Neurovascular Hypertension and Kidney Disease
Neurovascular Hypertension and Kidney Disease
Lambert G.W.,Baker IDI Heart and Diabetes Institute |
Lambert G.W.,University of Sfax |
Hering D.,Neurovascular Hypertension and Kidney Disease |
Hering D.,University of Western Australia |
And 20 more authors.
Journal of Hypertension | Year: 2015
Aim: To examine the effect of renal denervation (RDN) on blood pressure (BP) and health-related quality of life (QoL) in patients with resistant hypertension, pseudoresistant hypertension due to a white-coat effect and in patients with uncontrolled masked hypertension. Methods: Using the Medical Outcomes Study 36-Item Short-Form Health Survey (SF-36), Beck Depression Inventory (BDI) and Spielberger's state and trait anxiety questionnaires, we examined QoL, symptoms of depression and anxiety prior to and 12 months following RDN. BP was assessed from clinic and ambulatory blood pressure monitoring (ABPM) recordings. Results: Patients with uncontrolled masked hypertension had the highest BDI and anxiety scores among all groups at baseline. Twelve months following RDN clinic and ambulatory BP were reduced only in those patients with resistant hypertension (delta SBP: clinic-16±3 mmHg, ABPMday-8±2 mmHg, ABPMnight-8±2mmHg, all P<0.01). Clinic BP was reduced in the pseudoresistant group (-17±6mmHg, P<0.01) but was elevated in the uncontrolled masked group (R13±6mmHg, P0.02). In all patients, trait anxiety (P<0.05), BDI scores (P<0.05) and the SF-36 mental component summary (MCS) score (P<0.001) were improved. The improvement in the SF-36 MCS was confined to those patients with resistant hypertension (R4.0±1.1, P<0.01). The change in clinic BP after RDN was related to the baseline clinic BP (systolic: r=0.54, P<0.001; diastolic r=0.43, P<0.001), the number of ablations delivered (both clinic and mean day ABPM systolic r=0.24, P<0.05) and to the change in SF-36 MCS score (systolic: r=0.25, P=0.01; diastolic r=0.24, P=0.02). Conclusion: These results indicate that in patients with confirmed resistant hypertension, RDN is associated with a reduction in BP and a sustained improvement in mental health-related aspects of QoL. © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Reimann M.,University Hospital Carl Gustav Carus |
Hamer M.,University College London |
Malan N.T.,North West University South Africa |
Schlaich M.P.,Neurovascular Hypertension and Kidney Disease |
And 4 more authors.
Psychosomatic Medicine | Year: 2013
Objective: This study investigated the impact of stress on effectors of the L-arginine/nitric oxide (NO) system including the endogenous inhibitor asymmetric dimethylarginine (ADMA). Methods: Black (n = 168) and white (n = 206) South African teachers were exposed to a mental and a physical stressor for 1 minute, respectively. Serum samples for determination of L-arginine, NO metabolites, ADMA, and symmetric dimethylarginine (SDMA) were obtained at rest and during stress exposure. Perception of task stressfulness was assessed on a 7-point Likert scale, and psychological distress was estimated by the General Health Questionnaire. Results: Black South Africans exhibited higher resting levels of NO metabolites (adjusted mean [standard error of the mean] = 11.3 [1.3] versus 3.9 [1.1] μmol/l, p < .001) but lower circulating ADMA (0.62 [0.02] versus 0.70 [0.02] μmol/l, p = .004) and SDMA (0.41 [0.01] versus 0.53 [0.01] μmol/l, p < .001) than did white South Africans. Ethnicity-by-psychological distress interaction was observed for resting levels of ADMA (p = .002), SDMA (p = .038), and L-arginine (p = .048). Ethnic differences in responses to experimental stress were evident for NO metabolites (blacks versus whites: 5.94 [1.55] versus -0.74 [1.25] μmol/l, p = .004) and SDMA (blacks versus whites: -0.02 [0.01] versus 0.02 [0.01] μmol/l, p = .004). Ethnicity-by-psychological distress interaction for stress responses was found for L-arginine/ADMA ratio (p = .027). Conclusions: The L-arginine/NO system is affected by psychosocial distress with higher susceptibility in black South Africans. This interaction may contribute to the higher cardiovascular disease risk in black South Africans. Copyright © 2013 by the American Psychosomatic Society.
Straznicky N.E.,Human Neurotransmitters |
Grima M.T.,Human Neurotransmitters |
Lambert E.A.,Human Neurotransmitters |
Eikelis N.,Neurovascular Hypertension and Kidney Disease |
And 8 more authors.
Journal of Hypertension | Year: 2011
Objective: Metabolic syndrome (MetS) obesity is an independent risk factor for chronic kidney disease. This study was conducted to examine the effects of lifestyle interventions on renal parameters and putative metabolic, neuroadrenergic and hemodynamic mediators of renal injury. Methods: Untreated men and women (mean age 55 ± 1 years; BMI 32.7 ± 0.6 kg/m) without pre-existing renal dysfunction, who fulfilled MetS criteria were randomized to dietary weight loss (WL, n = 13), weight loss combined with aerobic exercise (WL + EX, n = 13), or no treatment (control, n = 12). Estimated glomerular filtration rate (eGFR), 24 h urinary albumin excretion, plasma renin activity (PRA), muscle sympathetic nerve activity (MSNA), baroreflex sensitivity (BRS), anthropometric, metabolic and fitness variables were measured at baseline and week 12. Results: Body weight decreased by -8.2 ± 0.8% in the WL and -10.7 ± 0.9% in the WL + EX groups (both P < 0.001). Fitness (maximal oxygen consumption) increased by 15 ± 5% and BRS by 5.5 ± 2.4 ms/mmHg in the WL + EX group only (P < 0.05). Serum creatinine decreased by -8.1 ± 4.8%, (WL, P = 0.016) and -14.9 ± 3.0% (WL + EX, P < 0.001). Estimated GFR increased commensurately but the increment was greater in the WL + EX group (P = 0.04). Albuminuria (P < 0.05) and MSNA (P < 0.001) decreased similarly in both groups, whereas PRA, high sensitivity C-reactive protein, uric acid and DBP decreased only in the WL + EX group (all P < 0.05). Conclusion: Moderate weight loss in obese MetS patients is associated with a reduction in albuminuria and an improvement in eGFR which is augmented by exercise co-intervention. © 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins.