In cross sectional studies, low levels of insulin like growth factor I (IGF-I) have been identified as a risk factor for cardiovascular disease, the incidence of which is strongly age associated. In the current study, we have used mice deficient in IGFBP-1 as an animal model to study the effects of increased IGF-I bioavailability on cardiovascular structure and function in ageing mice.Measurements of blood pressure in conscious mice (tail cuff photoplethysmography) and echocardiography in unconscious mice (under isoflourane anaesthesia) were recorded at 2, 6, 12 and 18 months of age (n=12-15). Mice were sacrificed and hearts used for left ventricular hypertrophy analysis by comparing cardiomyocyte cross-sectional area, fibrosis and apoptosis. Serum samples were used for total and free IGF-I and the Greiss reaction to estimate endogenous nitric oxide levels. Values are expressed as ±SEM and compared using student t-test or ANOVA. 8-12 week male IGFBP-1KO mice had an approx. 2.5 fold increase in free IGF-I compared to a matched WT cohort (WT 0.94±0.17ng/ml KO 2.58±0.34ng/ml p<0.01) with no change in circulating total IGF-I levels (WT 206.4±17.07ng/ml, 241.3±14.62ng/ml p=ns)As the cohorts aged, there was a greater fold-increase in left ventricular wall size in WT 18m old mice in comparison to young 2m old mice (At 18m IVSD WT 1.36±.06-fold KO 1.09±.04-fold p<0.01; IVSS WT 1.18±0.04-fold KO 1.04+0.06-fold P<0.05; LVPWD WT 1.36±0.06-fold KO 1.03±.0.03-fold p<0.001; LVPWS WT 1.25±0.04-fold KO 1.05±0.02-fold p<0.001). At 18months, the measurements of diastolic function E/A ratio (WT 1.18±0.03 KO 1.32±0.04 p<0.05) IVRT/RR (WT 0.109±0.004ms/ms KO 0.094 ±0.002ms/ms P<0.01) IVCT/RR (WT 0.138±0.01ms/ms KO.113±.0.01ms/ms) were all preserved in the KO cohort compared to the WT. Ejection fraction, stroke volume and fractional shortening were all preserved in the KO cohort at 18m (EF WT 48.77±1.53% KO 53.50±1.03% P<0.05; SV WT 42.01±2.66ul KO 60.69±3.88ul p<0.001; FS WT 28.50±1.06 KO31.91±0.74 p<0.05).KO mice were hypotensive at all time points compared to WT controls (at 2m WT 120.5±1.8mmHg KO 115.7±1.1mmHg p<0.05; 18m WT 123.5±2.6mmHg KO 114.5±2.2 p<0.05. This was abolished by chronic administration of L-NAME (at 2m WT 127.2±3.4mmHg KO 132.1±2.7 p2 KO 295.6±7.5um2 p<0.001). WT mice had a greater increase in apoptopic cells per slide in aging mice compared to KO (2m WT 4.67±0.67 18m WT 11±2.24 p<0.05; KO 2m 5.2±1.16 18m 8.33±2.67 P=ns). Fibrosis measured by picrosirus red staining and hydroxyproline analysis indicated that neither age nor genotype effected cardiovascular fibrosis. These results indicate that an increase in IGF-I bioavailability can help preserve cardiovascular structure and function in normal aging mice, possibly through increased nitric oxide production.