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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of experimental diabetes induced by streptozotocin on responses of rat isolated aortae and portal veins to noradrenaline, 5-hydroxytryptamine, and KCl was examined 7, 100, 180, and 360 days after the onset of diabetes. No significant changes in reactivity were seen 7 days after the onset of diabetes. After 100 days aortae from diabetic rats were supersensitive (defined as a significant increase in the pD2 value) to noradrenaline. However, 180 days after the onset of diabetes, the sensitivity of diabetic aortae to noradrenaline was not significantly different from control, while the responsiveness (defined as the maximum developed tension divided by cross-sectional area of aorta) to 5-hydroxytryptamine was reduced. A generalized increase in both the sensitivity and responsiveness of diabetic aortae to all three agonists was observed after 360 days of diabetes. In contrast, no changes in either the sensitivity or the responsiveness of portal veins to noradrenaline, 5-hydroxytryptamine, or KCl could be detected at any time after the onset of diabetes. These results indicate that changes in vascular reactivity can be detected with increasing duration of experimental diabetes. However, these changes do not follow a consistent pattern and are not seen in all parts of the vasculature.
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PMID:The influence of chronic experimental diabetes on contractile responses of rat isolated blood vessels. 315 32

The responsiveness to vasoactive agents in the perfused mesenteric vascular bed of streptozocin-induced diabetic rats was examined and compared with that of propylthiouracil-induced hypothyroid rats. Diabetic rats at 4 and 8 weeks after the induction of diabetes showed a significant decrease in isoproterenol-induced vasodilatation. In addition, the contractile responses to norepinephrine and 5-hydroxytryptamine and the vasodilative response to acetylcholine were significantly decreased in 12-week-diabetic rats. The contractile response to nerve stimulation was markedly decreased at 8 and 12 weeks. On the other hand, hypothyroid rats showed a decreased response to isoproterenol, but they did not show any change in the response to nerve stimulation. A decrease in plasma thyroid hormone levels in diabetic rats at any time period was similar in extent to that in hypothyroid rats. The data indicate that the progressive changes in vascular reactivity in diabetic rats may be divided into two stages. In the early stage, the altered reactivity of vasculature is likely to be mediated by hypothyroidism, whereas in the later stage, it is induced by other factors, e.g. hyperglycemia and hypoinsulinemia. Adrenergic neuropathy is not caused by hypothyroidism.
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PMID:Changes in vascular reactivity in experimental diabetic rats: comparison with hypothyroid rats. 316 24

The perivascular autonomic nerves of the major blood vessels on the ventral surface of the brain were studied in the streptozotocin-induced diabetic rat, an animal model for juvenile onset of diabetes. Histochemical and immunohistochemical techniques were used to determine the pattern and density of perivascular nerves containing catecholamine, 5-hydroxytryptamine (5-HT), vasoactive intestinal polypeptide (VIP) and neuropeptide Y (NPY). A significant reduction in the density and/or fluorescence intensity of 5-HT-immunoreactive nerves was observed in the circle of Willis and its main arterial branches namely: basilar, superior cerebellar, internal carotid, posterior communicating, middle cerebral and anterior cerebral arteries, while a significant reduction of VIP-immunoreactive nerves was observed in the internal carotid, middle cerebral and anterior cerebral arteries, but not in the basilar, superior cerebellar and posterior communicating arteries 8 weeks after the onset of diabetes. However, no changes were observed in the density of NPY- and catecholamine-containing nerves. The results are discussed in relation to autonomic neuropathy of the cerebral blood vessels in diabetes.
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PMID:Reduction of nerves containing vasoactive intestinal polypeptide and serotonin, but not neuropeptide Y and catecholamine, in cerebral blood vessels of the 8-week streptozotocin-induced diabetic rat. 329 10

Abnormal pressor responses are known to occur in the maternal circulation in pregnancy-induced hypertension (PIH), but little is know of the response of the foetal circulation. The responsiveness of umbilical arteries in PIH can be studied after delivery, and this is a useful model to explore the pathophysiological mechanisms involved. In the present experiments, the in vitro response of umbilical artery rings to bradykinin and 5-hydroxytryptamine (5-HT) was tested and ultrastructural changes investigated. Umbilical arteries from 48 cords were studied. Fifteen of the mothers had PIH, five had essential hypertension pre-dating the pregnancy and five had diabetes. Twenty-three women had pregnancies uncomplicated by hypertension or serious medical or obstetric problems and these served as controls. Umbilical arteries from the severe proteinuric PIH group were significantly more responsive to 5-HT as assessed by affinity constants (P less than 0.05). The responsiveness of arteries from all other groups did not differ from the normal cases. A probable mechanism for the findings is endothelial damage as a result of pre-eclamptic disease. This was substantiated by ultrastructural evidence.
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PMID:Umbilical artery reactivity and ultrastructural changes in pregnancy-induced hypertension and other complicated pregnancies. 342 82

Diabetes was induced in rats by a single intraperitoneal injection of streptozotocin (65 mg kg-1). Rabbits were rendered diabetic by injecting alloxan (100 mg kg-1) into the lateral ear vein. Diabetes was confirmed by a significant elevation of serum glucose in both species 8 weeks after injection. The maximum contraction to noradrenaline (NA), 5-hydroxytryptamine (5-HT) and KCl was markedly diminished in thoracic aortic rings (AR) from diabetic rats with no change in the EC50 of the agonists. There were no differences in the contractile properties of AR from diabetic rabbits to NA, 5-HT or KCl. Diabetes did not alter the responsiveness of AR from the rat to angiotensin II (AII). However, AR from diabetic rabbits displayed a decreased maximal contraction and an increased EC50 to AII. The magnitude of the acetylcholine-induced relaxation to precontracted AR was not different between diabetic and control rats and rabbits. The contractile responses of AR to NA, 5-HT and KCl were depressed in diabetic rats, regardless of the control tissue to which they were compared. The decrease in maximal contraction to NA, 5-HT and KCl seen in diabetic animals was prevented by insulin replacement. The results demonstrated that while both rats and rabbits exhibited a similar degree of hyperglycemia after treatment with a diabetogenic agent, aortic preparations from the rabbit are not affected in the same way as the aorta from the diabetic rat when exposed to NA, 5-HT and KCl. This feature may be related to the marked differences between the extent of sympathetic innervation of the aorta in the rabbit and rat. Furthermore, the decrease in maximal contraction in rat aorta was non-specific with respect to agonists since it could also be demonstrated with KCl. Therefore, it follows that the diabetic state may affect processes responsible for contraction beyond the level of receptor activation.
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PMID:A contrasting effect of the diabetic state upon the contractile responses of aortic preparations from the rat and rabbit. 360 57

1. Arachidonic acid (AA, 0.125-1.0 mg/kg) injected via the aorta into the autoperfused hindquarters caused dose-dependent increases in perfusion pressure. This effect was reduced after intravenous administration of the thromboxane receptor antagonist AH23848 (5 mg/kg) or indomethacin (5 mg/kg). 2. Responses to AA (0.125-1.0 mg/kg) were reduced markedly in the Krebs-perfused hindquarters when compared with those occurring in the blood-perfused preparation. 3. Doses of guanethidine (1 mg/kg) and pentacynium (1 mg/kg) blocking pressor responses to intravenous administration of the ganglion stimulants McN-A-343 and DMPP, respectively, did not affect responses to AA. 4. Constrictor responses to AA (0.5-1.0 mg/kg) in blood-perfused hindquarters were increased in 14 day alloxan-diabetic rats but those to the thromboxane A2-mimetic U46619 (0.5-8.0 micrograms/kg, i.a.) were reduced when compared with non-diabetic controls. 5. In 14 day alloxan-diabetic rats vasoconstrictor responses to noradrenaline and methoxamine were potentiated but those to 5-hydroxytryptamine were reduced compared with non-diabetic animals. 6. It is concluded that AA causes constriction in the blood-perfused hindquarters by release of a product of cyclo-oxygenase acting on thromboxane A2-receptors. A constituent of blood, perhaps the platelet, appears necessary for this effect. Conversion of AA to the constrictor metabolite is augmented during experimentally induced diabetes.
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PMID:Sensitivity changes of the perfused hindquarters' vasculature in rats with alloxan-induced diabetes mellitus. 367 85

The 5-hydroxytryptamine (5HT)-system of human blood platelets consists of a relatively specific uptake mechanism for 5HT at the plasma membrane, intracellular storage organelles (dense bodies), a metabolizing enzyme (monoaminoxidase B) and a 5HT2-receptor whose stimulation leads to activation of the phosphatidylinositide turnover, a rise in free cytoplasmic Ca2+, phosphorylation of proteins and a shape change reaction. There is neither a relevant 5HT-biosynthesis nor a marked physiological 5HT-turnover in platelets. Under physiological conditions the platelet 5HT-system may have a role as a scavenger for free extracellular 5HT and in hemostasis. Disturbances which have been described in pathophysiological states include impairment of 5HT-uptake (hypertension, migraine), impairment of 5HT-storage (storage pool deficiencies, thromboembolic disorders, hypertension) and increased sensitivity to activating agents like 5HT (cardiovascular disorders, diabetes). Besides their role in physiology and pathophysiology platelets may be useful partial models for vascular smooth muscle cells.
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PMID:The 5-hydroxytryptamine system of blood platelets: physiology and pathophysiology. 381 34

Platelets from patients with type 1 diabetes have exhibited more sensitivity to aggregation when compared with platelets from controls without diabetes after challenge with platelet-activating factor (PAF). The production of thromboxane B2 (TxB2) and 12-hydroxyeicosatetraenoic acid (12-HETE) and the release of 5-hydroxytryptamine (5HT) were increased when the platelets were challenged by PAF (5.0 X 10(-6) mol/L and 1.0 X 10(-6) mol/L). The production of TxB2 and 12-HETE and the release of 5HT were related to the irreversible biphasic aggregation profiles observed in the patients with diabetes. Inhibition of thromboxane A2 (TxA2) production by acetylsalicylic acid abolished the secondary wave of aggregation of platelets from patients with diabetes, changing an irreversible aggregation to a reversible one. Inhibition of both TxA2 and 12-HETE production by eicosatetraynoic acid did not contribute further to the inhibition caused by acetylsalicylic acid alone, indicating that 12-HETE was not involved in the secondary wave of aggregation. These data show that the increased aggregation observed in the platelets from the group with diabetes in response to PAF results in part from their higher production of TxA2 and release of 5HT.
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PMID:Action of platelet-activating factor on type 1 diabetic human platelets. 398 Oct 54

Diabetic rats (alloxan diabetes) were exposed to cadmium (2 mg kg-1 i.p.) daily for 21 days to investigate the levels of blood glucose, biogenic amines and iron, copper, zinc and cadmium in the brain. Cadmium exposure to diabetic rats produced a significant exacerbation in the hyperglycemic effect and accumulation of cadmium in the blood compared with that observed after diabetes or cadmium exposure alone. The elevation in the levels of brain dopamine and 5-hydroxytryptamine were also more pronounced in cadmium-exposed diabetic rats compared with either cadmium exposure or diabetes alone. Cadmium exposure to diabetic rats also produced significant changes in the concentrations of copper in the blood. These results indicated enhanced cadmium toxicity in diabetic rats.
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PMID:Biogenic amines and some metals in brain of cadmium-exposed diabetic rats. 407 19

The effect of diabetes induced by treatment of rats with streptozotocin on metabolism of circulating 5-hydroxytryptamine (5HT) was investigated using an in situ lung perfusion preparation. Tissue uptake of 5HT and production of its metabolite, 5-hydroxyindolacetic acid, were unaffected in lungs of diabetic animals provided 2 or 20 microM exogenous 5HT. At constant perfusion pressure, pulmonary flow was not altered by substrate concentration or by streptozotocin treatment. Thus, in the experimental models of diabetes used, metabolism of circulating 5HT by the pulmonary endothelium remained unaffected.
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PMID:Effect of diabetes on metabolism of 5-hydroxytryptamine by rat lungs perfused in situ. 617 31


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