Hyperuricemia and Risk of Cardiovascular Outcomes: The Experience of the URRAH (Uric Acid Right for Heart Health) Project.

The latest European Guidelines of Arterial Hypertension have officially introduced uric acid evaluation among the cardiovascular risk factors that should be evaluated in order to stratify patient's risk. In fact, it has been extensively evaluated and demonstrated to be an independent predictor not only of all-cause and cardiovascular mortality, but also of myocardial infraction, stroke and heart failure. Despite the large number of studies on this topic, an important open question that still need to be answered is the identification of a cardiovascular uric acid cut-off value. The actual hyperuricemia cut-off (> 6 mg/dL in women and 7 mg/dL in men) is principally based on the saturation point of uric acid but previous evidence suggests that the negative impact of cardiovascular system could occur also at lower levels. In this context, the Working Group on uric acid and CV risk of the Italian Society of Hypertension has designed the Uric acid Right for heArt Health project. The primary objective of this project is to define the level of uricemia above which the independent risk of CV disease may increase in a significantly manner. In this review we will summarize the first results obtained and describe the further planned analysis.

Severe obstructive sleep apnoea exacerbates the microvascular impairment in very mild hypertensives.

BACKGROUND: Different studies have shown that obstructive sleep apnoea syndrome (OSAS), frequently associated with hypertension, represents a harmful and independent risk for cardiovascular diseases. The aim of our study was to ascertain whether the occurrence of OSAS could worsen microcirculatory impairment in very mild hypertensives. MATERIALS AND METHODS: One hundred untreated very mild hypertensives underwent polysomnography and subdivided into 32 non-OSAS, 33 mild OSAS and 35 severe OSAS patients on standardized criteria. They underwent routine blood chemistry, ambulatory blood pressure monitoring and anthropometric analysis. Skin capillary density (n mm(-2)) of forearm (FAC) and periungueal (PUC) fields was obtained through videocapillaroscopy. By a venous congestion manoeuvre, PUC was maximized (CVC) and secondary capillary recruitment (GAIN) was calculated. These measurements served as indices of structural and functional capillary rarefaction, respectively. RESULTS: Severe OSAS hypertensives showed reduced FAC (P < 0.001) and PUC (P < 0.001) as compared to those with mild OSAS and non-OSAS, but a greater CVC (P < 0.01) and GAIN (P < 0.001). Multiple regression analysis showed that PUC was inversely related to total sleep time with oxyhaemoglobin saturation at < 90% (TST90) (P < 0.001) and FAC to the apnoea-hypopnoea index (AHI) (P < 0.001) and to the sleep propensity (P < 0.01). CVC was positively associated to AHI (P < 0.001) and GAIN to TST90 (P < 0.05). CONCLUSIONS: The findings suggest that OSAS, by means of reduced basal and functional capillarity rarefaction, might pose an additional risk of impaired peripheral perfusion in very mild hypertensives. A microcirculation study therefore should be a part of the clinical approach in patients at high cerebro-cardiovascular risk such as hypertensives and patients with OSAS.

Comparative genomic hybridisation in malignant deciduoid mesothelioma.

BACKGROUND: Malignant deciduoid mesothelioma is a rare variant of epithelioid mesothelioma. This tumour generally has poor prognosis, and can be asbestos related. AIM: To identify peculiar genetic changes responsible for critical phases in pathogenesis of malignant deciduoid mesothelioma and their prognostic relevance. METHODS: Comparative genomic hybridisation was carried out in six cases of malignant pleural deciduoid mesothelioma, four sporadic and two familial. All cases were found to be asbestos related. Four patients died during follow-up and the mean survival was 29.5 (SD 14.2, range 12-43) months. RESULTS: Genetic abnormalities were found in all the tumour tissues, the most frequent being chromosomal gains at 1p, 12q, 17, 8q, 19 and 20 and losses at 13q, 6q and 9p. Survival was found to be longer in those patients who presented a smaller number of losses (< or =2) in the tumorous chromosomes. CONCLUSIONS: Although numerous genetic changes are presented by deciduoid mesotheliomas, certain chromosomal regions are preferentially affected. The clinical outcome for this mesothelioma subtype is predicted by the number of losses.

Endothelin-1-receptor-mediated responses in resistance vessels of young and adult spontaneously hypertensive rats.

OBJECTIVE: To assess whether primary changes in endothelin-1 (ET-1) receptor responsiveness or secondary vessel functional modifications could characterize the effects evoked by ET-1 in the mesenteric vascular bed (MVB) of prehypertensive 5-week-old and 12-week-old spontaneously hypertensive rats (SHRs). DESIGN AND METHODS: We used male 5-week-old and 12-week-old SHRs and sex- and age-matched Wistar-Kyoto (WKY) rats as controls. ET-1 receptor responsiveness was evaluated by ET-1 (0.04-2 micromol/l) concentration-response curves and repeated with indomethacin and BQ-123 (0.1-0.5 micromol/l), the latter a selective ETA receptor antagonist. ETB receptor responsiveness was tested by sarafotoxin S6c (1-100 nmol/l) and IRL-1620 (0.1-10 nmol/l) concentration-response curves, obtained in the noradrenaline-precontracted MVB. RESULTS: At 5 weeks of age, ET-1 induced a similar concentration-dependent contraction in SHRs and WKY rats, with an overlapping BQ-123 pA2 value (negative common logarithm of the antagonist that produces an agonist dose ratio of 2) in the two strains. Indomethacin was ineffective in both groups. Sarafotoxin S6c and IRL-1620 both evoked an ETB-mediated, significant relaxation, only in WKY rats. In 12-week-old SHRs, ET-1 evoked a markedly increased maximal effect compared with the response in WKY rats (P< 0.01); this was prevented by treatment with indomethacin. The BQ-123 pA2 value was higher in SHRs than in WKY rats (P< 0.01). Both sarafotoxin S6c and IRL-1620 evoked a significant concentration-dependent relaxation in WKY rats, which was not detected in SHR preparations. CONCLUSIONS: Our results could suggest that the different responses evoked by ET-1 in the MVB of SHRs during the onset of hypertension may be related partially to primary alterations in the ET-1 receptorial pattern and partially to the onset of high blood pressure, leading to an impairment in the haemodynamic balance.

White-coat hypertension and carotid artery atherosclerosis: a matching study.

BACKGROUND: Blood pressure (BP) measurements obtained in the clinic have long served as the basis for determining risk of hypertensive vascular disease, yet many patients with high BP in the physician's office are normotensive elsewhere. It remains unclear whether such patients with "white coat" hypertension elude the risk of atherosclerosis. METHODS: Community residents 40 to 70 years of age and not receiving any cardiovascular medications were recruited to participate in a study of cardiovascular risk factors. On the basis of clinic and daytime ambulatory BP and a threshold criterion of 140/90 mm Hg, subjects were classified as having persistent hypertension, white-coat hypertension, or persistent normotension. One-to-one matching was conducted in male participants on the basis of race and BP. Subjects with persistent hypertension and white-coat hypertension were matched on clinic BP, and those with white-coat hypertension and normotension were matched on daytime ambulatory BP. RESULTS: The 3 matched groups of men (n=40 in each group) were similar in age, smoking status, and fasting glucose and lipid levels. Compared with the normotensive subjects, subjects with either persistent or white-coat hypertension had greater mean body mass index, waist-hip ratio, and fasting insulin concentration. On the basis of standardized duplex ultrasound examination of the carotid arteries, mean maximal intimal-medial thickness and plaque index in subjects with white-coat hypertension were greater than among normotensive subjects and equal to that of the subjects with persistent hypertension. CONCLUSION: When compared with unmedicated individuals with comparable elevations in clinic BP, individuals with white-coat hypertension appear not to be protected from the atherosclerotic sequelae of hypertension.

Insulin resistance in essential hypertension: a psychophysiological approach to the "chicken and egg" question.

AIMS: High levels of plasma insulin have frequently been found in patients with high blood pressure. The causal role of insulin resistance in essential hypertension, however, is still debated. Epidemiological and clinical studies have not provided complete responses to the original pathophysiological speculations, while the suggestion that enhanced sympathetic tone may induce both insulin resistance and hypertension is gaining ground. DATA SYNTHESIS: Many studies indicate that the high sympathetic drive in hypertensive patients originates within the brain, while other studies show that insulin resistance is associated with reduced vasodilatory capacity and increased vasoconstrictive functional responses ascribed to endothelial impairment. The sympathetic overdrive and enhanced cardiovascular reactivity, detectable since the earliest stages of hypertension lead to endothelial damage and, hence, impair the vasodilatory response, peripheral blood flow and flow-dependent metabolism. Thus, the link between hyperinsulinemia and high blood pressure might lie in the vascular abnormalities secondary to elevated sympathetic tone and exaggerated hemodynamic stress response. CONCLUSIONS: Examination of the literature and the results of recent pilot studies of the stress systemic and regional hemodynamic reactivity in the present paper suggests that behavioral characteristics and cardiovascular stress responses play a pivotal role in determining the hyperinsulinemic state in hypertensive patients. High sympathetic tone, with consequent vascular impairment and altered functional responses, may be the primary event causing hyperinsulinemia and start very early in patients with high blood pressure. In turn, hyperinsulinemia further contributes to vascular damage and aggravates the metabolic and hypertensive disease.

Distinct and combined vascular effects of ACE blockade and HMG-CoA reductase inhibition in hypertensive subjects.

Hypercholesterolemia and hypertension are frequently associated with elevated sympathetic activity. Both are independent cardiovascular risk factors and both affect endothelium-mediated vasodilation. To identify the effects of cholesterol-lowering and antihypertensive treatments on vascular reactivity and vasodilative capacity, we studied 30 hypercholesterolemic hypertensive subjects. They received placebo for 4 weeks, either enalapril or simvastatin for 14 weeks, and, finally, both medications for an additional 14 weeks. Postischemic forearm blood flow (MFBF) and minimal vascular resistance (mFVR) were used as indices of vasodilative capacity and structural vascular damage, respectively. Total (resting-stress-recovery phases) cardiovascular (blood pressure [BP] and heart rate [HR]) and regional hemodynamic (FBF and FVR) reactivity to stressful stimuli were calculated as area-under-the-curve (auc) (valuextime). Compared with baseline levels, simvastatin reduced total (TOT-C) and LDL cholesterol (LDL-C) (1.27 mmol/L, P<0.001 and 1.33 mmol/L, P<0.001, respectively). Enalapril also reduced TOT-C and LDL-C (0.6 mmol/L, P<0.001 and 0.58 mmol/L, P<0.05, respectively). MFBF was increased substantially by both treatments (P<0.001). Enalapril had a greater effect (-1.7 arbitrary units (AU), P<0.001) than simvastatin (-0.6 AU, P<0.05) on mFVR. During stress, FBF increased more with enalapril (4.4 FBFxminutes, P<0.001) than with simvastatin (1.8 FBFxminutes, P<0.01). Conversely, FVR stress response was reduced more with enalapril (9.1 FVRxminutes, P<0.001) than with simvastatin (2.9 FVRxminutes, P<0.01). During combination treatment, a significant (0.001>P<0.05) additive effect on hypercholesterolemia, structural vascular damage, BP, and FVR was shown. The findings suggest that angiotensin-converting enzyme (ACE) inhibition induces a larger reduction than HMG-CoA reductase blockade in vascular reactivity and structural damage in hypercholesterolemic hypertensive subjects.

Microvascular changes during laboratory stimuli and structural haemodynamic indices: the role of pulse pressure.

Office and ambulatory pulse pressure have been recognized as independent predictors of cardiovascular mortality and atherosclerosis in hypertensives as well as in normotensives. On the other hand, the vascular reactivity, in subjects with high pulsatile component of blood pressure, has not been studied yet. The purpose of our study was to identify the regional muscular hemodynamics and the cutaneous microvascular changes during laboratory stimuli in young adult very mild hypertensives with high pulse pressure. The cardiovascular (Finapres), the forearm vascular (plethysmography) and the microvascular cutaneous (laser-Doppler flowmetry and transcutaneous oximetry) responses to psychophysiological stimuli were measured. In addition, the hyperemic forearm vascular response to the ischaemic test was measured as haemodynamic index of vascular damage. We studied 15 very mild hypertensives with higher office pulse pressure and 15 patients with similar age, history of hypertension, metabolic parameters and systodiastolic blood pressure but lower pulse pressure values. Patients with high pulse pressure demonstrated reduced hyperemic response and increased residual vascular resistance at the forearm ischaemic test. They did not vary for all the parameters, except pulse pressure, during the baseline period but the total stress response, as residualized area-under-the-curve, was notably different. Patients with higher office pulse pressure demonstrated a significant increased heart rate, systolic and pulsatile blood pressure reactivity. On the contrary, they showed a reduced forearm and cutaneous blood flow response combined to a reduced transcutaneous tissutal oxygenation. The findings suggest that the increased pulsatile component of blood pressure might be associated to structural and functional vascular impairments since the very early stages of hypertension in young adults without metabolic disorders.

Reduced deformability of erythrocytes as feature of congenital dyserythropoietic anaemia type II (HEMPAS).

In this study we report results regarding erythrocytes deformability in congenital dyserythropoietic anemia type II (HEMPAS) by the use of LORCA (Laser-assisted Optical Rotational Cell Analyzer). The reduced erythrocytes deformability observed in seven case of CDA II is caused by changes in the structure of glycoproteins due to the incomplete glycosylation of erythrocytic and erythroblastic membrane. Erythrocytes deformability (EI) was shown to be inversely related with mean corpuscular volume (MCV) and mean haemoglobin concentration (MCH).

Antihypertensive treatment with verapamil and amlodipine. Their effect on the functional autonomic and cardiovascular stress responses.

Many biological and psychological factors induce haemodynamic and extra-cardiovascular functional changes mediated by the autonomic nervous system. Pharmacological blood pressure reduction, as a neurovegetative stimulus, can change the arousal of the sympathetic nervous system. We evaluated the effects of two calcium channel blockers, verapamil and amlodipine, both administered as monotherapies, upon the sympathetic stress response in 23 randomized mild-to-moderate essential hypertensives (161 +/- 2/98 +/- 1 mmHg). Patients performed four stress tests (mental arithmetic, colour word Stroop, cold pressor and handgrip) while extracardiovascular and haemodynamic functions were assessed non-invasively at every heart beat, during baseline, stress and recovery phases. The sympathetic response was evaluated by computing the 'area-under-the-curve' (value x time) measured during the psychophysiological session. The session was repeated at run-in, after placebo and during treatment. After one month's treatment, baseline blood pressure was significantly reduced in patients treated with amlodipine (139 +/- 1/84 +/- 1 mmHg; P < 0.001) and verapamil (140 +/- 2/85 +/- 1 mmHg; P < 0.001). The emotional arousal (frontalis muscular contraction, skin conductance) was unchanged, but the cutaneous vascular response was reduced (P < 0.05) in patients treated with verapamil. No changes in systolic or diastolic blood pressure were detectable, but amlodipine increased the heart rate response (P < 0.05). In contrast, verapamil reduced the heart rate (P < 0.05) without depressing the cardiac output response, which was increased with amlodipine (P < 0.05). Total vascular resistance was significantly (P < 0.001) reduced with both the treatments. Consequently, functional cardiac load, expressed by pressure-rate product and cardiac power, was significantly enhanced with amlodipine and reduced with verapamil. In conclusion, the abnormal sympathetic stress response, which characterizes the hypertensive patient, might be affected by the choice of medication. Verapamil in particular, moderated emotional arousal, the vasoconstrictive response and reduced cardiac load without lowering cardiac output demands. In contrast, in patients treated with amlodipine, in whom the cardiac output response was increased, the pattern was reversed and the functional cardiac load was also increased.

Glucose metabolism in abdominally obese hypertensive and normotensive subjects.

To determine whether the combination of obesity and hypertension results in additive defects in oxidative and nonoxidative glucose metabolism and the association of these changes with altered hemodynamic actions of insulin, we studied 11 abdominally obese hypertensive, 6 abdominally obese normotensive, and 7 lean normotensive nondiabetic subjects. Endogenous glucose production and glucose metabolized were calculated from a euglycemic clamp at 72 and 287 pmol insulin/m2 per minute. Glucose metabolized divided by insulin was lower at 72 pmol/m2 per minute in both obese groups than in lean normotensive subjects, at 148 +/- 14, 144 +/- 33, and 373 +/- 69 (mumol/m2 per minute)/(pmol/L), respectively (P < .01). Similar results were obtained during the higher insulin dose. Nonoxidative and oxidative glucose disposals by indirect calorimetry were lower in both abdominally obese groups (P < .05). Hepatic glucose production was completely suppressed in lean subjects at the lower insulin dose and in all three groups at the higher insulin dose. Hemodynamic responses during the clamp were not significantly different among the three groups. Abdominal obesity is associated with defects in insulin-regulated oxidative and nonoxidative glucose disposal as well as in insulin suppression of hepatic glucose production. Mild hypertension does not exacerbate these defects. Whereas the global impairment in glucose metabolism suggests the presence of an early defect or defects, including reduced tissue perfusion, systemic and regional hemodynamic responses to insulin were not altered. These findings do not support a direct role for insulin resistance in the pathogenesis of the hypertension associated with abdominal obesity.

Stress reactivity in responder and non-responder hypertensives treated with verapamil and enalapril.

Hypertension was found to be associated with sympathetic overdrive but it is still debated if the antihypertensive agents can differently affect the stress response in hypertensive subjects. Through a psychophysiological study, we evaluated the effect of verapamil (V) and enalapril (E), both as monotherapy and association. Office BP was successfully reduced (< 145/90 mmHg) in 11 patients treated with V (V-Resp) and in 10 patients treated with E (E-Resp). Both the drugs were prescribed in 9 patients (V+E) who did not sufficiently lower their blood pressure (N-Resp) with monotherapy. Patients performed three stressors (color word stroop, cold pressor and handgrip). Extracardiovascular and hemodynamic functions were measured during baseline, stress and recovery periods. The response was evaluated adding the changes occurred in every phase of the psychophysiological session. This was performed before run-in and after any modification of the therapeutic intervention. The emotional arousal (phrontalis muscular contraction, skin conductance, peripheral temperature) was reduced when BP was normal. No change in BP reactivity was found. HR response decreased in V-Resp and cardiac output increased in E-Resp while the vascular reaction was restrained in E-Resp and V-Resp. This was reduced also in N-Resp when they assumed V+E and normalized their arterial pressure. The findings indicate that the sympathetic reactivity may be modified by the therapy. In particular, verapamil restrained the cardiac stress response without lowering the cardiac output and was advantageously associated with enalapril to control the psychophysiological response in more resistant hypertensive patients.

Elevated blood pressures in obese young men with mild hypertension are sustained during the day and night.

The major goal of this study was to determine if the elevated blood pressures in obese men < 45 years old with mild hypertension persist outside the clinic. A secondary aim was to determine if hyperinsulinemia is associated with accentuated diurnal changes of blood pressure. To address these objectives, the clinic and ambulatory blood pressures as well as a 75-g, 2-h oral glucose tolerance test measurements were obtained from 9 lean normotensive, 9 lean hypertensive, and 22 obese hypertensive men < 45 years old. The week before study, volunteers ate an isocaloric diet with 220 mEq of NaCl/day. Obese hypertensives, subdivided by high (n = 11) and low (n = 11) insulin areas-under-the-curve (AUCs) in response to oral glucose, and lean hypertensives maintained higher ambulatory blood pressure than lean normotensives (130 +/- 3/74 +/- 1, 136 +/- 4/78 +/- 2, 132 +/- 5/77 +/- 3 v 118 +/- 4/65 +/- 2 mm Hg, respectively, P < .05). As expected, the insulin AUC during the glucose tolerance test was higher in obese hypertensives with higher insulin AUCs than in obese hypertensives with lower insulin AUCs, lean hypertensives, or lean normotensives (13.9 +/- 1.2 v 7.9 +/- 0.3, 7.2 +/- 0.7, 5.7 +/- 0.7 mU-min/dL, P < .05). Insulin AUCs were not significantly different in obese hypertensives with lower insulin levels, lean hypertensives, or lean normotensives. The diurnal increases of systolic and diastolic blood pressure as well as heart rate and pressure-rate product were similar in all four groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Diabetes modifies cardiovascular reactivity during hypertension.

Hypertension and diabetes often occur in the same patient, and this observation inspired the search for a new common pathogenetic hypothesis. The onset of diabetes during hypertension also could modify cardiovascular autonomic arousal. To identify a peculiar hemodynamic and psychophysiologic reactivity, a male population of mild essential hypertensive (166 +/- 6/102 +/- 8 mm Hg) patients (EH) and non-insulin-dependent hypertensive (169 +/- 10/101 +/- 7 mm Hg) diabetic subjects (HD) underwent a session of stress tests. Four tests, Mental Arithmetic, Incomplete Phrases, Cold Pressor, and Handgrip, were preceded and followed by a 10-minute recovery period. Functional tests were performed to identify any possible cardiac autonomic neuropathy. During the entire session, by means of a beat-to-beat noninvasive computerized device, hemodynamic and extracardiovascular functions were measured. The findings suggested the presence of a sympathetic hyperactivity in both HD and EH. In particular, HD showed a peculiar "tropism" for the peripheral vasculature. In these patients, in fact, total vascular resistance and peripheral temperature responses were 89.2% and -64.2%, respectively, versus 33.7% and -50.6%, which were found in EH. On the other hand, the ejection ventricular index was more depressed in HD (-27.9%) than in EH (-23.8%), although they did not seem to be affected by cardiac autonomic damage. The different profiles appear to confirm the increase of functional vascular damage in diabetic hypertensive patients, probably because of the insulin resistance or obsolete muscular cardiac damage.

Lipids and cardiovascular reactivity changes in hypertensive cigarette smokers: enalapril versus nifedipine treatment effects.

Cigarette smoking has many effects on the cardiovascular system, psyche, and serum lipids, which can create a vicious circle that is pejorative to the well-being of hypertensive patients, even if they are under pharmacologic treatment. To investigate the effect of two different antihypertensive agents, nifedipine and enalapril, on cardiovascular reactivity and lipoprotein patterns in cigarette smokers with hypertension, 92 essential hypertensive (175 +/- 11/103 +/- 8 mm Hg) subjects were studied, who had no sign of lipidosis, and subdivided into four groups in order of smoking habit and therapy. Over a 30-month follow-up period, the percentage changes in blood pressure (BP), heart rate (HR), triglycerides, total cholesterol, high density lipoprotein (HDL) and low density lipoprotein (LDL) cholesterol were evaluated while the patients underwent a session of psychophysiologic tests to assess sympathetic reactivity. The response was calculated through the difference in cumulative percentage changes (DC%) in systolic blood pressure (SBP), diastolic blood pressure (DBP), HR, muscular contraction (EMG), skin conductance (SCL), and peripheral temperature (TP). The office BP was reduced significantly in all groups. In the nonsmokers, enalapril reduced (p < 0.05) the SCL-, TP-, SBP-, and DBP-DC% reactivity, lowered (p < 0.05) TR, C-tot, and LDL, and increased (p < 0.05) the HDL. However, nifedipine magnified the sympathetic responses and the atherosclerotic lipoproteins and decreased (p < 0.05) the HDL.(ABSTRACT TRUNCATED AT 250 WORDS)

Insulin levels are similar in obese salt-sensitive and salt-resistant hypertensive subjects.

Evidence supports the hypothesis that hyperinsulinemia, especially in obesity, contributes to salt-sensitive hypertension by enhancing sodium retention and blunting the normal reduction of sympathetic drive and vascular resistance that occurs during a high versus low NaCl diet. To address these issues, we studied 18 obese (body mass index, > 27 kg/m2) subjects younger than 45 years old with mild hypertension to determine if the salt-sensitive versus salt-resistant subset had higher insulin levels, retained more volume, and failed to suppress sympathetic drive and vascular tone normally on a high (approximately 200 mEq/d) versus low (20 mEq/d) NaCl diet for 7 days each. Six obese subjects were salt sensitive, with an 8.4 +/- 2.1 (SEM) mm Hg increase of ambulatory mean blood pressure on the high versus low NaCl diet. Ten obese subjects were salt resistant, with a 7.1 +/- 0.9 mm Hg reduction of ambulatory mean blood pressure on high versus low NaCl. The salt-sensitive and salt-resistant groups had similar values, respectively, for the insulin area under the curve during an oral glucose tolerance test on low (14.6 +/- 1.8 versus 14.0 +/- 1.4 mU x min/dL, P = NS) and high (10.6 +/- 1.5 versus 10.6 +/- 1.0, P = NS) salt diets. Although insulin levels were similar, insulin raised calf blood flow in salt-resistant subjects (P < .05) but not in salt-sensitive subjects on the high NaCl diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Stress response and antihypertensive treatment.

Results from many studies suggest that the central nervous system may play an important role in enhancing and maintaining sympathetic, metabolic and haemodynamic effects in patients with hypertension. Likewise, emotional and mental stresses may provoke phasic and sustained adrenergic responses in normotensive and untreated hypertensive patients. Because the various antihypertensive medications have different mechanisms of action, and elicit different neurovegetative responses, it is useful to distinguish between the effects of different treatments on sympathetic activity. To identify the effect of stress on sympathetic reactivity, we evaluated the extracardiovascular and haemodynamic responses to various stressor agents using noninvasive techniques. This psychophysiological approach allowed us to standardise stress, to identify individual cardioneurovegetative responses both before and during treatment, and to establish the effects of various treatments on the cardioneurovegetative response. The extracardiovascular psychophysiological response of patients with a family history of hypertension and of normotensive patients who later became hypertensive was characterised by an inability to recover after mental challenge. Therefore, prolonged sympathetic activity resulting from mental stimulation may contribute to the development of hypertension. Antihypertensive medications affected sympathetic reactivity differently. For example, nifedipine worsened sympathetic reactivity, while verapamil was able to correct abnormal neuroadrenergic responses. Furthermore, verapamil was successfully combined with enalapril in patients whose hypertension was resistant to monotherapy with the angiotensin converting enzyme (ACE) inhibitor. Therefore, the functional and structural consequences of sympathetic stimulation resulting from daily activation and pharmacological blood pressure adjustments are important in hypertensive patients, because they may have abnormal sympathetic reactivity to various stimuli.

Psychological and physiological predictors of lipids in black males.

The association between lipids and both psychological and physiological measures were examined in this study of healthy black males. The results revealed that certain psychological measures, namely, State and Trait Curiosity and Trait Anger, explained a significant proportion of the variance in high-density lipoproteins (HDL), low-density lipoproteins (LDL), and triglycerides. Although psychological factors accounted for a significant proportion of the variance in lipids (29% for HDL, 25% for LDL, 64% for LDL/HDL, 29% for triglyceride), the amount of explained variance was significantly increased by the inclusion of both psychological and physiological variables in the regression equation. However, neither of the psychological variables explained any of the variance for total cholesterol when physiological variables were included in the regression analysis. The overall pattern of the findings suggests that black males who are at increased risk for elevated lipid levels may be identified by their level of mental vigilance, the frequency at which their anger is experienced, and the presence of other traditional risk factors.