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)

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

Chronic idiopathic constipation may be the result of an autonomic neuropathy. This hypothesis was tested in 23 constipated patients and 17 age matched controls, using the acetylcholine sweat spot test devised to test autonomic integrity in diabetes. Acetylcholine (0.01%) was injected in the dorsum of the foot painted with a mixture of starch and iodine. Active sweat glands appeared on the surface of the skin as small black dots which were photographed and counted, using a grid with 60 subareas. Two measurements were made: the number of dots per unit subarea (sweat spot test score) and the % number of abnormal subareas (with less than six spots). These two parameters were correlated. The median sweat spot test score was 9.53 in patients and 13.92 in controls (p = 0.0001), the receiver operating characteristic curve showing that a score of 12 delimited normal and abnormal subjects. Increasing age was correlated with a low score in patients, probably because of prolonged symptoms. Seventy per cent of patients and one control had a borderline or abnormal number of subareas. These results suggest that idiopathic constipation is associated with a degree of autonomic denervation. The sweat spot test is an easy, inexpensive method to test this hypothesis and deserves a place in the clinical assessment of slow transit constipated patients.
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PMID:Detection of subclinical autonomic neuropathy in constipated patients using a sweat test. 145 80

1. The effect of short- and long-term streptozotocin (STZ)-induced diabetes (12 and 52 weeks) on the vascular response to phenylephrine was examined in the isolated thoracic aorta with and without intact endothelium from diabetic, age matched control rats and diabetic rats treated with insulin. 2. Twelve weeks after induction of diabetes, aortae with intact endothelium demonstrated no changes either in sensitivity (defined as pD2) or contractility (defined as the maximal developed tension per aortic tissue wet weight) to phenylephrine. 3. In contrast, 52 weeks after induction of diabetes, aortae with intact endothelium demonstrated an increased sensitivity to phenylephrine while contractility to phenylephrine was not changed. Insulin treatment partially corrected the increased sensitivity to phenylephrine observed in diabetic rat aorta. 4. Removal of endothelium abolished the difference in phenylephrine sensitivity between diabetic and control aortae at 52 weeks. 5. Pretreatment of intact aortae with methylene blue, an inhibitor of endothelium-derived relaxing factor (EDRF), abolished the difference in phenylephrine sensitivity between control and diabetic rat aortae at 52 weeks, while pretreatment with indomethacin, an inhibitor of cyclo-oxygenase, had no effect. These results suggest that decreases in production or release of EDRF might be responsible for the increased vascular sensitivity to phenylephrine observed in long-term STZ diabetic rats. 6. Acetylcholine-induced relaxation, which is EDRF-dependent, was less in diabetic rat aortae with intact endothelium at 52 weeks, but not at 12 weeks. These results further support the theory that decreases in capacity of the endothelium to synthesize or release EDRF may occur in long-term STZ diabetic rats.
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PMID:Endothelium-dependent increase in vascular sensitivity to phenylephrine in long-term streptozotocin diabetic rat aorta. 146 44

The influences of chronically diabetic states on contraction and relaxation responses of the isolated basilar artery and aorta to various vasoactive agents were examined in alloxan-induced diabetic rabbits with 2 years duration. There were no significant differences in the reactivities of basilar artery to norepinephrine (NE), 5-hydroxytryptamine (5-HT) and KCl between age-matched control and diabetic rabbits. Maximal contractions of aorta with endothelium in response to NE and 5-HT were significantly enhanced in case concentration-response curves for NE and 5-HT-induced contractions in the aorta without endothelium from diabetic rabbits were not different from those from age-matched control rabbits. Acetylcholine-induced relaxations in both the basilar artery and aorta from diabetic rabbits were significantly attenuated compared with those from age-matched control rabbits. However, no differences were observed in concentration-response curves for sodiumnitroprusside-induced relaxations in both the basilar artery and aorta between diabetic rabbits and age-matched control rabbits. These results indicate that chronic diabetes induces an specific enhancement in the contractile responses to NE and 5-HT in aorta and an attenuation in the endothelium-dependent relaxation in both the basilar artery and aorta. These results further demonstrated that the cerebral artery is resistant to diabetes of 2 years duration as compared with the peripheral artery.
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PMID:Effects of chronic diabetes on vascular responses of basilar artery and aorta from rabbits with alloxan-induced diabetes. 180 Nov 4

The contribution of peripheral arterial tissue to the development of vascular changes in Diabetes Mellitus (DM) was studied using the perfused tail artery from rats treated with Streptozotocin (25 mg/kg ip for 5 days). Dose-response curves to KCl and phenylephrine (PE) were constructed; the response to PE was significantly higher in DM than control arteries. No difference was found in the response to KCl between DM and controls. The response to vasodilators Acetylcholine (Ach), Papaverine, PAF-Acether were independent of the type of vasoconstrictor used to increase the vascular tone (KCl or PE). The response in the diabetic was significantly smaller than in the control arteries. The infusion of Indomethacin had no effect on the vasodilator response but enhanced the response to PE. The mechanical removal of endothelium increased the response to PE; presumably the vasoconstriction elicited by PE is counterbalanced by the release of vasodilators such as PGI2 and EDRF of endothelium origin. Infusion of Methylene Blue, that inhibits intracellular accumulation of c-GMP, in DM and control preparations partially blocked papaverine response and totally abolished the response to Ach and PAF-Acether. These data support an active participation of the peripheral arterial wall to the pathological changes present in diabetes mellitus.
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PMID:Contribution of the arterial tissue to vascular pathology in diabetes mellitus. 237 18

Endothelium-dependent relaxations and vasoactive prostanoid production caused by acetylcholine were determined in the aortas of rabbits with diabetes mellitus induced by alloxan. Aortas of diabetic rabbits, contracted submaximally by phenylephrine, showed significantly decreased endothelium-dependent relaxations induced by acetylcholine compared with the aortas of normal rabbits. Indomethacin, a cyclooxygenase inhibitor, and SQ 29548, a prostaglandin H2-thromboxane A2 (PGH2-TxA2) receptor antagonist, normalized the sensitivity of diabetic aortas to acetylcholine, whereas these agents had no effect on the response of normal aortas. The relaxations in response to a nonreceptor-mediated endothelium-dependent vasodilator, A23187, and an endothelium-independent vasodilator, sodium nitroprusside, were not different between normal and diabetic aortas. Acetylcholine also caused contractions of resting aortic rings with endothelium from diabetic, but not normal rabbits; these contractions were inhibited by indomethacin. Synthesis of TxA2, measured as immunoreactive TxB2, was significantly increased in diabetic aortic segments only when the endothelium was present. These results suggest that in the diabetic state, the endothelium releases a major vasoconstrictor cyclooxygenase product that either directly counteracts the relaxation caused by or selectively interferes with the release of endothelium-derived relaxing factor(s) induced by cholinergic receptor stimulation. The vasoconstrictor is most likely TxA2 or possibly its precursor, PGH2.
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PMID:Contraction of diabetic rabbit aorta caused by endothelium-derived PGH2-TxA2. 251 65

1. Acetylcholine (ACh)-induced relaxation of aortic strips with endothelium and production of cyclic GMP between streptozotocin-induced diabetic and age-matched control rats were compared. 2. The concentration-response curve for ACh-induced relaxation was shifted to the right in diabetic rats. IC50 values for ACh were 4.57 +/- 0.67 x 10(-8) M and 1.00 +/- 0.87 x 10(-7) M in aortic strips from age-matched control and diabetic rats, respectively (n = 6, P less than 0.05). 3. Relaxations produced by atrial natriuretic peptide (ANP) in diabetic aortae were similar to those in age-matched vessels. 4. Relaxations produced by sodium nitroprusside (SNP) in diabetic aortae were similar to those in age-matched vessels. 5. Basal levels of cyclic GMP and ACh-induced production of cyclic GMP were significantly decreased in diabetic rats. 6. These results suggest that functional changes in endothelium but not in guanylate cyclase activity in the aorta may occur in diabetes, and thus, spontaneous and ACh-induced formation of cyclic GMP may be decreased. This decrease in production of cyclic GMP may be responsible for the decreased response of the aorta to the relaxant effect of ACh.
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PMID:Impairment of endothelium-dependent relaxation and changes in levels of cyclic GMP in aorta from streptozotocin-induced diabetic rats. 254 80

This paper describes the value of non-invasive neurovascular function tests in the clinical setting. Painful transcutaneous electrical nerve stimulation (TENS) of the dorsum of the foot evoked axon reflex vasodilatation, measured by laser Doppler flowmetry. In addition, acetylcholine and sodium nitrite (NaNO2) were iontophoresed to cause vasodilatation by endothelium-dependent and -independent mechanisms, respectively. Compared with healthy volunteers, diabetic patients with clinically diagnosed neuropathy showed reduced electrical axon reflex flare responses. These responses in one additional subject were absent in a region of denervated skin. Acetylcholine responses, but not NaNO2 responses, were also depressed in patients with diabetic neuropathy. Such reduced cutaneous nocifensor functions may contribute to some symptoms and complications of diabetes mellitus.
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PMID:Non-invasive tests of neurovascular function. 326 38

Acetylcholine (ACh) is localized in the syncytiotrophoblast layer of the human placental villous tissue. An attempt was made to correlate the ACh synthesis in different pathological placentas with the histopathology of the syncytiotrophoblast available in the literature. The ACh synthesis was estimated by 'in vitro' incubation of the placental tissue. Full-term (36-38 weeks) vaginally delivered pathological placentas and hydatid moles (28 weeks) were compared with normal placentas of the same age. The results suggested that: ACh synthesis is normal in states with normal syncytiotrophoblast (e.g., healthy greater than 42 week placenta, placenta praevia, twins, and hydramnios); high ACh synthesis is correlated with hormonal and immunological changes (e.g., diabetes mellitus and Rh-incompatibility); low levels of ACh synthesis occur in states with moderate syncytial degeneration (e.g., nephrotic syndrome and essential hypertension); very poor ACh synthesis occurs when syncytial degeneration is advanced (e.g., preeclampsia, eclampsia, intra-uterine death of fetus, vesicles of hydatid mole and placental tissue infarcts); and ACh synthesis is nil in material that is completely devoid of syncytiotrophoblast (e.g., placental tissue-like material, which rarely appears in between the vesicles of hydatid moles). In essence, the degree of reduction in ACh synthesis seems to correlate with the state of the syncytiotrophoblast in various pathological conditions; and ACh synthesis is greatly reduced during syncytial degeneration. It is concluded that the capacity of the placenta to synthesize ACh reflects the state of the syncytiotrophoblast.
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PMID:A correlative review of acetylcholine synthesis in relation to histopathology of the human syncytiotrophoblast. 379 52

Acetylcholine (ACh), choline acetyltransferases and cholinesterases occur in cornea, iris-ciliary body complex and retina of several vertebrates. In cornea, ACh may serve as a sensory transmitter as well as a local hormone, the function of which is not delineated. The function of ACh as the parasympathetic neurotransmitter at the iris and ciliary body is well established. The muscarinic receptors on the iris smooth muscle are similar to the muscarinic receptors (M2 type in two way classification) at other smooth muscles towards their interaction with agonists and antagonists. Binding studies using radiolabeled antagonists and their displacement by agonists indicate that muscarinic receptors in membranes of iris-ciliary body complex are heterogeneous indicating more than one subtype of muscarinic receptors. A subtype other than M2 receptors may occur at the presynaptic sites of parasympathetic nerves, which have yet to be investigated using specific agonists and antagonists. Cholinergic markers, choline acetyltransferase and acetylcholinesterase, differ quantitatively and qualitatively in retinas of different species. However, amacrine cells are cholinergic in all vertebrate species. Although they make up 1% of retinal neurons, they influence the activity of a majority of ganglion cells. Cholinergic effects in ganglia are mediated through nicotinic and muscarinic receptors. Both of these types of cholinergic receptors are heterogeneous. They have yet to be investigated for their subtypes using specific agonists and antagonists. Although the role of cholinergic retinal neurons in the processing of visual information is not known, their input to ganglion cells generally increases the rate of spontaneous activity or the number of action potentials in light-evoked responses. Thus, the cholinergic input seems to modify the overall neuronal input to the ganglion cells from the receptive fields. Endothelial cells of blood vessels contain muscarinic receptors, which are activated by ACh to cause relaxation. Although retinal blood vessels provide recognizable characteristic signs in diabetes mellitus and hypertensive disease, no information is available on the muscarinic receptors of these vessels.
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PMID:Cholinergic systems and multiple cholinergic receptors in ocular tissues. 391 49


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