Behavioral consequences of mild hypertension.

We studied plasma levels of cyclic nucleotides and their responses to submaximal exercise as an endogenous adrenergic stimulation in normal subjects, untreated and treated patients with essential hypertension to assess the roles of various hormones and the autonomic nervous system in essential hypertension. Plasma c-AMP level was significantly higher in untreated, diuretic-treated patients and those treated with propranolol than in normal subjects, but plasma c-GMP level was comparable in normal subjects and untreated patients. Plasma c-AMP decreased significantly, whereas plasma c-GMP increase significantly, after chronic propranolol therapy. Plasma c-AMP increased significantly after submaximal exercise in normal subjects, untreated patients and those treated with propranolol, but plasma c-GMP increased significantly only in normal subjects. The increase in plasma c-AMP was significantly higher in untreated patients than in normal subjects and patients treated with propranolol. Moreover, the percent increase in plasma c-AMP was significantly higher in untreated patients than in those treated with propranolol. Therefore, it is suggested that the sympathetic nervous system may be hyperactive, and that a hyperreactivity of the beta-adrenergic receptors may play an important role in essential hypertension.

Aim. To assess an incidence of microalbuminuria (MAU) depending on gender and its relation to intrarenal hemodynamic, glomerular filtration rate (GFR), and leptin serum level in essential hypertension (HT). Material and methods. 149 patients (61 men and 88 women, aged 49.4±7.1 years, body mass index 32.2±3.8 kg/m2) with HT degree 2-3 were examined. Clinical characteristics in men and women were comparable. Ultrasonography of intrarenal vessels was performed in all patients. GFR was calculated by isotope nephroangioscintigraphy. Leptin serum level was determined\ by radioimmunoassay. MAU was detected by semiquantitative test. Results were processed with SPSS-11.0 software package. Results. MAU incidence was higher among female hypertensives in contrast to males: 40% vs 26% (p=0.056). Hypertensives with MAU of both genders demonstrated higher both resistance index (RI) and pulsatility index (PI). Gender differences of both RI and PI in patients with MAU were highly significant (p<0.001) at all levels of arterial visualization (renal, segmental and interlobar). Female hypertensives with MAU had lower GFR (79.1±13.2 ml/min/1.73m2) than those without MAU (89.3±17.2 ml/min/1.73m2). Male hypertensives with MAU had higher GFR than those without MAU: 126±32.5 vs 105.4±16.7 ml/min/1.73m2, respectively. Serum leptin level in females with MAU was higher than this in female patients without MAU: 103.5±38.7 vs 76.7±46.4 ng/ml (p=0.04), respectively. Leptin levels did not differ in males with or without MAU. In males MAU positively correlated with GFR (r=0.372, р=0.003), where-as in females – correlation was negative (r=-0.34, р=0.02). Besides, in females MAU correlated with serum leptin level (r=0.48, p=0.01) Conclusion. Female hypertensives with MAU demonstrate more stable elevation of RI and PI in contrast to hypertensive males with MAU. MAU level correlates with GFR in opposite ways: in males positively whereas in females — negatively.

A high prevalence of hypercalciuria has been reported in patients with essential hypertension. Nevertheless, the clinical and therapeutic implications of this finding have scarcely been studied. This study was designed to determine the prevalence of hypercalciuria in an unselected population with essential hypertension and to analyze the relationship between the urinary calcium and the clinical and therapeutic status of these patients. This article presents a prospective study of 112 patients with essential hypertension and 49 healthy normotensive control subjects. Urinary excretion rates of calcium, sodium, chloride, potassium, urinary calcium/creatinine index, the fractional excretion of sodium, potassium and uric acid, the creatinine clearance and serum values of creatinine, urea, uric acid, electrolytes, total proteins, parathormone (intact molecule), plasma renin activity, aldosterone, glucose, and insulin (fasting and after an oral glucose load) were performed in every patient and control subject. Untreated hypertensive patients had a higher prevalence of hypercalciuria (35% had a urinary calcium/creatinine ratio > 0.20 versus 20% of treated hypertensives and 2% of control subjects; P < 0.001). Patients on thiazide or beta-blocker monotherapy had lower urinary excretion rates of calcium and urate than patients on calcium-antagonist monotherapy or untreated patients. Urinary calcium, sodium, and urate correlated positively both in treated and untreated essential hypertension patients. Patients with the higher urinary calcium levels also had higher excretion rates of sodium and urate, higher creatinine clearance rates, and lower serum creatinine and serum uric acid levels. It was concluded that hypercalciuria is a frequent finding of untreated essential hypertension. The association of high urinary calcium levels with high urinary urate excretion rates in the same patient may predispose to development of lithiasis in patients with essential hypertension. Antihypertensive drugs have a variable effect on calciuria-uricosuria, which may constitute an additional criterion in the selection and individualization of therapy. Thiazides and beta-blockers can decrease calciuria and uricosuria and, therefore, the lithogenic risk in these patients.

Body fluid volumes, cardiac output, PRA and pressor responses to angiotensin II (AT) and norepinephrine (NE) were compared between untreated patients with essential hypertension aged younger than 35 (EH-I) and those aged older than 36 years (EH-II). Men blood volume, total body water and extracellular volume were not significantly different between the patients with essential hypertension and normotensive subjects. There were no difinite differences in each volume between the EH-I and EH-II patients either. However, the distribution of blood volume was significantly larger in the essential hypertensive patients than in the normotensive subjects, suggesting that the changes in blood volume might not be homogenous in essential hypertension. In addition, blood volume was noted to have a significant inverse correlation with PRA. Cardiac output at rest was slightly but not significantly less in the EH-I and EH-II groups than in the normotensive group. A decline in blood pressure following 'bed-rest' was accompanied by a decrease in total peripheral resistance index (TPRI). Thus, elevated peripheral vascular resistance seems to be responsible for the mild to moderate hypertension even in the younger patients. PRA and its increases in response to standing or furosemide were normal in the EH-I patients, while they were markedly suppressed in the EH-II patients as compared to the age-matched normotensive subjects. In addition, PRA had a significant inverse correlation with the blood pressure and the scores of the severity of hypertension in the patients with essential hypertension. Thus, it seems likely that low renin in essential hypertension is secondary to long-lasting hypertension. Pressor response to AT significantly correlated with mean blood pressure and that to NE did so with 24 hours' urinary sodium excretion in essential hypertensive patients. The influence of aging on the pressor responses were obscure: the relationships of the pressore responses to blood pressure or to urinary sodium excretion were not different between the EH-I and EH-II groups. The examinations were repeated in 16 patients with essential hypertension (16 to 48 year-old) in 11 to 30 days after the initial study. Twelve of the 16 patients had declines in blood pressure and TPRI at the second study. In 7 of the patients whose blood pressure declined following 'bed-rest', there were significant decreases in pressor response to AT and in blood volume and a significant increase in PRA (group A). The other 5 patients showed a significant decrease in PRA and an enhanced pressor response to NE (group B). The blood volume in the group A was significantly larger than that in the group B at the initial study. It is suggested that the cause of essential hypertension is not homogeneous in that the increased vascular resistance may have been attributed to sodium excess in some patients and to an increased sympathetic activity in others. Some additional factors remain to be taken into account to clarify the complicated aspects of essential hypertension.

Involvement of genetic polymorphisms in arterial hypertension has already been reported, including GST genes, with contrasting results. The present research evaluates the possible association between GST gene polymorphisms and essential hypertension (EH) in an Italian population sample. 193 hypertensive subjects and 210 healthy controls were recruited. Buccal cells were collected from each subject using an oral swab and DNA was extracted using the phenol:chloroform:isoamilic alcohol method. GST SNPs were determined using the PCR-RFLP method, while GST null polymorphisms were determined using a Multiplex PCR. Among GST polymorphisms, only the frequency of the GSTT1 null phenotype was significantly higher in hypertensive patients than in normotensive participants. GSTT1 null individuals were significantly associated with increased risk of hypertension [P < 0.001; adjusted OR 2.24 (1.43-3.50)]. In sex-based analysis, the risk was significantly higher in female hypertensives [P < 0.001; adjusted OR 3.25 (1.78-5.95)] but not in male subjects. This study analyzed all GST gene that, in other research, have been studied in relation to arterial hypertension and the GSTO polymorphisms, showing an association only with GSTT1. The results for the GSTO genes represent the first analysis of this GST class in relation to blood pressure regulation. The association between the GSTT1 null phenotype and EH was confirmed in the overall population and in women, but not in men. These data suggest that GSTT1 could be a sex-specific candidate gene for EH.

The ease with which humans usually perform everyday activities masks their inherit complexity. Tasks such as setting a table prior to a meal or preparing a hot beverage require the coordination of several cognitive abilities. At the same time, many everyday activities are simple enough to afford investigation in controlled lab settings. One main goal of this issue is to raise awareness of everyday activities as a topic and a field of study in its own right, which allows investigating (a) selected cognitive abilities with high ecological validity and (b) the interplay and integration of key cognitive abilities. To this end, this topic consists of eight papers that span different aspects of everyday activities, ranging from neuroscience through philosophical considerations and implications to lessons fromrobotics.

The increasing use of ambulatory blood pressure monitoring (ABPM) devices in the investigation of hypertension has allowed detailed study of the circadian rhythm of blood pressure variability, the assessment of resistant hypertension, and the syndrome of “white coat” hypertension. The relevance of ABPM to target-organ damage and the complications of hypertension, such as heart attacks and strokes, has only recently gained prominence. There are more than 30 cross-sectional studies that have linked ABPM to hypertensive target-organ damage, including left ventricular hypertrophy (LVH),1 2 microalbuminuria,3 hypertensive retinal changes, and cerebrovascular disease.4 The majority of these studies have consistently reported that patients with an absent or reduced fall in blood pressure at night (referred to as “nondippers”) have more severe target-organ damage, including LVH5 and cerebrovascular disease,4 6 when compared with patients who demonstrate a normal nocturnal fall in blood pressure. For example, Verdecchia et al,7 in a prospective cohort of over 1100 hypertensive patients, reported higher mortality rates both in nondippers and “reverse dippers” and higher cardiovascular morbidity rates in female nondippers compared with dippers.8 In addition, Yamamoto et al9 recently reported that progressive cerebrovascular disease, including silent ischemic lesions and symptomatic stroke, was associated with a reduced nocturnal blood pressure fall in patients with a history of lacunar infarction. In a cross-sectional study of patients admitted with acute stroke (ictus <12 hours), Lip at al10 reported that such patients could generally be classed as nondippers, with higher blood pressures recorded using ABPM (but not using casual manual measurements) in black/Afro-Caribbean patients and also in patients with hemorrhagic stroke. These studies therefore suggest the potential usefulness of ABPM in epidemiological, cohort, or cross-sectional studies and the assessment of ethnic differences, stroke subtypes, and prognosis. A nondipper status …

There is evidence that the subgroup of patients with essential hypertension who are also insulin resistant is at increased risk of cardiovascular disease (CVD). We are unaware of the frequency of insulin resistance in patients with essential hypertension as well as the CVD risk in this subgroup of patients. This analysis was aimed at providing the prevalence of insulin resistance and associated CVD risk factors in treated and untreated patients with essential hypertension. The study population consisted of 126 patients with hypertension: 56 untreated and 70 in a stable treatment program. Body mass index (BMI), blood pressure, plasma glucose and insulin responses to an oral glucose challenge, lipid and lipoprotein concentrations, and steady-state plasma glucose (SSPG) concentration during the insulin suppression test were measured. Insulin resistance was defined operationally as a SSPG concentration >180 mg/dl. Demographic characteristics and metabolic CVD risk factors were comparable in both groups, with 30-50% of both treated and untreated patients having abnormalities of all risk factors measured. Approximately 50% of patients met the criteria for insulin resistance in both groups, and the prevalence of abnormal CVD risk factors in this group was increased two to threefold as compared to the other half of the subjects. Approximately 50% of patients with essential hypertension, both treated and untreated, appear to be insulin resistant, and CVD risk factors are greatly accentuated in this subset of patients.

Accumulating data suggests that catestatin, an eclectic neuroendocrine peptide, is involved in the pathophysiology of primary hypertension (PH). Nevertheless, clinical studies concerning its role in PH are still scarce. Therefore, in the present study, we aimed to explore an association between serum catestatin levels, ambulatory blood pressure (BP) and arterial stiffness in patients with PH and healthy controls. In this single-center study, 72 patients aged 40–70 diagnosed with PH, and 72 healthy controls were included. In patients with PH, serum catestatin concentrations were significantly higher in comparison to the healthy controls (29.70 (19.33–49.48) ng/mL vs. 5.83 (4.21–8.29) ng/mL, p < 0.001). Untreated patients had significantly higher serum catestatin than patients treated with antihypertensive drugs (41.61 (22.85–63.83) ng/mL vs. 24.77 (16.41–40.21) ng/mL, p = 0.005). Multiple linear regression analysis showed that serum catestatin levels retained a significant association with mean arterial pressure (β ± standard error, 0.8123 ± 0.3037, p < 0.009) after model adjustments for age, sex and body mass index. Finally, catestatin levels positively correlated with pulse wave velocity (r = 0.496, p < 0.001) and central augmentation index (r = 0.441, p < 0.001), but not with peripheral resistance. In summary, increased serum catestatin concentration in PH, predominantly in the untreated subgroup, and its association with ambulatory BP and arterial stiffness address the role of this peptide in PH.

Improvement of insulin sensitivity for glucose metabolism with the long-acting Ca-channel blocker amlodipine in essential hypertensive subjects

Essential arterial hypertension and stone disease

Management of the patient with primary (essential) hypertension

The Relationship of Aldosterone to Mild Essential Hypertension

Introduction. Insomnia may increase risk of cardiovascular events. There is little data available reporting the prevalence and clinical relevance of insomnia in patients with essential hypertension. Therefore, the aim of the study was to investigate the relationship between insomnia and different clinical and biochemical parameters in essential hypertension patients. Methods. Four hundred and thirty‐two patients (mean age: 47±13 years; 253 male, 179 female) with essential hypertension were screened for insomnia using the Athens Insomnia Scale (AIS). Several variables including age, sex, known duration of hypertension, body mass index, creatinine, left ventricular mass index, coexisting disorders, smoking status and alcohol use were analysed. Twenty‐four‐hour ambulatory blood pressure measurements (ABPM) were performed. Results. Among patients included in the study, 207 subjects (mean age: 49±13 years; 47.9%) had an AIS score of 15 or higher and were identified as insomniacs. Insomnia was more frequent in women than in men (60.9% vs 38.7%, p<0.001) and was reported more frequently in patients with coronary artery disease. Subjects with insomnia were older and had longer duration of hypertension. There were no differences between insomniacs and non‐insomniacs in ABPM parameters. A relationship was found between the number of antihypertensive drugs and insomnia frequency. There were correlations between AIS score and age (r = 0.21; p<0.001) and duration of hypertension (r = 0.22; p<0.001). In the sub‐group of untreated essential hypertension patients, there were negative correlations between AIS score and night fall in systolic and diastolic blood pressure. Conclusion. Our results showed that insomnia is common in patients with essential hypertension and indicate an association between insomnia and gender, known duration of hypertension and number of antihypertensive drugs taken. Untreated essential hypertension insomniacs were characterized by less pronounced nocturnal fall in both systolic and diastolic blood pressure compared with non‐insomniacs.

The determinants and significance of urinary albumin excretion have been studied in normal subjects and in hypertensive patients; however, they are unknown in patients with primary aldosteronism. From a population of 114 patients with documented primary aldosteronism, we selected 23 never-treated patients (12 males, 11 females; 11 tumoral, 12 non-tumoral) and compared them to patients with never-treated essential hypertension with low renin (supine plasma renin activity <1 ng/ml per h, n = 23) or normal renin (supine plasma renin activity between 1 and 4 ng/ml per h, n = 23), matched for age, body mass index, mean arterial pressure, renal function and known duration of hypertension. The patients with primary aldosteronism had lower serum potassium and higher plasma aldosterone concentrations than those with essential hypertension. Urinary albumin and beta2-microglobulin excretion were greater in untreated patients with primary aldosteronism than in those with low- or normal-renin essential hypertension. Among the patients with essential hypertension, the renin activity was not a determinant of albuminuria. These findings indicate that primary aldosteronism is associated with excessive urinary albumin excretion. This albuminuria could be due to impairment of proximal tubular reabsorption caused by hypokalemic nephropathy and/or by high levels of circulating aldosterone; however, it could be an indicator of target-organ damage associated with primary aldosteronism.