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Background: Hypertension is a growing clinical problem in pediatric population. Also, the cause of hypertension is usually unknown and it may result from systemic inflammation related to tooth decay., Aim: To estimate the potential association in cross-sectional study between tooth decay and hypertension in children and adolescents., Patients and Methods: Study group-65 children diagnosed with primary arterial hypertension; control subjects-44 normotensive children. Blood pressure, dental examination, measurement of salivary cortisol, alpha-amylase, secretory IgA, and lysozyme concentrations were performed in all of the children., Results: Hyper- and normotensive children had similar peripheral blood morphology and serum biochemical parameters, except of uric acid concentration, which was significantly higher in the study group (p = .047). Salivary evening concentrations of cortisol and alpha-amylase were significantly higher in hypertensive children (p = .002 and p = .004, respectively). Although 24-hr systolic blood pressure (SBP), including daytime and nighttime SBP, correlated with "decay," "microalbuminuria," "BMI," and "glomerular filtration rate" (r > .75, r > .7, r < .68, and r < .43, respectively), in multivariate analysis only "decay" was associated with hypertension both in children and in adolescents (p < .0001)., Conclusion: Tooth decay in children/adolescents might be regarded as a potent trigger factor of hypertension in individuals in whom all other causes of secondary arterial hypertension have been excluded., (© 2020 Wiley Periodicals LLC.)

Introduction: Excessive intake of fructose increases serum uric acid concentration. Hyperuricemia induces a negative effect on atherosclerosis and inflammation. Hyperuricemia is common in patients with arterial hypertension. Several antihypertensive drugs including diuretics increase serum uric acid concentration. In contrast, the angiotensin II receptor antagonist (ARB) losartan was found to lower serum uric acid though it may increase renal excretion while other ARBs showed mostly a neutral effect. In this study, effects of two AT1 receptor antagonists losartan and eprosartan on serum uric acid changes induced by oral fructose load were directly compared., Methods: The randomized, crossover, head-to-head comparative study comprised 16 ambulatory patients (mean age 64.5 ± 9.8 years). The patients fulfilled AHA/NHLBI 2005 criteria of metabolic syndrome. A daily single morning dose of each study drug (50 mg of losartan or 600 mg of eprosartan) was given during two 3-month periods in a random order separated by 2-week washout time. The oral fructose tolerance test (OFTT) was performed at baseline and after each two 3-onth treatment periods. Before and during OFTT, urine excretion of uric acid and creatinine was assessed in the first morning portion of urine. Blood samples for the measurement of serum uric acid and lipids were taken at baseline and 30, 60, and 120 minutes after oral intake of 75 g of fructose., Results: After 3-month treatment with eprosartan and losartan, both systolic and diastolic blood pressure decreased significantly and to a similar extent. After the treatment, serum uric acid and its baseline and postfructose urine excretion were unchanged. No significant changes of plasma lipids before and after OFTT were observed throughout the study., Conclusions: The study showed that in patients with hypertension and metabolic syndrome, both losartan and eprosartan have a neutral effect on fasting and postfructose load serum uric acid concentration and its urinary excretion. This trial is registered with NCT04954560., Competing Interests: The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article., (Copyright © 2021 Anna Masajtis-Zagajewska et al.)

The aim of this case-control study was the evaluation of the association between biomarkers of early primary arterial hypertension (HA) and oral diseases among children and adolescents. Material and methods. Subjects suspected of primary HA (n = 180) underwent a complex evaluation of their vascular status: blood pressure, heart rate, vascular stiffness, sympathetic activity in a 24 h ambulatory examination, followed by measurement of serum uric acid (UA), cystatin C, and creatinine. This procedure allowed the identification of children with primary (n = 58) and secondary HA (n = 74), as well as of children with normal arterial blood pressure, who served as a control group (n = 48). All subjects with secondary HA were excluded from further investigation. Oral examination included the measurement of caries intensity (using the decayed, missing, filled index for permanent teeth DMFT /primary teeth dmft), bacterial plaque (by the plaque control record index, PCR%), and gingivitis (by the bleeding on probing index, BOP%). For statistical analysis, a linear regression model and Spearman rank correlation were used. Results. UA, cystatin C, and creatinine were not altered in the HA group. However, the number of decayed permanent teeth (DT) and the DMFT, PCR%, and BOP% indexes were significantly higher in the primary HA group compared to the control group ( p = 0.0006; p = 0.02; p = 0.0009; p = 0.003). Our results are not sufficient to prove the important role of caries and gingival inflammation in the modulation of HA symptoms, although they prove the association of oral diseases with primary HA symptoms. This may indicate future strategies for preventive measures for hypertensive children and adolescents.

Background: Regular physical activity is widely recommended for patients with arterial hypertension as an essential component of lifestyle modification. Much less is known about the impact of physical exercise on the management of treatment of resistant hypertension (RH). The aim was to assess the effect of physical activity program intensified by mobile phone text reminders on blood pressure control in subjects with RH managed in the primary care., Methods: In total, 53 patients with primary hypertension were qualified, including 27 who met the criteria for RH and 26 with well-controlled hypertension (WCH). Ambulatory 24-h blood pressure was monitored and body composition evaluated with bioimpedance and habitual physical activity profile was determined continuously over 72 h with accelerometer. All measurements were performed at baseline and after three and six months. The patients were asked to modify their lifestyle according to American Heart Association Guidelines that included regular aerobic physical activity tailored to individual needs.FindingsPhysical activity in RH increased significantly after six months compared with control subjects (P=0.001). Office systolic blood pressure (SBP) and diastolic blood pressure (DBP) in the RH group decreased significantly after three months but after six months only office DBP remained significantly lower. After three months 24-h SBP decreased by 3.1±11 mmHg (P=0.08) and DBP by 2.0±6 mmHg (P=0.17) in RH, whereas in WCH respective changes were +1.2±10 and -0.3±6 mmHg. After six months 24-h BP changes were similar., Conclusion: Individualized structured physical activity program increases physical activity in the treatment of resistant hypertensives in primary care but the effect on 24-h blood pressure is only transient.

Subclinical kidney disease is associated with developing hypertension in the general population, but data are lacking among HIV-infected people. We examined associations of kidney function and injury with incident hypertension in 823 HIV-infected and 267 HIV-uninfected women in the Women's Interagency HIV Study, a multicenter, prospective cohort of HIV-infected and uninfected women in the United States. Baseline kidney biomarkers included estimated glomerular filtration rate using cystatin C, urine albumin-to-creatinine ratio, and 7 urine biomarkers of tubular injury: α-1-microglobulin, interleukin-18, kidney injury molecule-1, neutrophil gelatinase-associated lipocalin, liver fatty acid-binding protein, N-acetyl-β-d-glucosaminidase, and α1-acid-glycoprotein. We used multivariable Poisson regression to evaluate associations of kidney biomarkers with incident hypertension, defined as 2 consecutive visits of antihypertensive medication use. During a median follow-up of 9.6 years, 288 HIV-infected women (35%) developed hypertension. Among the HIV-infected women, higher urine albumin-to-creatinine ratio was independently associated with incident hypertension (relative risk =1.13 per urine albumin-to-creatinine ratio doubling, 95% confidence interval, 1.07-1.20), as was lower estimated glomerular filtration rate (relative risk =1.10 per 10 mL/min/1.73 m 2 lower estimated glomerular filtration rate; 95% confidence interval, 1.04-1.17). No tubular injury and dysfunction biomarkers were independently associated with incident hypertension in HIV-infected women. In contrast, among the HIV-uninfected women, urine albumin-to-creatinine ratio was not associated with incident hypertension, whereas higher urine interleukin-18, α1-acid-glycoprotein, and N-acetyl-β-d-glucosaminidase levels were significantly associated with incident hypertension. These findings suggest that early glomerular injury and kidney dysfunction may be involved in the pathogenesis of hypertension in HIV-infected people. The associations of tubular markers with hypertension in HIV-uninfected women should be validated in other studies., (© 2016 American Heart Association, Inc.)

Intensive physical exercise may facilitate potassium release from skeletal muscles that may result in hyperkalemia. Commonly used drugs including angiotensin converting enzyme inhibitors (ACEI) and statins increase a risk of hyperkalemia. It is not known whether the effect of these drugs on serum potassium during physical exercise is additive. The study compared the effect of physical exercise on the changes of serum potassium in hypertensive patients receiving ACEI alone or in combination with statin. Eighteen patients with arterial hypertension with normal renal function were included in a prospective placebo-controlled cross-over study. The patients underwent 3 exercise tests on a bicycle ergometer with 55 - 60% of maximum oxygen consumption each lasting 30 minutes, i.e. after being treated with ACEI alone for six months, and then in a random order after the administration of ACEI with statin or ACEI with placebo each time for eight weeks separated by 2-week wash-out. Serum potassium was measured with atomic emission flame spectrometry before and after 15 and 30 minutes exercise and after 30-minute recovery. During the exercise serum potassium concentration increased moderately but significantly during all exercise tests. Mean serum potassium during exercise remained within the normal range. There were no differences in the exercise-induced changes of serum potassium during the exercise tests performed after ACEI combined with statin or with placebo. Addition of statin to ACEI does not increase the risk of hyperkalemia in hypertensive patients with preserved renal function during physical exercise with intensity typical for routine daily activities.

Background: There are limitations of the use of several classes of antihypertensive drugs in patients after kidney transplantation (KTx), as well as contradictory opinions on their effects on progression of graft dysfunction. In this study we assessed the prevalence of arterial hypertension (HA) and the antihypertensive agents used by the patients long after KTx., Material/methods: This retrospective evaluation of the number and classes of antihypertensive drugs was based on medical records of 348 patients (140 F, 208 M; mean age 49 ± 13 years) late after KTx (mean time after KTx 78 ± 43 months). The data were related to graft function., Results: Ninety-three percent of patients after KTx required antihypertensive therapy. Only 8.7% were treated with 1 agent (mean eGFR 65.1 ± 27.4 ml/min), 26.3% received 2 drugs (eGFR 60.0 ± 25.8 ml/min), 34.2% received 3 drugs (eGFR 55.5 ± 23.4 ml/min), 20.1% received 4 drugs (eGFR 54.9 ± 24.9 ml/min), and 10.5% received ≥ 5 drugs (eGFR 45.9 ± 22.0 ml/min). The number of antihypertensive medications increased along with the deterioration of graft function. Dihydropyridine calcium antagonists (CCB) were the most common class of drugs recommended to the patients after KTx (81%), followed by β-adrenergic antagonists (74.4%); α-antagonists (40.2%), angiotensin-converting enzyme inhibitors (38.7%), diuretics (34.1%), clonidine (17.8%) and angiotensin II receptor blockers (9.5%)., Conclusions: HA is highly prevalent in KTx patients. Multidrug therapy is usually required for the treatment of HA in this population. Dihydropyridine CCB is the most common class of antihypertensive drugs used by them. Graft function is a determining factor in the number of antihypertensive agents.,

Most hypertensive dialysis patients are currently treated with angiotensin converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARB). Aliskiren, the direct renin inhibitor, has not been specifically studied in peritoneal dialysis patients. The aim of the study was to compare hypotensive effects of aliskiren and ramipril and their influence on serum potassium and inflammatory parameters in hypertensive peritoneal dialysis patients. Eighteen hypertensive patients on chronic peritoneal dialysis were enrolled in an open-label comparative fixed-order study. The patients had been off RAAS blocking drugs for ≥4 weeks prior to an inclusion. At each of 3 study visits (baseline and after each of the treatment periods) blood pressure, serum lipids, potassium, renin, aldosterone, C-reactive protein (CRP) and monocyte chemotactic protein-1 (MCP-1) were measured. After the baseline visit aliskiren was started (150 mg/d) and after 12 weeks replaced with ramipril (5 mg/d) for the next 12 weeks. Blood pressure was 142/88±15/11 mmHg at baseline, 137/84±10/8 mmHg after aliskiren (ns) and 126/81±11/7 mmHg after ramipril (p<0.05 vs baseline and aliskiren). No incidents of hyperkalemia were observed. Plasma renin concentration increased significantly during aliskiren treatment compared to ramipril (227,6±844 vs. 58,3±765 pg/mL). CRP was similar after both therapies (8,8±34 vs. 8,4±32 µg/mL) but MCP-1 concentration was significantly lower after aliskiren than after ramipril (294,0±172,6 vs. 358,9±183,3 pg/mL). Aliskiren 150 mg/day decreases blood pressure less effectively than ramipril 5 mg/day in peritoneal dialysis patients. It does not influence serum potassium. The decrease of MCP-1 concentration after aliskiren treatment may provide an indirect evidence for its blood pressure independent cardioprotective and anti-inflammatory effects., (Copyright © 2012 S. Karger AG, Basel.)

Moxonidine is a selective imidazoline receptor agonist with comparable blood pressure-lowering efficacy to first-line antihypertensives and favorable metabolic effects. YKL-40 (chitinase-3-1-protein) has been proposed as a new marker of inflammation, atherosclerosis and endothelial dysfunction in neoplastic, cardiovascular and metabolic diseases but has not yet been studied in the context of essential hypertension. Fifteen patients (10 M, 5 F; age 48+/-14 years) with arterial hypertension and insulin resistance (HOMA-IR index >2.77) on at least two antihypertensive drugs were randomized to receive either moxonidine (0.4 mg) or amlodipine (10 mg) for two 8-week periods with a 7-day wash-out. Serum insulin, glucose, C-reactive protein (CRP), lipids, uric acid, YKL-40 and blood pressure were measured and insulin sensitivity was calculated (HOMA) at the beginning and end of each study phase. Mean BP decreased significantly with both moxonidine and amlodipine (-9.8+/-7.6 and -10.4+/-7.3 mm Hg, respectively). Serum high-density lipoprotein cholesterol increased with both therapies, but only moxonidine-affected serum triglycerides. No significant changes in serum uric acid, CRP, YKL-40 (2.3 and 3.3 ng ml(-1), respectively) or HOMA index (0.70+/-2.4 and 0.76+/-2.8) were observed. There was a strong negative correlation between serum uric acid and YKL-40 concentration at baseline (r=-0.77, P=0.01). Serum YKL-40 did not correlate with blood pressure, biochemical parameters or HOMA index. Moxonidine is an effective adjunctive antihypertensive agent for use in patients with hypertension and insulin resistance that induces beneficial effects on serum lipid profile but does not reduce insulin resistance, inflammation or serum YKL-40 concentration.

Background: For some hypertensive patients, conventional blockade of the renin-angiotensin-aldosterone system with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers does not adequately protect against target organ damage. This may be particularly true for hypertensive patients with obesity, a condition often associated with elevated aldosterone levels., Methods: We conducted a pre-post study of fixed, low-dose spironolactone (12.5 mg/d), added to chronic ACE inhibitor-based antihypertension regimens, in obese subjects with essential hypertension and preexistent target organ damage. Outcomes of interest were changes in blood pressure (office, 24-h, and nocturnal), urinary albumin excretion, and potassium., Results: 21 subjects with mean age 57.3 +/- 7.1 years, BMI 32.4 +/- 3.4 kg/m2 and 12.0 +/- 7.0 years of antihypertensive therapy were enrolled. The mean aldosterone level before spironolactone treatment was 10.1 +/- 7.3 ng/dl, and over 40% of subjects had baseline levels greater than mean population levels. During 4 weeks of low-dose spironolactone, mean office (110.6 +/- 7.8 to 105.0 +/- 8.1 mmHg, p = 0.004), 24-hour ambulatory (100.6 +/- 9.4 to 95.5 +/- 7.1 mmHg, p = 0.03) and nocturnal (95.3 +/- 11.5 to 87.5 +/- 8.2, p = 0.004) blood pressures all declined significantly. Log urine albumin : creatinine ratios also significantly dropped during spironolactone treatment (p = 0.002); in multivariate analysis, this decline did not appear to be due to changes in blood pressure but was influenced by concomitant changes in estimated glomerular filtration rate. Both the reductions in blood pressure and albumin excretion reversed after withdrawal of spironolactone. Serum potassium levels were essentially unchanged by low-dose spironolactone (p = 0.9)., Conclusions: A fixed, low-dose of spironolactone, added to chronic ACE inhibitor therapy, reduced blood pressure and urinary albumin excretion in obese subjects with hypertension and preexistent target organ damage. A relative hyperaldosteronism due to aldosterone escape and/or obesity may explain the beneficial effects of spironolactone therapy in this study.

Background: The aim of this nationwide analysis was to assess the incidence and current treatment profile of arterial hypertension in children undergoing chronic haemodialysis or peritoneal dialysis and attitudes of paediatric nephrologists towards the choice of antihypertensive drugs in their patients., Methods: The study group consisted of 134 children (89 males, 45 females, mean age 10.7+/-5 years) from all 13 paediatric dialysis centres in Poland. The data were gathered through a questionnaire for each patient dialysed in November 2004., Results: The overall incidence of hypertension in the study group was 55% (74 of 134 patients; 47 males, 27 females). The incidence rate was similar in boys and girls (53 vs 60%) and in those on haemodialysis and peritoneal dialysis (56 vs 54%). Chronic glomerulonephritis as an underlying renal disease was significantly more frequent in the hypertensive than in the normotensive subjects (37 vs 10%, P = 0.004). Residual urine output was higher in normotensives (41 vs 10 ml/kg body weight; P < 0.001). Among those treated with antihypertensives: 32% were treated by monotherapy, 36% received two drugs, 22% received three drugs, while 7% received > or = 4 drugs. The therapy was effective in only 57% of subjects. We observed no differences in biochemical and clinical parameters between those who responded to the therapy and those who failed to do so. Calcium channel blockers constituted the most frequently administered class of drugs [73% of children; in 43 out of 48 (90%) combined with other drugs, but in 11 out of 24 (46%) as a monotherapy]. In monotherapy, angiotensin-converting enzyme inhibitors and calcium channel blockers were administered most frequently., Conclusion: We conclude that the incidence of hypertension in dialysis children in Poland is high (55%). The effectiveness of antihypertensive treatment is rather low (58%) and the choice of drugs is limited.

The term hypertension in pregnancy stands either for a high blood pressure, which has already developed before pregnancy (i.e., chronic hypertension in pregnancy), or for a pregnancy-associated disease (i.e., pregnancy-induced hypertension). Each form of hypertension may be an isolated phenomenon or constitute a part of the syndrome of preeclampsia or eclampsia. This review focuses mainly on the risk factor assessment, prevention and treatment of hypertension developing during pregnancy. Despite a frequent occurrence of this disease its prevention and treatment is still a subject of debates, and only a limited number of studies, which fulfill the criteria of "evidence-based medicine" have so far been performed in this field. Although the impressive advances in treatment of hypertension in the general population have been done, the choice of drugs and control of hypertension developing during pregnancy is still far from being satisfactory.

Insulin resistance and hyperinsulinaemia are presumed to participate in the pathogenesis of essential hypertension (EH). Insulin resistance is characterised by an impaired insulin-mediated glucose uptake. Participation of the renin-angiotensin system in the development of hyperinsulinaemia in EH patients has not been unanimously proven. The present study aimed to asses the influence of antihypertensive therapy with angiotensin converting enzyme inhibitor (ACEI, enalapril = 10 mg/day) (9 male patients) or angiotensin II AT-1 receptor blocker (A II RB = losartan 50 mg/day) (9 male patients) respectively on insulin sensitivity in patients with EH. 3-hours euglycaemic clamp test with constant infusion of insulin (50 mU/m2/min) was performed twice: before and after 8 weeks of therapy with ACEI or A II RB respectively. The control group (CG) consisted of 12 healthy males (clamp test was performed once). Serum insulin concentration (I) was estimated by radioimmunoassay. Glucose disposal rate (M-value = mg/kg/min) and tissue insulin sensitivity (M/I value = mg/kg/min per mU/l) were calculated in subjects of the CG and in patients with EH before and after antihypertensive therapy with ACEI or A II RB, respectively. In CG the M-value (7.38 +/- 0.13) and tissue insulin sensitivity (M/I = = 6.76 +/- 0.19) were significantly higher than in EH before treatment with ACEI (M-value = 5.44 +/- 0.16; M/I = = 4.57 +/- 0.18) or A II RB (M-value = 5.75 +/- 0.21; M/I = 4.77 +/- 0.31), respectively. ACEI therapy was followed by a significant increase of both M (6.82 +/- 0.25) and M/I (5.68 +/- 0.25) values. In contrast to ACEI, treatment with A II RB did not influence neither M (5.75 +/- 0.21) nor M/I (4.79 +/- 0.21) values respectively. In contrast to A II RB, ACEI shows a beneficial effect on insulin sensitivity in EH patients. This effect does not seem to be mediated by an influence on the AT-1 receptor.

Insulin stimulates the production of endothelin-1 (ET-1) and nitric oxide (NO) by isolated endothelial cells. Additionally, insulin-dependent glucose transport and insulin-mediated NO production partially share common elements in signal transduction. There are discordant data on plasma ET-1 levels during acute euglycemic systemic hyperinsulinemia in normotensive men and men with essential hypertension (EH) (known to be insulin-resistant), as well as on the relations between insulin sensitivity and vascular function. Our aim was to assess the response of approximate measures of whole-body generation of NO and ET-1 to acute euglycemic hyperinsulinemia in EH patients and controls. We studied 17 newly diagnosed untreated men with uncomplicated EH and 10 normotensive controls. Plasma ET-1 and urinary excretion of nitrite plus nitrate, stable NO metabolites (Uno(x)), were measured before and during a 3-hour hyperinsulinemic-euglycemic clamp. Both in hypertensives and normotensives, plasma ET-1 levels were reduced after 2 hours of the clamp (EH: baseline, 3.1+/-1.9 pg/mL; 2 hours, 1.9+/-1.2 pg/mL, P = .04 v baseline; controls: baseline, 4.2+/-2.6 pg/mL; 2 hours, 2.8+/-1.4 pg/mL, P = .04 v baseline). No significant changes in Uno(x) during the clamp were observed. Changes in Uno(x) during the clamp (deltaUno(x)) and differences in plasma ET-1 measured before the end and before the beginning of the clamp (deltaET-1) were correlated in the controls (r = .75, P = .01) but not in EH (r = -.01, P = .97). No parameter of glucose metabolism correlated with basal Uno(x), basal plasma ET-1, deltaUno(x), and deltaET-1, whether absolute or percent values, in either group. Thus, acute euglycemic hyperinsulinemia produces a decrease in plasma ET-1 in both EH patients and controls. The lack of correlation between deltaUno(x) and deltaET-1 under these conditions in EH may suggest an impairment of systems governing interactions between the NO-dependent pathway and ET-1. In addition, insulin actions on glucose metabolism and on the endothelial mediators appear dissociated.

Our aim was to investigate systemic nitric oxide (NO) production and its potential determinants such as insulin resistance, dyslipidemia, and circulating methylated analogs of L-arginine in uncomplicated essential hypertension (EH). Nineteen newly diagnosed, untreated male subjects with mild pure uncomplicated EH and 11 normotensive controls were studied at rest after an overnight fast. The groups had comparable age, body mass index, creatinine clearance, cholesterol, fasting glucose, and insulin. In hypertensives, the urinary excretion rate of nitrite plus nitrate (Unox), an index of endogenous NO production, was depressed (56+/-17 vs. 77+/-23 micromol/mmol creatinine; p < 0.05), whereas plasma levels of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NO synthesis, were increased (2.4+/-1.1 vs. 1.1+/-0.7 microM; p < 0.005). Circulating concentrations of symmetric dimethylarginine were similar in both groups (1.4+/-1.3 vs. 1.5+/-1.1 microM; p = NS). The L-arginine-to-ADMA ratio was reduced in hypertension (3.3+/-0.5 vs. 4.5+/-0.8; p < 0.001 for In-transformed data). There was no correlation between Unox and either the magnitude of insulin resistance or dyslipidemia in EH. Thus in male subjects with EH, endogenous systemic NO formation appears depressed, which is unrelated to accompanying insulin resistance or dyslipidemia. Circulating ADMA levels are increased in uncomplicated EH, which may be of potential relevance.

Erythropoietin (Epo) is a glycoprotein hormone responsible for the control of the proliferation and differentiation of cells of erythroid lineage. Recombinant erythropoietin (rHuEpo) is widely used as a pharmacological agent for the treatment of the anaemia of renal failure. Efficacy of rHuEpo and its superiority over blood transfusions have been proven in large multicentre trials. The most important side-effect of the therapy is the increase of BP which is observed in approximately 30-35% of dialysis patients receiving rHuEpo. It appears that the haemodynamic resetting that occurs with partial correction of anaemia may be inappropriate resulting in an altered vascular resistance in relation to the cardiac output. This is in turn due to the combination of increased blood viscosity and loss of hypoxic vasodilatation. Both these factors, however, cannot account completely for the rise in vascular resistance, and therefore the possibility of a direct and/or hormonally-mediated vasopressor effect of rHuEpo has recently been raised. Moreover, scarce information exists on the possible involvement of endogenous erythropoietin in the pathogenesis of arterial hypertension and haematological disturbances observed in primary and some secondary forms of hypertension.

Adrenergic alpha 2-receptors mediate important regulatory functions in both the brain and the periphery. Activation of these receptors lowers blood pressure through a decrease in sympathetic and vasomotor nerve activity. Agonists of the alpha 2-adrenoceptors are often used in the treatment of arterial hypertension. As recently discovered, their chemical structure includes so called "imidazoline ring" and compounds with such chemical structure bind to nonadrenergic sites known as imidazoline receptors. These receptors are localized in midportions of the brain but they are also present in other organs such as lungs, heart, adrenal medulla, liver and kidneys. Their selective activation lowers blood pressure without inducing sedation typical for alpha 2-agonists. Several substances binding with high selectivity to imidazoline receptors have recently been synthesized. Some of them as rilmenidine and moxonidine have successfully been introduced to the treatment of arterial hypertension in humans.

Albuminuria is more prevalent in patients with primary hypertension than in normotensive subjects of the general population. The presence of albuminuria predicts the presence of more severe target organ damage and is related to the risk of cardiovascular events. Preliminary results show albuminuria even in some normotensive individuals with a genetic risk of hypertension and in association with insulin resistance. While albuminuria is generally more frequent in the elderly, it is also found in young patients with mild to moderate primary hypertension. It is uncertain whether in these circumstances albuminuria indicates some "renal component" in the etiology of primary hypertension. Massive albuminuria may occur in subjects with "benign" nephrosclerosis. Whether albuminuria is a predictor of hypertensive renal damage requires further study. Albuminuria is reduced by antihypertensive treatment, but diverse effects on albuminuria are seen with different antihypertensive agents.

We assessed the influence of hyperoxemia on erythropoietin secretion in patients with various etiological forms of arterial hypertension (essential, n = 15; renoparenchymal, n = 16; renovascular, n = 15) and in 15 healthy subjects. On the first day of the study, blood was withdrawn at 1-hour intervals for the estimation of erythropoietin during a total of 6 hours and at 2-hour intervals for the assessment of PO2. Three days later the same parameters were assessed again at identical time intervals, but the subjects were breathing pure oxygen during the first 2 hours. Breathing with pure oxygen resulted in a significant increase of blood PO2 (184.85 +/- 4.47 versus 85.92 +/- 2.28 in essential, 185.21 +/- 5.52 versus 84.55 +/- 3.04 in renoparenchymal, and 181.7 +/- 3.14 versus 87.49 +/- 2.25 in renovascular hypertension groups and 189.84 +/- 5.2 versus 85.89 +/- 1.73 mm Hg in healthy subjects; P < .001 in all groups). Baseline plasma erythropoietin was not different among the groups (29.33 +/- 4.14 in essential, 24.56 +/- 3.09 in renoparenchymal, and 27.77 +/- 3.29 in renovascular hypertension groups and 24.23 +/- 2.70 mU/mL in the control group). The pattern of erythropoietin decline was different in the groups of hypertensive patients. In patients with essential hypertension, unlike in healthy subjects and patients with other etiological forms of arterial hypertension, only a very short-term suppression of erythropoietin levels was observed during hyperoxemia. No significant changes in blood pressure during breathing with pure oxygen were found in any of the studied groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Recent data indicated the importance of urinary losses of erythropoietin (Epo) in the pathogenesis of anaemia in patients with nephrotic syndrome. In the present study we aimed to investigate plasma and urinary Epo levels and their renal handling in relation to beta 2-microglobulin (beta 2m), sodium metabolism and the renin-angiotensin-aldosterone system (RAAS), respectively, in patients with sub-nephrotic range proteinuria (SNP), microalbuminuric diabetics and hypertensives, and in healthy subjects studied on a standardized diet containing 120 mmol sodium and 70 g protein per day. We found that patients with SNP were characterized by lower plasma levels of Epo than healthy subjects but no differences were found in urinary excretion of Epo, endogenous Epo clearance and its fractional excretion (FEEpo). There were no differences between groups in FE beta 2m and FENa and plasma aldosterone levels but plasma renin activity was higher in patients with SNP than in the controls. No relationships were found between Epo levels and activity of the RAAS and sodium metabolism, respectively. Our data suggest that lower levels of plasma Epo in patients with SNP and normal renal excretory function are not due to urinary losses of Epo but rather to the decreased production/degradation ratio.

Regulation of renal erythropoietin (EPO) production has not yet been clearly established in physiologic as well as in pathologic conditions. Recent studies suggest a possible role for renin-angiotensin system in control of EPO production. An elevation in blood pressure occurs commonly in patients with various forms of anaemia treated with recombinant human EPO. Furthermore it has been found that EPO can alter secretion of hormones engaged in regulation of intravascular fluid volume and vascular resistance. The aim of this study was to determine whether patients with essential hypertension (EH) and healthy subjects differ in EPO secretion and whether EPO serum level is related to renin response to dietary sodium restriction and upright position of the body. 63 patients with EH and 12 healthy subjects were investigated. Patients with EH were divided into subgroups on the following criteria: renin response to dietary sodium restriction and upright position of the body. 63 patients with EH and 12 healthy subjects were investigated. Patients with EH were divided into subgroups on the following criteria: renin response to dietary sodium restriction and upright position of the body and severity of existing hypertension. In all subjects haematocrit value, haemoglobin concentration, erythrocyte count, sodium, potassium, creatinine, iron, ferritin serum levels, total iron binding capacity, plasma renin activity (PRA), erythropoietin serum level and mean arterial blood pressure (MAP) were measured in basic conditions (normal sodium diet). Additionally PRA, EPO and MAP were measured after dietary sodium restriction for three days and upright position of the body for three hours.(ABSTRACT TRUNCATED AT 250 WORDS)

Recent studies suggest the existence of a relationship between the renin-angiotensin system and erythropoietin (EPO) secretion. It has been studied whether patients with various forms of arterial hypertension (essential, renal, renovascular, in the course of arteritis) differ with respect to EPO secretion and whether EPO serum levels are related to renin response induced by dietary sodium restriction to 10-20 mmol Na/24 h for 3 days and upright body position for 3 h. Patients with different forms of hypertension and normal renal excretory function and healthy subjects did not differ in hematocrit value, markers of iron metabolism, and EPO secretion except for patients with arteritis who had higher ferritin values. In these patients a positive correlation between EPO levels and hematocrit values suggests the existence of an altered regulation of EPO secretion. In essential hypertension a negative correlation found between changes in EPO and PRA levels in response to sodium restriction and upright body position may also reflect an altered regulation of both EPO and renin production.

QT/QS2 ratio has been assessed in 26 patients with both borderline and mild hypertension and mitral valve prolapse syndrome (19 patients), and hyperthyroidism (16 patients) in comparison with method control groups. The following polycardiographic parameters have been analyzed: QT, QTp, QS2, QT/QS2, and QTp/QS2. Higher values of QT/QS2 ratio have been noted in patients with mitral valve prolapse syndrome and hyperthyroidism than that in the control group. There has been no difference in patients with mild hypertension while the values of the analyzed parameter have been significantly lower in patients with borderline hypertension. QT has been longer than QS2 (QT)QS2 1/in 9 (56%) patients with hyperthyroidism. A positive correlation between QT/QS2 ratio and ++thyroxine levels have been noted in these patients. QT values have been higher than QS2 values only in 1 patient with mild hypertension. It seems that QT/QS2 value has limited value as an indirect index of the adrenergic activity in the dysfunction of the autonomic nervous system.

In 30 patients with renovascular hypertension, 50 with hypertension in a course of arteries, 71 hypertensive subjects with coexisting parenchymal nephropathy and in 63 with primary hypertension the captopril test was performed after 8 hours night rest and within high sodium diet. Positive test result was stated in 76.67% of patients with renovascular hypertension, in 70.59% of patients with arteritis, in 53.52% of patients with hypertension and coexisting parenchymal nephropathy and in 63.49% of patients with primary hypertension. Significant correlation between increase of plasma renin activity and blood pressure decrease after captopril administration was only stated in patients with renovascular hypertension and in those with arteritis. Results of performed studies impaired the captopril test value in diagnostics of renin-dependent hypertension.