The effect of gingival aging in diabetic and non-diabetic status: an experimental study.

Major gingival-periodontal changes according to age have been observed in both diabetic and non-diabetic rats. Male Wistar rats weighing 200-220 g were divided into two groups: 1) Nondiabetic (ND) and 2) Diabetic (D) by receiving an intraperitoneal (ip) dose of streptozotocin (STZ) (50 mg /kg). Animals from both groups (ND and D) were euthanized at 4, 8, 12, 17 y 25 weeks after treatment with saline solution or STZ.

Oxidative stress in the optic nerve and cortical visual area of steptozotocin-induced diabetic Wistar rats: Blockade with a selective bradykinin B receptor antagonist.

The role of bradykinin B receptors on the oxidative stress as measured by the levels of Na+/K+ ATPase activity, malondialdehyde (MDA) and glutathione (GSH) in male Wistar rat optic nerve and visual cortex area 1 and 4weeks after STZ treatment was studied. Rats were divided into 4 groups (n=6-7): 1. Controls (non-diabetics); 2.

Blockade of early and late retinal biochemical alterations associated with diabetes development by the selective bradykinin B1 receptor antagonist R-954.

The chronic hyperglycemia measured alongside diabetes development is associated with significant long-term damage and failure of various organs. In the present study it was shown that hyperglycemia induced early and long term increases in nitric oxide (NO) levels, kallikrein activity and vascular capillary permeability measured as plasma extravasation, and decreases of Na/K ATPase activity in diabetic rat retina 4 and 12 weeks after streptozotocin (STZ) injection. Treatment of the animals for 5 consecutive days with a novel selective bradykinin B(1) receptor (BKB(1)-R) antagonist R-954 (2mg/kg s.

Activation of peritoneal macrophages during the evolution of type 1 diabetes (insulitis) in streptozotocin-treated mice.

The effects of lipopolysaccharide (LPS) and desArg9Bradykinin (DBK) on the release of nitric oxide (NO) from macrophages of mice 8, 12 and 18 days after having been treated with low doses of streptozotocin (STZ; 5 × 45 mg/kg) were studied. The results showed that LPS stimulated the release of NO from macrophages of untreated animals by 50% whereas the bradykinin B(1) agonist desArg9Bradykinin (DBK) increased the level of NO by 20%. This increased NO production was totally abolished by incubating the cells with R-954, a selective bradykinin B(1) antagonist.

Antidiabetic efficacy of bradykinin antagonist R-954 on glucose tolerance test in diabetic type 1 mice.

Insulin-dependent diabetes mellitus (type 1 diabetes) is an inflammatory autoimmune disease associated with many complications including nephropathy, retinopathy, neuropathy and hyperalgesia. Experimental evidence has shown that the bradykinin B1 receptor (BKB1-R) is involved in the development of type 1 diabetes and found to be upregulated alongside the disease. In the present study the effects of the selective BKB1-R antagonist the R-954 (Ac-Orn-[Oic(2), alpha-MePhe(5), D-beta Nal(7), Ile(8) ]des-Arg(9)-BK and the BKB1-R agonist des Arg(9)-BK (DBK) were studied on diabetic hyperglycemia.

Side effects of cyclosporine-A treatment in rats: gingival overgrowth and early hyperglycemia.

Gingival overgrowth is an adverse side effect of cyclosporine A (CsA) in the treatment of transplanted patients. The purpose of this study was to evaluate the effects of CsA on new-onset diabetes mellitus and gingival overgrowth in rats, by measuring collagen, nitric oxide and microvascular permeability. Blood glucose level, collagen, nitric oxide level and vascular permeability were determined.

Diabetes and its effects on dental pulp.

Uncontrolled or poorly controlled diabetes mellitus may be a risk factor for the development of oral complications. The objective of this investigation was to determine the effect of diabetes mellitus progression on inflammatory and structural components of dental pulp. Male Wistar rats were given a single injection of Streptozotocin (STZ), and induction of diabetes was confirmed 24 h later.

The development of insulitis and the kallikrein-kinin system.

Data derived from animals and humans suggest that the onset of diabetes is associated with hemodynamic changes in the renal circulation leading to increased renal plasma flow (RPF), glomerular capillary hyperfusion, and an increased glomerular transcapillary hydraulic pressure gradient. The duration of diabetes is one of the most important factors in predicting the development of diabetic nephropathy. On the other hand, diabetic nephropathy has been associated with the degree of hyperglycemia; thus, hyperglycemia may therefore contribute to alterations in structure and function of the kidney.

The diabetic nephropathy and the development of hypertension in rats.

The present study was designed to examine the development of hypertension in diabetic rats treated with streptozotocin (STZ, 1 mg/g bw). The rats were studied at 3, 6, 9, 12 and 15 weeks. From the third week the rats were divided in diabetic rats according their glycemias and controls, along 15 weeks.

Renal function in the diabetic pregnant rats.

Diabetic nephropathy is associated with increased urinary albumin and reduce kallikrein excretion. Increased activity of the renal kallikrein-kinin system has been suggested as one of the possible mechanisms underlying diabetic hyperfiltration. The present study shown that the Kallikrein-kinin system is progressively increased in the diabetic-pregnant rats at 7, 14, 21 days; 48 and 7 days after pregnancy (P < 0.

The involvement of kallikrein-kinin system in diabetes type I (insulitis).

Islet inflammation or insulitis is followed by selective destruction of the insulin secreting B-cell. Animal models of insulin-dependent diabetes mellitus (IDDM) have been used to characterize more fully insulitis, and our results with C57/BL/Ks mdb with low doses of streptozotocin (STZ) confirmed the disease. B1 receptor antagonist [Leu8]des-Arg9-BK has shown a significant effect on diabetic glycemia and renal control parameters.

Renal ischemia-induced increase in vascular permeability is limited by hypothermia.

The purpose of the present work was to evaluate the kallikrein-kinin system and effects of hypothermia during renal ischemia and reperfusion. Male C57BL/KSJmdb mice were subjected to 20 or 60 min ischemia for different periods of reperfusion. Our results demonstrate that short periods of ischemia followed by reperfusion did not cause significant alterations in kallikrein activity, Evans Blue (EB) extravasation, prokallikreins, myeloperoxidase activity or plasma creatinine concentration.

Constitutive nitric oxide synthase (cNOS) activity in Langerhans islets from streptozotocin diabetic rats.

Nitric oxide synthase activity was measured in Langerhans islets isolated from control and streptozotocin diabetic rats. The activity of the enzyme was linear up to 150 micrograms of protein from control rats and was optimal at 0.1 microM calcium, when it was measured after 45 min of incubation at 37 degrees C in the presence of 200 microM arginine.

Effects of L-NAME and L-Arg on arterial blood pressure in normotensive and hypertensive streptozotocin diabetic rats.

The present study was designed to examine blood pressure response to nitric oxide synthase-pathway inhibition and stimulation in normotensive and hypertensive diabetic rats. Rats treated with streptozotocin (60 mg/Kg i.p.

Effects of aprotinin on the kallikrein-kinin system in type I diabetes (insulitis).

Sub-diabetogenic doses of streptozotocin (STZ) produce insulitis, beta cell destruction and diabetes in mice. Since kinin have been proposed as an inflammatory mediator in several diseases, we decided to evaluate the role of the kallikrein-kinin system in the evolution of insulitis. Male C 57 BL/KsJ mdb mice were injected with STZ (40 mg/kg) for 5 consecutive d.

Effects of B1 and B2 kinin receptor antagonists in diabetic mice.

Streptozotocin (STZ) has been extensively used to produce type I diabetes in animals. This experimental disease is characterized by a mild inflammatory reaction in the Langerhans islets. Because kinins have been proposed as prominent inflammatory mediators in the pathogenesis of several diseases, we decided to evaluate the role of kinins and their receptors in the evolution of insulitis.

Effects of HOE 140 on some renal functions in type I diabetic mice.

To investigate in mice the mechanisms underlying renal functions in a type I diabetes model, we have suppressed B2 kinin receptors local activities by their specific antagonist D-Arg [Hyp3-Thi5-D-Tic7-Oic8]BK (HOE 140). Mice made diabetic with low consecutive doses of streptozotocin (STZ) (45 mg/k BW during 5 days) were injected with HOE 140 (15 micrograms/twice a day) for 15 days. This drug did not modify glycemia of STZ treated animals but a significantly reduction of urinary proteins, nitrites and kallikrein was observed.

Streptozotocin-induced hyperglycemia is decreased by nitric oxide inhibition.

1. Diabetes mellitus type I was induced in 3-month old male C57 BL/KS-mdb mice (N = 24) by ip injection of streptozotocin (STZ, 45 mg/kg body weight) for 5 days. 2.

The kallikrein-kinin system of sweat in normal and cystic fibrosis subjects.

The mechanisms of kallikrein secretion was studied in 25 normal subjects (11 male, 14 female) and 5 subjects with cystic fibrosis (identified by the usual criteria). The results obtained show a decreasing of prekallikrein and total kallikrein in cystic fibrosis stimulated by IPR or pilocarpine compare to controls. On the other hand sweat from males shows more prekallikrein and total kallikrein than females.

The kallikrein-kinin system in early state of diabetes.

The kallikrein-kinin system was studied in 9 normals, healthy subjects (6 men, 3 women, age range 1 to 14 years) and 15 diabetic patients (9 men, 6 women age range 2 to 14 years) with an evolution of the disease between 1 to 14 years. Diabetic patients with low microalbuminuria (6.62 +/- 0.

Renal alteration and development of hypertension in diabetic rats.

Unlabelled: There is a close association between diabetes and hypertension. Many studies have demonstrated an increased incidence of hypertension in the presence of diabetic nephropathy. The aim of the present work was to study the kallikrein-kinin system during the diabetic states with hypertension.

The kallikrein-kinin system in the colon and lung fluid from a cribriform degeneration (cri) mutant mouse.

The cribriform degeneration (cri) mutant mouse was widely studied in regard to the electrolyte and kallikrein metabolism because of its potentiality as a cystic fibrosis (CF) genetic animal model. In this paper the activity of the kallikrein-kinin system, and the kininase activity and glycoproteins concentration in colon and pulmonary lavage fluid (PLF) in homozygous mutant (cri/cri) and control sibling mice are described. The mutant mice showed a diminished kininogenase and kininase activity and glycoproteins concentrations in both studied organs.