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ABSTRACT
In creased plasma atrial natriuretic peptide levels accompany the expansion of effective plasma volume in diabetic patients. Atrial natriuretic peptide has a deleterious effect on the pathogenesis of diabetic nephropathy by increasing renal plasma flow and glomerular filtration rate. Angiotensin converting enzyme inhibitors decrease plasma atrial natriuretic peptide levels. We aimed to show the effect of losartan, a specific angiotensin II receptor antagonist, on plasma atrial natriuretic peptide levels in diabetic rat model. Thirty-six female, 10-week-old wistar rats were enrolled in the study. Diabetes was induced by 65 mg/kg streptozotocin in pH 4.5 sodium citrate buffer injection via intraperitoneal route. The rats did not receive any kind of antidiabetic treatment throughout the study period. Following the first month of diabetes induction, the rats were separated into two groups, the first group was treated with 10 mg/kg losartan via oro-gastric lavage and the second served as a diabetic control group. Following the second month of diabetes induction, including the one-month treatment period, atrial natriuretic peptide levels were studied in trasylol and EDTA treated plasma samples. Six healthy and age- matched rats were also studied as a healthy control group. Plasma atrial natriuretic peptide levels in diabetic untreated rats were not different from the healthy control group (104.6±4.7 pg/ml vs. 100.7±10.8 pg/ml, respectively ). In the losartan treated diabetic group, plasma atrial natriuretic peptide levels were significantly lower than the diabetic control group (93.2±4.4 pg/ml, p<0.01 ), but not different from the healthy controls. As a result, treatment with angiotensin II receptor blockers decreases the plasma atrial natriuretic peptide levels in diabetic rats. A similar effect of angiotensin converting enzyme inhibitors had been shown previously. This finding may be explained by the inhibition of the renin-angiotensinaldosterone system leading to a reduction of effective plasma volume expansion.
In creased plasma atrial natriuretic peptide levels accompany the expansion of effective plasma volume in diabetic patients. Atrial natriuretic peptide has a deleterious effect on the pathogenesis of diabetic nephropathy by increasing renal plasma flow and glomerular filtration rate. Angiotensin converting enzyme inhibitors decrease plasma atrial natriuretic peptide levels. We aimed to show the effect of losartan, a specific angiotensin II receptor antagonist, on plasma atrial natriuretic peptide levels in diabetic rat model. Thirty-six female, 10-week-old wistar rats were enrolled in the study. Diabetes was induced by 65 mg/kg streptozotocin in pH 4.5 sodium citrate buffer injection via intraperitoneal route. The rats did not receive any kind of antidiabetic treatment throughout the study period. Following the first month of diabetes induction, the rats were separated into two groups, the first group was treated with 10 mg/kg losartan via oro-gastric lavage and the second served as a diabetic control group. Following the second month of diabetes induction, including the one-month treatment period, atrial natriuretic peptide levels were studied in trasylol and EDTA treated plasma samples. Six healthy and age- matched rats were also studied as a healthy control group. Plasma atrial natriuretic peptide levels in diabetic untreated rats were not different from the healthy control group (104.6±4.7 pg/ml vs. 100.7±10.8 pg/ml, respectively ). In the losartan treated diabetic group, plasma atrial natriuretic peptide levels were significantly lower than the diabetic control group (93.2±4.4 pg/ml, p<0.01 ), but not different from the healthy controls. As a result, treatment with angiotensin II receptor blockers decreases the plasma atrial natriuretic peptide levels in diabetic rats. A similar effect of angiotensin converting enzyme inhibitors had been shown previously. This finding may be explained by the inhibition of the renin-angiotensinaldosterone system leading to a reduction of effective plasma volume expansion.