TY - JOUR
T1 - Effect of treatment with nebivolol on parameters of oxidative stress in Type 2 diabetics with mild to moderate hypertension
AU - Peter, P
AU - Sharma, A
AU - Martin, Una
AU - Dunne, F
PY - 2006/4/1
Y1 - 2006/4/1
N2 - AIM: The aim of this study was to examine the effect of the cadioselective B(1)-adrenoceptor blocker nebivolol on glycaemic control, lipid profile and markers of oxidative stress in patients with type 2 diabetes over a 6-month period. METHODS: Twenty-six patients with mild to moderate hypertension (140-160 mmHg systolic, 90-105 mmHg diastolic) confirmed on 24-h blood pressure monitoring, were treated with nebivolol 5 mg daily for 6 months. Total serum cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol and low-density lipoprotein (LDL) subfractions, lipid hydroperoxides (LHPs) and total antioxidant capacity (TAC) were measured before and after 6 months of treatment. RESULTS: Nebivolol, as expected, reduced mean daytime systolic and diastolic pressures on ambulatory monitoring (149 +/- 9 to 140 +/- 13 mmHg, P = 0.02 and 84 +/- 7 to 77 +/- 9 mmHg, P <0.001). There were no significant changes in serum cholesterol or triglycerides following treatment but a significant increase in HDL cholesterol was noted (1.12 +/- 0.19 to 1.25 +/- 0.36 mmol/L, P = 0.008). Patients showed a highly significant reduction in TAC from 501 +/- 57 to 422 +/- 29 trolox equivalent (P <0.001). Baseline LHPs were very high and showed no significant change over the 6-month period (18.7 +/- 7.4 and 18.7 +/- 10.9 micromol/L). The LDL score increased significantly from 1.7 +/- 0.7 to 2.3 +/- 0.7 (P = 0.0002) at 6 months suggesting a change to a more atherogenic lipid profile. Neither weight nor glycaemic control changed during treatment. CONCLUSION: Nebivolol appears to be lipid neutral and may even have a positive effect on HDL cholesterol. Despite this it may promote the formation of potentially atherogenic LDL subfractions possibly as a result of reduced antioxidant defences. Further studies are needed to clarify the changes observed in parameters of oxidative stress.
AB - AIM: The aim of this study was to examine the effect of the cadioselective B(1)-adrenoceptor blocker nebivolol on glycaemic control, lipid profile and markers of oxidative stress in patients with type 2 diabetes over a 6-month period. METHODS: Twenty-six patients with mild to moderate hypertension (140-160 mmHg systolic, 90-105 mmHg diastolic) confirmed on 24-h blood pressure monitoring, were treated with nebivolol 5 mg daily for 6 months. Total serum cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol and low-density lipoprotein (LDL) subfractions, lipid hydroperoxides (LHPs) and total antioxidant capacity (TAC) were measured before and after 6 months of treatment. RESULTS: Nebivolol, as expected, reduced mean daytime systolic and diastolic pressures on ambulatory monitoring (149 +/- 9 to 140 +/- 13 mmHg, P = 0.02 and 84 +/- 7 to 77 +/- 9 mmHg, P <0.001). There were no significant changes in serum cholesterol or triglycerides following treatment but a significant increase in HDL cholesterol was noted (1.12 +/- 0.19 to 1.25 +/- 0.36 mmol/L, P = 0.008). Patients showed a highly significant reduction in TAC from 501 +/- 57 to 422 +/- 29 trolox equivalent (P <0.001). Baseline LHPs were very high and showed no significant change over the 6-month period (18.7 +/- 7.4 and 18.7 +/- 10.9 micromol/L). The LDL score increased significantly from 1.7 +/- 0.7 to 2.3 +/- 0.7 (P = 0.0002) at 6 months suggesting a change to a more atherogenic lipid profile. Neither weight nor glycaemic control changed during treatment. CONCLUSION: Nebivolol appears to be lipid neutral and may even have a positive effect on HDL cholesterol. Despite this it may promote the formation of potentially atherogenic LDL subfractions possibly as a result of reduced antioxidant defences. Further studies are needed to clarify the changes observed in parameters of oxidative stress.
KW - nebivolol
KW - hypertension
KW - type 2 diabetes
KW - oxidative stress
UR - http://www.scopus.com/inward/record.url?scp=33645472417&partnerID=8YFLogxK
U2 - 10.1111/j.1365-2710.2006.00718.x
DO - 10.1111/j.1365-2710.2006.00718.x
M3 - Article
C2 - 16635049
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
SN - 1365-2710
VL - 31
SP - 153
EP - 159
JO - Journal of Clinical Pharmacy and Therapeutics
JF - Journal of Clinical Pharmacy and Therapeutics
ER -