Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intravenous glucose tolerance tests (GTT) were performed in 13 metabolically healthy patients at the first and second day after abdominal surgery. GTT were carried out during an additional infusion of bradykinin (BK) (80 microgram/h) in six of these patients at the first day (group A) and in seven patients at the second day (group B). Furthermore, GTT were performed in six patients with chemical diabetes with and without BK-infusion. In addition, the effect of BK on blood glucose concentration in the postabsorptive state was investigated in nine maturity onset diabetics and in five healthy volunteers. As a control, another nine diabetics received physiological saline. In both groups of surgical patients BK improved glucose tolerance (k-values: group A without BK 1.03 +/- 0.12, with BK 1.31 +/- 0.07; group B without BK 0.85 +/- 0.18, with BK 1.25 +/- 0.21). This was also true in chemical diabetics (without BK 0.81 +/- 0.03, with BK 1.08 +/- 0.04). While BK did not change blood glucose concentration in healthy volunteers, it reduced that of diabetics by 12.2 +/- 1.4% continuously during 100 min. No spontaneous drop of blood glucose was observed in diabetics receiving saline. These results are in good accord with the present view that kinins may play a role within the regulation of carbohydrate metabolism.
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PMID:[Improvement of pathological glucose tolerance by bradykinin in diabetics and in surgical patients (author's transl)]. 71 29

Kinin system was investigated in 82 patients suffering from diabetes mellitus of various severity. To make pathogenetically substantiated pharmacological correction of the kinin system activity prodectin--kinin antagonist--was used in these patients. A conclusion was drawn that the blood plasma kinin system was activated in the patients with moderately severe and severe diabetes. The activity of total kallikrein and kininogen became normal against the background of prodectin treatment. The blood plasma kinin system activity was normalized simultaneously with the improvement of the diabetic angiopathies course.
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PMID:[Plasma kinin system indices in diabetes mellitus patients before and after treatment with prodectin]. 72 71

The carrageenin-induced foot oedema in rats is considerably decreased by insulin pretreatment, but increased in alloxan diabetes. Maximum inhibition by insulin occurs in the early phase of the oedema reaction and the insulin action is even further increased when it is administered 30 min after carrageenin. Doses of insulin as low as 1 U/kg intravenously produce significant inhibition. Determinations of the components of the kinin system indicate that the kininogenase activity is increased, and both the kininogen and kininase content are in turn decreased in the plasma of insulin-treated animals. When the carrageenin-induced oedema fluid of the paw after insulin is analysed for kininogen and kininase, their levels are significantly decreased when compared with those of oedema fluid without insulin. Histamine content in the oedema fluid is significantly enhanced by insulin. The anti-inflammatory effect of insulin under these conditions therefore appears to involve changes in the kinin system.
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PMID:Involvement of the kinin system in the insulin-induced inhibition of carrageenin oedema in rats. 91 16

The goal of this study was to determine whether responses of the basilar artery are altered during diabetes mellitus. We measured the diameter of the basilar artery in vivo in non-diabetic and diabetic rats (streptozotocin; 50-60 mg/kg i.p.). Responses of the basilar artery to agonists, which presumably produce dilatation by releasing endothelium-derived relaxing factor (EDRF), were impaired in diabetic rats compared to non-diabetic rats. Acetylcholine (1.0 and 10 microM) dilated the basilar artery by 13 +/- 2 and 26 +/- 4% (means +/- S.E.M.), respectively, in non-diabetic rats, but by only 4 +/- 1 and 9 +/- 2%, respectively, in diabetic rats (P less than 0.05). Bradykinin (1.0 and 10 microM) dilated the basilar artery by 14 +/- 2 and 35 +/- 6% (means +/- S.E.M.), respectively, in non-diabetic rats, but by only 5 +/- 1 and 6 +/- 2%, respectively, in diabetic rats (P less than 0.05). The response to nitroglycerin was similar in non-diabetic and diabetic rats. Thus, impairment of vasodilatation in diabetic rats in response to acetylcholine and bradykinin is not related to non-specific impaired of vasodilatation. Next, we examined the possibility that impaired dilator responses of the basilar artery in response to acetylcholine and bradykinin in diabetic rats may be related to the activation of the thromboxane A2-prostaglandin H2 receptor. SQ 29548 (a specific thromboxane A2-prostaglandin H2 receptor antagonist) did not alter responses of the basilar artery to acetylcholine and bradykinin. These findings suggest that diabetes mellitus impairs endothelium-dependent dilatation of the basilar artery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impairment of endothelium-dependent dilatation of the basilar artery during diabetes mellitus. 138 36

Streptozotocin-induced diabetes resulted in diminished vasodilator responses to bradykinin in the preconstricted isolated perfused kidney of the rat which were associated with decreased renal phospholipase A2 activity and reduced release of PGE2 into the renal venous effluent.
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PMID:Influence of diabetes mellitus on renal vascular responses to bradykinin. 146 37

Diabetes provokes a greater responsiveness of rat urinary bladder preparations to bradykinin and a greater formation and release of prostaglandin F2 alpha, without affecting prostaglandin E2 release significantly. Inhibition of cyclooxygenase by indomethacin (1 microM) inhibits the contraction elicited by bradykinin and leads to identical contractile responses of control and diabetic urinary bladder strips. Removal of the urinary bladder epithelium does not modify the contractile response evoked by bradykinin in control preparations but significantly decreases the contraction of preparations of diabetic tissues. Quantitatively, the activity of control urinary bladder strips with epithelium and the activity of diabetic preparations without epithelium are the same. More prostaglandin F2 alpha is released into the medium by urinary bladder strips devoid of epithelium in both control and in diabetic rats. These results indicate a role for epithelial cells in the smooth muscle contraction evoked by bradykinin in diabetic rats.
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PMID:A possible role for urinary bladder epithelium in bradykinin-induced contraction in diabetic rats. 151 35

The vascular endothelial cells have the ability to modulate local vascular tone by releasing relaxing factors such as nitric oxide or the vasoconstrictor peptide endothelin-1. Although this regulatory system is found in all vertebrates, there is a great heterogeneity in the release of these endothelium-derived substances, from one organ to an other, between large and small vessels, and between different species. Therefore, observations made in certain vascular beds or animals do not necessarily apply to human ophthalmic circulation. The present study was designed to investigate endothelial mediators in the human ophthalmic artery. The results show that in the human ophthalmic artery, nitric oxide is released under basal conditions and that its production can be markedly stimulated by bradykinin, acetylcholine, and particularly histamine, which cause profound vascular relaxation. In contrast, endothelin-1 evoked potent contractions, which were unaffected by the calcium antagonist nifedipine. However, upon re-exposure of the blood vessels to the peptide, marked tachyphylaxis occurred. These findings demonstrate that in the human ophthalmic artery, endothelium-derived nitric oxide and endothelin are very potent modulators of vascular tone, suggesting that they play an important role in the regulation of local blood flow in the eye. Hence, endothelium dysfunction may represent a new pathogenetic mechanism in disease states associated with altered blood flow to the eye, such as diabetes, hypertension, and some forms of low-tension glaucoma.
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PMID:Nitric oxide and endothelin-1 are important regulators of human ophthalmic artery. 160 46

In 1928, Frey and co-workers discovered kallikrein in human urine and described its prolonged hypotensive effect in the dog. Four years later, the same authors first reported a blood glucose-lowering effect of orally administered kallikrein in diabetic patients. However, the observed blood glucose-lowering effect of kallikrein appeared to fade with repeated administration, and therefore its possible metabolic role was not further investigated and fell into disregard. One decade ago, experimental data yielded indirect evidence that the regulation of local skeletal muscle blood flow and glucose uptake during work was mediated by proteolytically cleaved kinins. Further experiments demonstrated that in insulin-resistant states such as postoperative stress and type II diabetes, reduced muscular insulin sensitivity was increased and partly restored by continuous low-dose infusion of synthetic bradykinin. Recent work showing that tissue kallikrein is present in a number of different tissue sites, including skeletal muscle and our own observation of local kinin overflow after muscle work in healthy subjects, but not in type II diabetics, support the concept of a skeletal muscle kallikrein-kinin system (KKS) that is locally activated upon contraction. Moreover, in isolated perfused rat heart preparations, favorable effects of kinins on myocardial glucose uptake, oxidation, and glycolytic flux have been reported. Most interestingly, cardioprotective effects of kinins have been observed and attributed to improved energy and substrate metabolism in ischemic hearts. Taken together, these data gave rise to the concept that tissue KKS might be involved in the local modulation of skeletal muscle and myocardial tissue blood flow and substrate metabolism, and that activation of the KKS is defective in insulin-resistant states.
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PMID:Metabolic effects of kinins: historical and recent developments. 169 62

Late diabetic effects are the sequelae of for a long time super elevated blood sugar levels. The diabetic nephropathy is the cause of the secondary arterial hypertension. The investigation seeks for the connections between the diabetes mellitus and the essential, that is primary hypertension. The two diseases frequently appear and clearly increase in the second half of life. Moreover, they are above average frequently associated with each other. Among brothers and sisters of diabetic hypertensives in comparison to normal cohorts clearly increased high blood pressure prevalences were found. The insulin resistance which could be proved in a great number of hypertensive and which has been known since more than two decades might be the connecting link between hypertension and diabetes mellitus. Like the obesity the essential hypertension can be associated with all degrees of an insulin hyposensitiveness. The sodium-retaining effect of the insulin might explain the increased sodium content of the body in hypertensives. The differential diagnostics of the essential hypertension should therefore seek for conditions of an insulin resistance. The type II diabetic lacks a release of bradykinin during muscle work. Thus the glucose uptake into the cell is unfavourable influenced and demands an increased insulin excretion. This genetically (?) fixed defect is found also in essential hypertensives. It could be the connecting link between the two diseases. ACE-inhibitors have via a kininase II inhibition an effect also on the bradykinin decomposition and can favourable influence the glucose uptake into the muscle. An improved insulin effect among the ACE-inhibitors was described. Therefore, they should be preferred in the treatment of hypertensive diabetics.
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PMID:[Diabetes mellitus and arterial hypertension. In search of the connecting link]. 177 26

This study evaluated the possible impairments to endothelium-mediated vasodilation by structural and functional properties of the intestinal arterioles in adult (20-21-week-old) rats after 8-11 days or 7-8 weeks of streptozotocin-induced diabetes. Arteriolar intravascular pressures and luminal diameters were simultaneously measured during iontophoretic application of acetylcholine, bradykinin, and nitroprusside to the outer vessel wall, and passive diameter-pressure relations were obtained during maximal vasodilation. Microvascular pressures and circumference-passive wall tension relations were similar between all diabetic and normal rats and did not appear to significantly influence vasodilation. Both acute and chronic hyperglycemia were associated with near complete suppression of acetylcholine-induced vasodilation in large arterioles, and the threshold dose for vasodilation of intermediate arterioles was approximately 10-fold higher in diabetic rats. In both diabetic groups, dilatory responses to nitroprusside were normal, and in chronically diabetic rats, the relative vasodilation in response to various doses of bradykinin was equivalent to that found in normal rats. These observations indicate that a very specific deficit of acetylcholine-induced endothelium-derived relaxing factor action rapidly develops in intestinal arterioles of diabetic rats, but the arteriolar wall mechanical properties, cGMP-mediated muscle relaxation, and endothelial release of the bradykinin-stimulated relaxing factor are not compromised after 7-8 weeks of chronic hyperglycemia.
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PMID:Structural and functional origins of suppressed acetylcholine vasodilation in diabetic rat intestinal arterioles. 193 56


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