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

1. Endothelial cells of blood vessels generate factors which can modulate underlying smooth muscle tone, inducing vasorelaxation, (endothelium-derived relaxing factor, EDRF, and endothelium-derived hyperpolarizing factor) and/or vasoconstriction (endothelium-derived contracting factors, EDCFs, including the peptide endothelin). 2. EDRF is nitric oxide (NO) or a RNO compound from which this oxide is released. Its half-life is very short (6-50 sec), and it produces rapid vasodilations and inhibits platelet aggregation. 3. NO is formed from the terminal guanidino of L-arginine, but not of D-arginine. NO effects and NO formation are inhibited by NG-monomethyl-L-arginine (L-NMMA), but not by D-NMMA. These inhibitory effects are blocked by L-arginine. 4. Removal of endothelium or pathological situations that can induce endothelial dysfunction (atherosclerosis, diabetes, hypertension or subarachnoid hemorrhage) cause increases on the vascular contractility elicited by agonists (noradrenaline, serotonin, EDCFs, etc.). These findings suggest that EDRF produces a physiological inhibitory modulation of vascular smooth muscle tone and its alteration produces or facilitates the development of diseases such as hypertension or coronary and cerebral vasospasm.
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PMID:Role of endothelium-formed nitric oxide on vascular responses. 227 79

In order to find out objective indices for "hidden" hypoglycemia in diabetic patients the urine excretion of the catecholamines adrenaline, noradrenaline, dopamine and the serum levels of cortisol and somatotrophic hormone (STH) were followed up. 45 diabetics on insulin treatment were included in the study: 32 patients with type I diabetes mellitus and 13 patients with diabetes mellitus type II with secondary resistance to sulfanilurea drugs and insulin. The patients were classified into the following groups: I. without hypoglycemia--28 patients; 2. with diurnal hypoglycemia--6 patients and 3. with nocturnal hypoglycemia--II patients. In the patients with hypoglycemia the 24 h adrenaline urine excretion was higher than in the patients without hypoglycemia. No such differences were found for noradrenaline and dopamine. The separate examination of the diurnal and nocturnal catecholamines excretion showed in all groups that they cannot serve as an objective index for determination of hypoglycemia. The STH showed no differences in all groups of diabetics. Disturbances in the circadian rhythm of cortisol secretion in diabetics were found. This could be a good and available marker for detecting "hidden" hypoglycemia in diabetics.
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PMID:[Catecholamine excretion in diabetics on insulin treatment]. 228 57

This study was aimed at evaluating cardiac function, both systolic and diastolic, in young type 1 diabetics with a mean duration of the disease of 10.9 +/- 6 years and without evidence of cardiac autonomic neuropathy and micro- or macroangiopathy. Thirteen diabetics, with good metabolic control, and 10 normal matched subjects were studied by echocardiography at rest and by radionuclide ventriculography both at rest and during effort. The level of plasma catecholamines was also determined. The echocardiographic data were comparable in the two groups. Scintigraphic data showed an increased peak ejection and peak filling rate (P less than 0.001) in diabetics while the other indices of cardiac function were comparable. Norepinephrine (P less than 0.01) and epinephrine (P less than 0.001) were higher in diabetics. A hypothesis is formulated that the higher indices of flow velocities in type 1 diabetics are supported by a sympathetic overactivity.
Diabetes Res Clin Pract 1990 Jan
PMID:Cardiac function and sympathetic activity in young diabetics. 230 95

The influence of alloxan-induced diabetes mellitus on the sympathetic neuroeffector junction of the rabbit carotid artery denuded of endothelium was studied. Six weeks of diabetes resulted in a neuropathy characterized by a 38% reduction in the arterial content of norepinephrine. Norepinephrine release from the nerves measured from electrically stimulated superfused arterial segments was decreased. The cocaine-sensitive accumulation of [3H]-norepinephrine (NE) was also reduced, reflecting decreased neuronal uptake. The consequences of these prejunctional changes were studied by measuring isometric contractions of arterial rings caused by electrical nerve stimulation or by exogenous norepinephrine. Despite the reduced release of norepinephrine, neurogenic contractions were normal, suggesting an increased sensitivity of the smooth muscle. After neuronal uptake was blocked, the neurogenic contractions of diabetic arteries were less than normal, reflecting the reduction in transmitter release. The sensitivity of diabetic arteries to exogenous norepinephrine was increased under control conditions; maximal contractions were unchanged. Blockade of norepinephrine uptake increased norepinephrine sensitivity more in normal than in diabetic arteries, and there was no longer a significant difference in sensitivity. Thus, under control conditions, neurogenic contractions of the partially denervated diabetic rabbit carotid artery are paradoxically normalized by increased alpha-adrenergic sensitivity of the smooth muscle. The increased sensitivity caused by reduced neuronal uptake can thus preserve neurogenic vasoconstriction and cause supersensitivity to exogenous catecholamines in the sympathetic neuropathy caused by diabetes mellitus.
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PMID:Adrenergic denervation in rabbits with diabetes mellitus. 237 13

Platelet and plasma vasoactive amine concentrations were measured in healthy controls and in type 1 (insulin-dependent) diabetic patients with or without vascular disease. Platelet concentrations of serotonin and noradrenaline were similar in all groups and were unrelated to age or gender, or to duration of diabetes, blood pressure, glycaemia or renal function in the diabetic subjects. Plasma concentrations of serotonin in the diabetic groups were comparable (118 +/- 16 (mean +/- SEM) and 127 +/- 21 pmol/mL), and were significantly higher in comparison to the healthy controls (66 +/- 12 pmol/mL, P = 0.002).
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PMID:Platelet and plasma vasoactive amines in type 1 (insulin-dependent) diabetes mellitus with and without vascular disease. 238 58

Penile tissue (consisting of corpus cavernosum and tunica albuginea) was obtained from 19 patients undergoing surgery for the implantation of penile prostheses. The tissue was examined for vasoactive intestinal polypeptide-like immunoreactivity in nerves, acetylcholinesterase-positive staining in nerves and noradrenaline content. Impotence was due to a variety of causes; 11 patients were classified as a 'non-neuropathic' group on the basis of their clinical history which included Peyronie's disease, vascular disease, hypertension and psychogenic impotence. Vasoactive intestinal polypeptide-like immunoreactive and acetylcholinesterase-positive nerves were present and the pattern and distribution were similar in each patient in this group. The noradrenaline content of the tunica albuginea was significantly lower than the corpus cavernosum (p less than 0.02), although there was a linear relationship between the noradrenaline contents of the two regions (r = 0.95, p less than 0.01). By comparison, a complete absence of vasoactive intestinal polypeptide-like immunoreactivity in nerves was observed in a patient with a cauda equina lesion. Five out of six diabetic patients studied revealed a marked reduction in vasoactive intestinal polypeptide-like immunoreactivity in nerves associated with the cavernous smooth muscle, while acetylcholinesterase-positive staining was reduced in three out of five diabetic patients studied. The noradrenaline content of the corpus cavernosum from diabetic patients was significantly lower (p less than 0.02) than that of the 'non-neuropathic' group. The noradrenaline content of the tunica albuginea, however, was similar in both groups. The results provide evidence that VIPergic, cholinergic and adrenergic nerves in the penis are affected in diabetes mellitus and thus may contribute to the development of impotence in diabetic patients.
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PMID:Changes in the VIPergic, cholinergic and adrenergic innervation of human penile tissue in diabetic and non-diabetic impotent males. 243 29

Streptozotocin-induced diabetes produced marked alterations of monoamine concentrations in several hypothalamic nuclei of male and female rats. Norepinephrine (NE) concentrations were significantly elevated in the median eminence (ME), supraoptic nucleus (SON) and periventricular nucleus (PEVN) in both sexes of diabetic rats. NE concentrations in the suprachiasmatic nucleus (SCN) and ventromedial nucleus (VMN) of male and female diabetic animals remained unaltered. Serotonin (5-HT) concentrations were increased in PEVN of male and female diabetic rats. No significant changes in hypothalamic dopamine (DA) concentrations were observed. Insulin treatment reversed the diabetes-related changes in monoamine concentrations in most of the nuclei. The significance of these biochemical changes relative to the endocrine and behavioral abnormalities in diabetes is discussed.
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PMID:Diabetes-induced changes in monoamine concentrations of rat hypothalamic nuclei. 243 7

The gross anatomy and autonomic innervation of the ventral prostate glands was examined in control and streptozotocin-induced diabetic rats. The most striking finding was the consistent reduction in size and the gross atrophy of the prostates from diabetic rats. No change was detected in the total content of noradrenaline in the alveolar lobes or in the levels of vasoactive intestinal polypeptide, neuropeptide Y and substance P in the whole prostates of diabetic rats. However, histochemical and immunohistochemical investigations revealed localized reductions in density and/or fluorescence intensity of noradrenaline-containing nerve fibres and increased density and/or fluorescence intensity of vasoactive intestinal polypeptide- and neuropeptide Y-containing nerve fibres in the alveolar smooth muscle of a majority of diabetic animals. No changes in acetylcholinesterase-staining nerve fibres were seen. The adrenergic component of the autonomic nervous system in this gland appears to be particularly susceptible to change in diabetes.
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PMID:Histochemical and biochemical investigation of adrenergic, cholinergic and peptidergic innervation of the rat ventral prostate 8 weeks after streptozotocin-induced diabetes. 244 38

The effect of progression of diabetes on adrenergic, serotonergic, and peptidergic innervation of the proximal colon of the rat at 8, 16, and 25 wk after induction of diabetes with streptozotocin was investigated using immunohistochemical, biochemical, and immunochemical methods. Two different responses to diabetes emerged from the present study. The first response, which involves noradrenaline and vasoactive intestinal peptide, was characterized by a sign of degeneration, where there was an initial increase in tissue level and immunoreactivity of the transmitters followed by a decrease in tissue level and density of nerve fibers at 16 and 25 wk after induction of diabetes. The second response, which involves 5-hydroxytryptamine, substance P, and calcitonin gene-related peptide, was characterized by changes in tissue level and immunoreactivity of the transmitters with no evidence of degeneration. The third feature was one of resistance to change due to diabetes, which was demonstrated by neuropeptide Y-containing nerves, where there was neither a change in tissue level of neuropeptide Y nor a change in immunoreactivity. It seems likely that the overall changes described will have profound implications in the function of the gut in the streptozotocin-diabetic rat model that may have some parallels in diabetic humans.
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PMID:Progressive changes in adrenergic, serotonergic, and peptidergic nerves in proximal colon of streptozotocin-diabetic rats. 245 87

Content of noradrenaline was decreased in neocortex and brain stem of rat brain by 70% and 50%, respectively, and that of serotonin--by 50% in the neocortex after development of the diabetic syndrome. At the same time, the RNA synthesizing ability of brain chromatin from the experimental animals was 3-fold higher as compared with controls. Catecholamines (L-DOPA, dopamine, noradrenaline) activated the RNA synthesis in controls by 40-50%, whereas in the animals with alloxane diabetes the effect was distinctly decreased. In vitro inhibitory effect of serotonin on the RNA synthesis was markedly decreased in preparations of brain chromatin from diabetic rats. Inhibitory effect of actinomycine D on the RNA synthesis was neutralized completely in controls after preincubation of the brain chromatin with L-DOPA, while only partial influence was detected in diabetic rats.
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PMID:[RNA-synthesizing activity of brain chromatin in rats with experimental alloxan diabetes]. 246 37


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