Key result
Streptozotocin-induced diabetic rats show ~119% higher plasma DNP and increased kidney receptor binding versus controls.
Why the study?
The characteristics of dendroaspis natriuretic peptide and its receptor in the context of diabetes remain to be fully elucidated.
STZ-induced diabetes in rats increases plasma and tissue levels of DNP and alters its receptor properties in the kidney, suggesting a role in diabetic renal function.
Caution against extrapolating rat DNP changes to patients; leaves open targeted human studies in diabetic heart disease.
Dendroaspis natriuretic peptide (DNP) shares a functionally important sequence homology with other natriuretic peptides. However, the characteristics of DNP and its receptor in the context of diabetes remafin to be fully elucidated. In the present study, alterations in the plasma levels and tissue contents of DNP and the properties of its receptor in diabetic rats, induced by streptozotocin (STZ) injection, were investigated. The plasma levels of DNP were 90.01 ± 4.12 and 196.68 ± 5.60 pg/ml in the control and STZ-induced diabetic rats, respectively. The tissue contents of DNP in the cardiac atrium, ventricle, renal cortex and inner medulla of the STZ-induced diabetic rats were also significantly increased compared with the control rats. Specific (125)I-DNP-binding sites were located predominantly in the glomeruli and inner medulla of the rat kidney. In the glomeruli of the kidney, the apparent dissociation constants (Kd) of (125)I-DNP in the control and STZ-induced diabetic rats were 0.41 ± 0.03 and 0.56 ± 0.06 nM, respectively. The maximum binding capacities (Bmax) of (125)I-DNP in control and STZ-induced diabetic rats were 2.98 ± 0.21 and 6.22 ± 1.06 fmol/mg protein, respectively. However, no differences were observed in the apparent Kd and Bmax of (125)I-DNP in the inner medulla of the kidney between the control and STZ-induced diabetic rats. In the glomerular and inner medullary kidney membranes, DNP stimulated the production of cyclic guanosine monophosphate (cGMP) in a dose-dependent manner. The magnitude of cGMP production in glomerular membranes was greater in the STZ-induced diabetic rats, whereas the magnitude of cGMP production in the inner medullary membranes was lower in the STZ-induced diabetic rats compared with the control rats. These results indicated that STZ-induced diabetes modulate DNP and its receptor, and also suggested that modulation of the DNP system is involved in the renal function of diabetic animals via the intracellular domain of the kidney NP receptor.
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Park et al. (2015) studied Streptozotocin-induced diabetes (n=49). Streptozotocin-induced diabetes vs. Age-matched controls was evaluated on Plasma levels of DNP (pg/ml) (p=<0.01). Streptozotocin-induced diabetic rats exhibited significantly elevated plasma DNP levels (196.68 vs 90.01 pg/ml) and increased specific 125I-DNP binding capacities in kidney glomeruli compared to controls.
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