 men (80 normotensives, 112 white-coat hypertensives, and 572 essential hypertensives) and 442 women (53 normotensives, 81 white-coat hypertensives and 308 essential hypertensives) who were a nonrandom subset of a larger cohort of patients being assessed to determine the prognostic significance of ambulatory blood pressure measurements. Physician-measured technician-measured and ambulatory (average awake and asleep) blood pressures, daytime blood pressure variability, the difference between awake and sleeping blood pressures, cholesterol levels, plasma renin activity (PRA) and anthropometric and demographic characteristics were compared across the patient classifications within each sex group and between male and female white-coat hypertensives using one-way analysis of variance. Student's t tests and chi squared analysis. RESULTS: Among men, cholesterol levels of normotensives were significantly lower than those of either white-coat or essential hypertensives (P < 0.05 and P < 0.01, respectively). White-coat hypertensives were significantly younger than the essential hypertensives. The ambulatory and technician-measured blood pressures of the white-coat hypertensives were similar to those of the normotensives, as were most measures of variability of blood pressure. Among women, there were no differences in cholesterol level; however, white-coat hypertensives had lower PRA than did the essential hypertensives (P < 0.01) In contrast to the men, women with white-coat hypertension were similar in age to those with essential hypertension, and 10 years older than normotensives (P < 0.01). The ambulatory blood pressures of white-coat hypertensives were similar to those of normotensives, but their technician-measured blood pressures were intermediate between those of the normotensive and essential hypertensive groups. The daily variability of diastolic blood pressure among the white-coat-hypertensive women was greater than that of the normotensive women and similar to that of the essential hypertensive women. For all other measures of variability, data for white-coat-hypertensive women were similar to those for the normotensive women. There was no anthropometric or demographic difference among the patients either for men or for women. White-coat-hypertensive women were older than white-coat-hypertensive men and had higher systolic blood pressures and variabilities of blood pressure (P < 0.05). They also had lower PRA. CONCLUSIONS: These results are consistent with the ideas that the phenomenon of white-coat hypertension is similar for the two sexes, women may exhibit white-coat hypertension at a greater age than do men, and women with white-coat hypertension may further exhibit a broader white-coat effect, reflected in blood pressures measured by other medical personnel.     

Natriuretic hormones in young hypertensives and in young normotensives with or without a family history of hypertension.

The behavior of plasma atrial natriuretic factor (ANF) and digoxin-like substance (DLS), and the daily urinary excretion of kallikrein (uKK) were evaluated in young hypertensives and in young normotensives with or without a family history of essential hypertension. Each group was also evaluated, separating those with low plasma renin activity from the total sample. The sample group was made up of 75 young males; 31 hypertensives (mean age 22.7 +/- 2.5 years), 28 normotensives with hypertensive heredity (normotensives F+) (mean age 22.2 +/- 1.9 years) and 16 normotensives (mean age 22.0 +/- 2.1 years). An inverse correlation between ANF and PRA was shown in all groups. In hypertensives, ANF was inversely correlated with uKK (r = -0.664, P less than .0001). Plasma ANF (P less than .012) and DLS (P less than .0001) were higher in hypertensives than in normotensives, while uKK excretion was lower (P less than .0001). Plasma levels of DLS were higher in F+ normotensives than in normotensives (P less than .003). Low renin hypertensives showed the lowest uKK excretion (P less than .0001 v normal-high renin hypertensives). Furthermore, low renin hypertensives showed the highest plasma levels of ANF (P less than .0001 v normal high renin hypertensives) and DLS (P less than .012 v normal-high renin hypertensives). Plasma ANF (P less than .0001) was higher, while uKK was lower (P less than .045) in low renin F+ normotensives than in normal-high renin ones. In conclusion, our data indicate that plasma ANF and DLS are elevated since the early phase of hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)     

Baroreflex sensitivity and heredity in essential hypertension.

BACKGROUND. Abnormalities in baroreflex control of heart rate may be important in the pathogenesis of essential hypertension. METHODS AND RESULTS. To investigate the influence of heredity on baroreflex function, we measured baroreflex sensitivity in 40 untreated patients with essential hypertension grouped by the presence (FH+) or absence (FH-) of a family history of hypertension and in 24 normotensive counterparts. Baroreflex sensitivity was assessed by both high-pressure (phenylephrine bolus) and low-pressure (amyl nitrite inhalation) stimuli. Subject groups were matched for age, blood pressure, body weight, and race. Baroreflex sensitivity (in milliseconds per millimeter of mercury) assessed by amyl nitrite inhalation was 24.3 +/- 2.8 in FH- normotensives, 12.3 +/- 1.7 in FH+ normotensives, 15.4 +/- 3.3 in FH- hypertensives, and 8.1 +/- 1.2 in FH+ hypertensives. Baroreflex sensitivity assessed by phenylephrine bolus was 28.8 +/- 5.6 in FH- normotensives, 19.3 +/- 2.8 in FH+ normotensives, 19.1 +/- 2.0 in FH- hypertensives, and 13.6 +/- 1.3 in FH+ hypertensives. Two-factor analysis of variance showed significant effects on baroreflex sensitivity for blood pressure status (normotensive versus hypertensive) and for family history of hypertension. After control line (controlling) for the effects of several variables, including age, mean arterial pressure, body weight, and race through multiple linear regression analysis, the effect of family history of hypertension on baroreflex sensitivity was still highly significant. Indeed, of all variables investigated, family history of hypertension was the strongest unique baroreflex sensitivity predictor. CONCLUSIONS. These data suggest that the impairment in baroreflex sensitivity in hypertension is in part genetically determined and may be an important hereditary component in the pathogenesis of essential hypertension.     

Enhanced antinatriuresis in response to angiotensin II in essential hypertension

Angiotensin II regulates sodium homeostasis by modulating aldosterone secretion, renal vascular response, and tubular sodium reabsorption. We hypothesized that the antinatriuretic response to angiotensin II is enhanced in human essential hypertension. We therefore studied 48 white men with essential hypertension (defined by ambulatory blood pressure measurement) and 72 normotensive white control persons, and measured mean arterial pressure, sodium excretion, renal plasma flow, glomerular filtration rate, and aldosterone secretion in response to angiotensin II infusion (0.5 and 3.0 ng/kg/min). Hypertensive subjects exhibited a greater increase of mean arterial pressure (16.7+/-8.2 mm Hg v 13.4+/-7.1 mm Hg in normotensives, P < .05) and a greater decrease of renal plasma flow (-151.5+/-73.9 mL/ min v -112.6+/-68.0 mL/min in controls, P < .01) when 3.0 ng/kg/min angiotensin II was infused. The increase of glomerular filtration rate and serum aldosterone concentration was similar in both groups. Sodium excretion in response to 3.0 ng/kg/min angiotensin II was diminished in both groups (P < .01). However, the decrease in sodium excretion was more pronounced in hypertensives than in normotensives (-0.18+/-0.2 mmol/min v -0.09+/-0.2 mmol/min, P < .05), even if baseline mean arterial pressure and body mass index were taken into account (P < .05). We conclude that increased sodium retention in response to angiotensin II exists in subjects with essential hypertension, which is unrelated to changes in glomerular filtration rate and aldosterone concentration. Our data suggest a hyperresponsiveness to angiotensin II in essential hypertension that could lead to increased sodium retention.     

Moderate sodium restriction enhances the pressor response to hyperlipidemia in obese,hypertensive patients

The effect of dietary sodium restriction on insulin, lipids, and blood pressure has been controversial. Evidence suggests that adverse short-term effects in response to very low-salt diets do not persist long-term with modest sodium restriction. In this study, the effects of modest dietary sodium restriction (60 and 120 mmol sodium) were measured for 3 weeks in 12 lean normotensives and 10 obese hypertensives. Blood pressure, plasma lipids, and the pressor response to an infusion of Intralipid and heparin were obtained. In contrast to previous reports concerning very low-salt diets, obese hypertensives did not manifest a pressor response or an adverse lipid effect with moderate salt restriction. Obese hypertensives were not more salt-sensitive than lean normotensives and did not manifest a different hemodynamic response to 4-hour infusion of Intralipid and heparin while on the 120-mmol/day salt diet. During the 60-mmol/day salt diet, however, plasma triglycerides increased more in obese than in lean volunteers during the Intralipid and heparin infusion (398+/-38 vs. 264+/-18 mg/dL; p<0.05), and there were greater increases in mean blood pressure (12+/-2 vs. 7+/-2 mm Hg; p<0.05) and systemic vascular resistance (111+/-38 vs. 225+/-44 dyne.sec.cm-5) as well as a larger decrease in small artery compliance (22.5+/-0.6 vs. 20.4+/-0.6 mL/mm Hg x 100; p<0.05). These data suggest that modest dietary sodium restriction in obese hypertensives does not adversely affect baseline blood pressure or lipids, but it does magnify their adverse lipid and hemodynamic response to fat loading.     

Ethnic differences in blood pressure with observations on noradrenaline and renin. A hospital hypertensive population.

100 patients with essential hypertension (77 whites, 23 black) were studied with measurements of plasma noradrenaline concentration and plasma renin activity. Black patients had higher blood pressure than whites. There were no ethnic differences in mean plasma noradrenaline, but plasma renin activity was lower in blacks than whites, and this difference was not related to differences in sodium intake. Plasma noradrenaline increased with age in blacks, and in a white control group. Young white hypertensive patients (< 45 years) had higher plasma noradrenaline than controls, and in white hypertensives plasma noradrenaline was positively correlated with plasma renin.     

Clinic and ambulatory heart rate in sustained and white-coat hypertension

BACKGROUND: Sustained and white-coat hypertensives show hypertension in the office setting but different blood pressure values outside the clinical environment. So far, only a few incomplete data on heart rate are available inside and outside the clinical setting in these groups of patient. The aim of this study was to evaluate clinic and ambulatory heart in sustained hypertensives, white-coat hypertensives and normotensives. METHODS: We selected 236 sustained hypertensives, 236 white-coat hypertensives and 236 normotensives matched for age, gender and body mass index, and with a similar occupation. The subjects had been submitted to clinic evaluation and the non-invasive monitoring of blood pressure and heart rate. White-coat hypertension was defined as clinic hypertension and a daytime blood pressure of less than 135/85 mmHg. RESULTS: The clinic heart rate was significantly higher in sustained hypertensives and white-coat hypertensives than in normotensives (76 +/- 11 versus 75.5 +/- 10 versus 70 +/- 9 beats/min [bpm], respectively, P < 0.05). The daytime heart rate was significantly higher in sustained hypertensives than in white-coat hypertensives and normotensives (79.4 +/- 10 versus 74.6 +/- 8.5 versus 74.5 +/- 8.5 bpm, respectively, P < 0.05), as were the night-time heart rate (67 +/- 8.5 versus 63 +/- 8 versus 63 +/- 8 bpm, respectively, P < 0.05) and 24 h heart rate (76.3 +/- 9 versus 72 +/- 7.8 versus 72 +/- 8 bpm, respectively, P < 0.05). When men and women were analyzed separately, the same trend was observed. CONCLUSIONS: The clinic heart rate is similar in sustained and white-coat hypertensives, but the ambulatory heart rate is lower in white-coat hypertensives. As ambulatory heart rate is more representative of 24 h heart rate load and may be a better indicator of the detrimental effect of heart rate, our findings suggest that white-coat hypertensives are at lower cardiovascular risk than sustained hypertensives.     

Platelet sodium-proton exchange is increased in essential hypertension

Transmembrane sodium-hydrogen (Na+-H+) exchange was measured indirectly in human platelets as the amiloride-sensitive change in volume during incubation in isosmotic sodium propionate. After first establishing the reproducibility of the assay, we measured propionate-activated volume increases in platelets from 24 male essential hypertensive patients and 20 male normotensives. For the entire group, platelet Na+-H+ exchange was significantly (P less than 0.006) higher in hypertensives compared with normotensives. Unlike red blood cell (RDC) cation transport markers of hypertension, platelet Na+-H+ exchange was elevated in both black and white hypertensives. Na+-H+ exchange was significantly positively correlated with diastolic blood pressure and did not correlate significantly with age, body weight or body mass index. In addition, platelet Na+-H+ exchange did not correlate significantly with red blood cell lithium-sodium countertransport activity. Platelet Na+-H+ exchange deserves further study as a marker for pathophysiological abnormalities in human hypertension.     

Ca2+i:K+i ratio and total intracellular calcium in essential and renal hypertension

The calcium ion (Ca2+) and potassium ion (K+) content in the ashed material from red blood cells was determined by flame photometry in 61 essential hypertensives, 11 renal hypertensives and in 47 normotensive controls, and intracellular K+ concentration was measured in the haemolysate. The ratio between Ca2+ and K+ content in ashed red blood cells (Ca2+i:K+i) was 2.07 +/- 0.91 X 10(-3) in normotensives, 4.91 +/- 2.17 X 10(-3) in essential hypertensives (P less than 0.01) and 3.48 +/- 2.04 X 10(-3) in renal hypertensives (P less than 0.05). Intracellular K+ concentration was 94.3 +/- 3.1 mmol/l in normotensives, 94.7 +/- 3.8 mmol/l in essential hypertensives and 93.8 +/- 3.9 mmol/l in renal hypertensives. Therefore intracellular total Ca2+ concentration is increased in the red blood cells from essential hypertensives and, to a lesser extent, in the red blood cells from renal hypertensives. The use of Ca2+i:K+i ratios in red blood cells may thus be useful in assessing cellular Ca2+ content in hypertension.