Blood Pressure Response to Physical Exercise in Healthy Adolescents and Adolescents with Insulin-Dependent Diabetes Mellitus

1994 ◽  
Vol 86 (4) ◽  
pp. 425-432 ◽  
Author(s):  
H. Nordgren ◽  
U. Freyschuss ◽  
B. Persson

1. Reference values for systolic blood pressure during exercise are provided for 88 healthy adolescents (12–22 years of age) of both sexes. Data were related to oxygen uptake, heart rate, blood lactate concentration, rate of perceived exertion, age, sex, body size and physcial fitness. 2. The same variables were measured in 55 adolescents of both sexes with insulin-dependent diabetes mellitus of about 12 years duration and were analysed with respect to the healthy control group, to degree of metabolic control and to late diabetic complications. 3. In healthy adolescents the pressure response was not related to sex or age. When compared with control subjects diabetic patients had a higher diastolic blood pressure at rest and a more marked blood pressure increase, 23 versus 19 mmHg W−1 kg−1 body weight, during exercise with no sex difference. The blood pressure rise was not related to metabolic control, glomerular hyperfiltration or physical fitness. 4. Prolonged exercise tests were no more informative regarding the blood pressure response to exercise than the stepwise increased load test. Analysing the blood pressure increase versus relative work load (W/kg body weight) during exercise reveals blood pressure differences otherwise not noted. A diabetic patient with blood pressure above the 97.5% confidence limit during exercise seems to have a higher risk of developing incipient nephropathy 5 years later.

1999 ◽  
pp. 341-349 ◽  
Author(s):  
M Kawaguchi ◽  
K Koshimura ◽  
Y Murakami ◽  
M Tsumori ◽  
T Gonda ◽  
...  

It has been reported that insulin treatment improves hypertension in patients with diabetes mellitus. The mechanisms of the antihypertensive effect of insulin, however, remain to be fully elucidated. In the present study, we investigated a possible involvement of nitric oxide (NO) in insulin-induced reduction of blood pressure using the Zucker diabetic fatty (ZDF) rat, an animal model of non-insulin-dependent diabetes mellitus. The animals were divided into three groups and treated for 4 weeks with daily subcutaneous injections of insulin (25U/kg body weight) with or without oral administration of l-nitro-arginine methyl ester (L-NAME, 50mg/kg/day body weight as drinking water), an inhibitor of NO synthase (NOS). Saline solution was injected subcutaneously in the control groups. During the experimental period, body weight gain was greater in the insulin-treated groups than in the control groups whereas water intake was considerably decreased in the insulin-treated groups. Insulin treatment resulted in a decrease in plasma glucose and blood pressure, and an increase in both NO metabolites (NOx) in the plasma and NOS activity in the aorta tissue. L-NAME treatment blunted not only the antihypertensive effect of insulin but also the changes in NOx and NOS activity. These findings suggest that insulin reduces blood pressure in the ZDF rat by stimulating NOS activation and NO production.


Hypertension ◽  
1997 ◽  
Vol 30 (5) ◽  
pp. 1162-1168 ◽  
Author(s):  
Jan Lambert ◽  
Rik Pijpers ◽  
Frans J. van Ittersum ◽  
Emile F.I. Comans ◽  
Mieke Aarsen ◽  
...  

1998 ◽  
Vol 133 (1) ◽  
pp. 46-50 ◽  
Author(s):  
Laura A. Young ◽  
Thomas R. Kimball ◽  
Stephen R. Daniels ◽  
Debra A. Standiford ◽  
Philip R. Khoury ◽  
...  

1995 ◽  
Vol 23 (6) ◽  
pp. 467-472 ◽  
Author(s):  
S Okada ◽  
K Ishii ◽  
H Hamada ◽  
K Ichiki ◽  
S Tanokuchi ◽  
...  

The possibility that glycosylated haemoglobin levels and/or blood pressure might correlate with cardiac sympathetic neuropathy and/or diabetic somatic neuropathy was investigated in patients with non-insulin-dependent diabetes mellitus. Sympathetic nerve function was quantified by analysis of [123I]metaiodobenzylguanidine accumulation in the cardiac muscle. Somatic nerve function was assessed by measuring the motor nerve conduction velocities of the peroneal and tibial nerves, and the sensory nerve conduction velocity of the sural nerve. None of the parameters of cardiac sympathetic neuropathy or diabetic somatic neuropathy showed any correlation with blood pressure, nor was there any evidence of a correlation between cardiac sympathetic neuropathy and glycosylated haemoglobin levels; there was, however, a significant correlation between diabetic somatic neuropathy (as indicated by tibial nerve conduction velocity) and glycosylated haemoglobin levels. The results are consistent with the view that different mechanisms are involved in the two types of neuropathies.


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