The aims of the study were to (1) compare peripheral bone mineral density (BMD) in men with diabetes to peripheral BMD in non-diabetic men, and (2) explore factors which may predict BMD in diabetic men. Ninety men with type 2 diabetes and 35 men with type 1 diabetes were randomly selected for participation via a computerised database. Fifty healthy males were also recruited. All patients had peripheral BMD measured by dual energy Xray absorptiometry (DEXA) at the non-dominant distal radius. Information on a number of clinical parameters was obtained by direct questioning, and from patient case notes. The mean age (95% confidence interval (CI)) of the type 1 diabetic group, type 2 diabetic group and control group were, respectively: 49.3 years (44.6-53.9), 62.8 years (60.7-64.8) and 38.5 (34.9-42.1) years. Median (95% CI) Z-scores for the three groups were: -0.18 (-0.68 to +0.32), +0.19 (-0.14 to +0.49) and -0.02 (-0.4 to +0.31), respectively (p=not significant). Only body mass index (BMI) was correlated with BMD in the type 1 diabetic group, and only BMI and age were correlated with BMD in type 2 diabetics. There was no correlation between BMD and glycosylated haemoglobin concentration (HbA(1)c), disease duration or presence of microvascular or macrovascular complications in either of the diabetic groups. We did not find any significant difference in peripheral BMD between patients with type 1 diabetes, type 2 diabetes and controls.
Experiments were performed in dogs to determine the effects of the intravenous administration of the dipeptide hydrolase inhibitor SQ 20,881 on renal hemodynamics, intrarenal blood flow distribution, and renal function. Dipeptide hydrolase converts angiotensin I to angiotensin II and inactivates bradykinin. SQ 20,881 causes an inhibition of the vasoconstrictor response after angiotensin I and potentiation of the vasodilatory activity of bradykinin. Total renal blood flow, cortical distribution of blood flow, and glomerular filtration rate were determined. In seven animals administration of SQ 20,881 (1 mg/kg) resulted in a decrease in mean systemic blood pressure of 11 mmHg, an increase in total renal blood flow of 0.71 ml/min per g, and a significant fall in glomerular filtration rate. Fractional blood flow to the superficial cortex decreased and to the juxtamedullary cortex increased. Absolute flow was unchanged in the superficial cortex and increased significantly in the deep cortex. The findings are compatible with reported effects of bradykinin on intrarenal blood flow distribution, although the experiments do not distinguish between potentiation of bradykinin or inhibition of angiotensin I conversion.
Angiotensin I1 is a potent vasoconstrictor agent which will produce changes in renal blood flow. Since the renin-angiotensin system has been implicated in the control of renal hemodynamics (1, 2 ) , it is important to determine if angiotensin I1 has a preferential action on the kidney. Recently, several peptides which inhibit the conversion of angiotensin T to angiotensin I1 have become available ( 3 ) . Reports indicate that these peptides are active in vivo, and effectively block the pressor response following injection of angiotensin I. We have utilized one of these peptides (SQ 20,881)3 to study the redistribution of blood flow to several organs in the rat. Materials and Methods. At least 4 daysprior to the actual experiments, a polyethylene catheter was implanted into the left ventricle or ascending aorta via the right carotid artery in 250-300 g female rats. On the day of the experiment, the animals were anesthetized with pentobarbital sodium ( 60 mg,/kg) and the ventricular catheter was exposed and flushed with saline. A femoral vein was cannulated for injection of SQ 20,881, and a femoral artery was cannulated to measure mean systemic blood pressure using a strain gauge pressure transducer (Statham P23Dd) and Grass polygraph or Beckman dynograph.Blood flow redistribution was determined in the intestine, liver, kidneys, spleen, adrenals, stomach and skeletal muscle. blood flow in this organ from animal to anin-ma1 was found to be too great to yield valid results, In addition, similar studies were performed on three pregnant rats in order to observe the possible effects of the peptide in this situation.Radioactive microspheres (3M Co.) with a diameter of 15 pm and labeled with either ICr)Yb or 8*iSr were used. The microspheres were diluted in a glucose solution with a density of 1.3 g/cm3 which is the same as the density of the spheres. After injection of the microspheres, the animals were killed and the organs or pieces of organs were counted in a two-channel well-type scintillation counter.In control experiments, microspheres were injected in random order and the distribution was calculated for the first and second injection. In experimental animals, SQ 20,881, in doses of 4 or 40 mg/kg, was given between the two injections of microspheres. The injection of microspheres was again randomized and distribution was calculated before and after administration of the peptide.Percentage distribution of microspheres in various organs was calculated as the counts per minute of either Yb or Sr in a given organ divided by the total counts to all of the organs. The data were analyzed using the Student's t test with a .05 probability level of significance.In order to test the effectiveness of the peptide in inhibiting angiotensin I converting enzyme activity, various doses of angiotensin I and angiotensin I1 were administered intravenously to 250-300 g rats. The changes in blood pressure were recorded and SQ 20, 881 administered. The animals were then injected with identical doses of angiotensin I and angiotensin I1 an...
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