Search

Hypertension terms 'dipper' and 'non-dipper' are propounded by the change that occurs during ambulatory blood pressure (BP) monitoring. The purpose of this study is to present whether the serum urotensin II levels are different in patients with dipper and non-dipper hypertension and to put forward the effects causing this difference, if there are any. Patients recently diagnosed with hypertension were included in the study. With ambulatory BP monitoring, 81 patients with high BP were divided into two groups, dipper ( n = 40) and non-dipper ( n = 41). Serum urotensin II levels were analyzed by ELISA method. Serum urotensin II levels were higher in patients with non-dipper hypertension than in patients with dipper hypertension (204 [106-533] vs. 140 [96-309], P = .004). There was a positive correlation between total systolic BP and serum urotensin II levels ( r = 0.408 and P = .009), but the relation in the non-dipper hypertension group was not significant ( r = 0.194 and P = .2). In conclusion, serum urotensin II levels were higher in non-dipper HT patients than dipper HT patients. This higher urotensin II level might be responsible for poor prognoses. [ABSTRACT FROM AUTHOR]

Background. We aimed to determine the status of the autonomic nervous system in patients with autosomal-dominant polycystic kidney disease (ADPKD) who were normotensive and had normal renal function. Methods. A total of 28 normotensive ADPKD patients with normal renal function and 30 healthy control subjects consented to participate in the study. Heart rate recovery (HRR) indices were defined as the reduction in heart rate from the rate at peak exercise to the rate at the 1st, 2nd, 3rd and 5th minutes after the cessation of the exercise stress test; these results were indicated HRR1, HRR2, HRR3 and HRR5, respectively. Results. The 1st- and 2nd-minute HRR indices of patients with ADPKD were significantly lower than those of the healthy control group (27.1±7.9 vs 32.0±7.9; p=0.023 and 46.9±11.5 vs 53.0±9.0; p=0.029, respectively). Similarly, HRR indices after the 3rd and 5th minutes of the recovery period were significantly lower in patients with ADPKD when compared with indices in the control group (56.7±12.0 vs 65.1±11.2; p=0.008 and 62.5±13.8 vs 76.6±15.5; p =0.001, respectively). Conclusion. Impaired HRR index is associated with normotensive early-stage ADPKD patients. Increased renal ischemia and activation of the renin-angiotensin-aldosterone system (RAAS) may contribute to impairment in the autonomic nervous system in these patients before the development of hypertension. Even if ADPKD patients are normotensive, there appears to be an association with autonomic dysfunction and polycystic kidney disease. [ABSTRACT FROM AUTHOR]

The Seventh Report of the Joint National Committee on the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure classifies blood pressure (BP) as normal, prehypertension, and hypertension. Although it has been shown that there is a relationship between hypertension and arterial stiffness, there is not sufficient data about arterial stiffness in patients with prehypertension. The present study was designed to evaluate arterial stiffness and wave reflections in subjects with prehypertension. We evaluated arterial stiffness and wave reflections of 45 subjects with prehypertension and an age-matched control group of 40 normotensive individuals, using applanation tonometry (Sphygmocor, AtCor Medical, Sydney, Australia). Aortic pulse wave velocity (PWV) was measured as indices of elastic-type aortic stiffness. The heart rate-corrected augmentation index (AIx@75) was estimated as a composite marker of wave reflections and arterial stiffness. Aortic PWV (10 ± 2.5 vs. 8.6 ± 1.7, m/s, p = 0.004) and AIx@75 (21 ± 8.3 vs. 10 ± 9.1, %, p = 0.0001) were significantly higher in subjects with prehypertension than in the control group. In multiple linear regression analysis, we found that the presence of the prehypertension was a significant predictor of aortic PWV (β = 0.26, p = 0.009) and AIx@75 (β = 0.46, p = 0.0001). Our results suggest that arterial functions were impaired even at the prehypertensive stage. [ABSTRACT FROM AUTHOR]

Augmentation index (AIx), a measure of wave reflection, is regulated by a number of factors, including endothelial function and vascular smooth muscle tone. The relationship between local endothelium-derived factors and AIx is well known; however, association between endothelial damage markers and AIx has not been sufficiently studied. This study investigates whether endothelial damage markers—von Willebrand factor (vWF) soluble thrombomodulin (sTM)—are associated with wave reflections. We studied 46 (48.5 ± 10.6, years) never-treated patients with hypertension (HT) and an age-matched control group of 40 (47 ± 8.6, years) normotensive individuals. von Willebrand factor and sTM levels were determined in all subjects. We evaluated the aortic AIx of the study population using applanation tonometry (Sphygmocor, AtCor Medical, Sydney, Australia). The heart rate-corrected augmentation index (AIx@75) was estimated as a marker of wave reflections. Endothelial damage markers and AIx@75 were significantly higher in hypertensive patients than in controls. In the whole population, the vWF level (β = 0.24, p = 0.01) was an independent determinant of AIx@75 in multivariate analysis. However, the sTM level was not associated with AIx@75. We found that the vWF level was an independent determinant of AIx@75. Our results suggest that increased an vWF level contributes significantly to increased wave reflections. [ABSTRACT FROM AUTHOR]

Background. The role of endogenous relaxin on hypertensive cardiovascular damage remains unknown. We investigated the relaxin level and its relation to cardiovascular function in patients with never treated hypertension (HT). Methods. We studied 42 (47.8±10 years) never treated patients with HT and 40 age-matched (47±8.6 years) normotensive individuals. Serum relaxin levels were determined in all subjects using enzyme-linked immunosorbent assay. Left ventricular (LV) diameters were evaluated by transthoracic echocardiography. Ejection fraction and LV mass index were measured. Diastolic functions were evaluated with both conventional and tissue Doppler echocardiography. We evaluated central aortic pressures, heart rate-corrected augmentation index (AIx@75), a marker of wave reflections, and aortic pulse wave velocity (PWV) as indices of elastic-type aortic stiffness of the study population using applanation tonometry (SphygmoCor). Results. Relaxin levels were significantly lower in hypertensive patients as compared with controls (36.5±7.3 vs 49.7±39.8 pg/ml, p=0.03). The relaxin level was negatively correlated with brachial and central aortic pressure. However, serum relaxin was not significantly associated with LV diameters, ejection fraction, LV mass index, LV diastolic function, AIx@75 or aortic PWV in our study. Conclusion. Serum relaxin is decreased in patients with HT. However, low endogenous relaxin is not related to cardiovascular function. [ABSTRACT FROM AUTHOR]