1. |
- Andersson, Michael, 1980, et al.
(författare)
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Muscarinic receptor subtypes involved in urothelium-derived relaxatory effects in the inflamed rat urinary bladder.
- 2012
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Ingår i: Autonomic neuroscience : basic & clinical. - : Elsevier BV. - 1872-7484. ; 170:1-2, s. 5-11
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Tidskriftsartikel (refereegranskat)abstract
- Functional studies have shown altered cholinergic mechanisms in the inflamed bladder, which partly depend on muscarinic receptor-induced release of nitric oxide (NO). The current study aimed to characterize which muscarinic receptor subtypes that are involved in the regulation of the nitrergic effects in the bladder cholinergic response during cystitis. For this purpose, in vitro examinations of carbachol-evoked contractions of inflamed and normal bladder preparations were performed. The effects of antagonists with different selectivity for the receptor subtypes were assessed on intact and urothelium-denuded bladder preparations. In preparations from cyclophosphamide (CYP; in order to induce cystitis) pre-treated rats, the response to carbachol was about 75% of that of normal preparations. Removal of the urothelium or administration of a nitric oxide synthase inhibitor re-established the responses in the inflamed preparations. Administration of 4-diphenylacetoxy-N-methylpiperidine (4-DAMP) inhibited the carbachol-induced contractile responses of preparations from CYP pre-treated rats less potently than controls. Pirenzepine and p-fluoro-hexahydro-sila-diphenidol (pFHHSiD) affected the carbachol-induced contractile responses to similar extents in preparations of CYP pre-treated and control rats. However, the Schild slopes for the three antagonists were all significantly different from unity in the preparations from CYP pre-treated rats. Again, l-NNA or removal of the urothelium eliminated any difference compared to normal preparations. This study confirms that muscarinic receptor stimulation in the inflamed rat urinary bladder induces urothelial release of NO, which counteracts detrusor contraction.
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2. |
- Andersson, Michael, 1980, et al.
(författare)
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Pharmacological modulation of the micturition pattern in normal and cyclophosphamide pre-treated conscious rats.
- 2011
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Ingår i: Autonomic neuroscience : basic & clinical. - : Elsevier BV. - 1872-7484. ; 159:1-2, s. 77-83
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Tidskriftsartikel (refereegranskat)abstract
- In the current study, we wanted to assess the influence of muscarinic receptors, nitric oxide and purinoceptors on the micturition pattern of conscious normal and cyclophosphamide (CYP) pre-treated rats. The micturition parameters were assessed using a metabolic cage. Rats were pre-treated with either saline or CYP, to induce cystitis, followed by treatment with either the muscarinic M1/M3/M5 receptor antagonist 4-diphenylacetoxy-N-methylpiperidine (4-DAMP), the nitric oxide synthase blocker N(ω)-nitro-L-arginine methyl (L-NAME), the P2 purinoceptor antagonist pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid (PPADS) or a combination of 4-DAMP with PPADS or L-NAME. Voiding volumes per micturition event were significantly lower in CYP pre-treated than in saline pre-treated rats. Neither 4-DAMP nor L-NAME had any effect in the normal rats, whereas PPADS reduced the micturition volume per event. In CYP pre-treated rats, 4-DAMP and L-NAME significantly increased voiding volumes per event and micturition frequency, respectively. 4-DAMP dose-dependently reduced the differences in micturition activity between saline and CYP pre-treated rats. We show that cystitis changes the urodynamics in conscious rats and that this change seems to depend on the production of NO and on altered muscarinic receptor effects. The altered muscarinic receptor responses are likely to per se involve NO-mediated mechanisms.
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3. |
- Aronsson, Patrik, 1983, et al.
(författare)
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Adenosine receptor antagonism suppresses functional and histological inflammatory changes in the rat urinary bladder.
- 2012
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Ingår i: Autonomic neuroscience : basic & clinical. - : Elsevier BV. - 1872-7484. ; 171:1-2, s. 49-57
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Tidskriftsartikel (refereegranskat)abstract
- Cyclophosphamide (CYP) induces an interstitial cystitis-like inflammation. The resulting bladder dysfunction has been associated with increased release of adenosine-5'-triphosphate (ATP), structural bladder wall changes and contractile impairment. Due to the inflammatory modulatory effects of purines it was presently wondered if pre-treatment with P1 and P2 purinoceptor antagonists affect the CYP-induced alterations. Rats were pre-treated with saline or antagonists for five days, and 60h before the in vitro functional examination the rats were administered either saline or CYP. Histological examination revealed CYP-induced bladder wall thickening largely depending on submucosal enlargement, mast cell invasion of the detrusor muscle, increase in muscarinic M5 receptor expression and macrophage migration inhibitory factor (MIF) occurrence in large parts of the urothelium. Functionally, methacholine- and ATP-evoked contractions were smaller in urinary bladders from CYP-treated rats. Pre-treatment with the P2 purinoceptor antagonist suramin and the P1A2B antagonist PSB1115 did not to any great extent affect the CYP-induced changes. The P1A1 antagonist DPCPX, however, abolished the difference of methacholine-evoked contractions between saline- and CYP-treated rats. ATP-evoked contractions were reduced in control after the DPCPX pre-treatment, but not in cystitis. The functional observations for DPCPX were supported by its suppression of CYP-induced submucosal thickening, muscarinic M5 receptor expression and, possibly, detrusor mast cell infiltration and the spread of urothelial MIF occurrence. Thus, P1A1 is an important pro-inflammatory receptor in the acute CYP-induced cystitis and a P1A1 blockade during the initial phase may suppress CYP-induced cystitis. P1A1 purinoceptors seem to regulate contractility in healthy and in inflamed rat urinary bladders.
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4. |
- Billhult, Annika, et al.
(författare)
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The effect of massage on immune function and stress in women with breast cancer - A randomized controlled trial.
- 2009
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Ingår i: Autonomic neuroscience. - : Elsevier BV. - 1872-7484 .- 1566-0702. ; 150:1-2, s. 111-115
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: To examine the short-term effects of light pressure effleurage on circulating lymphocytes by studying the number and activity of peripheral blood natural killer (NK) cells in patients with breast cancer compared to a control group. Furthermore, the effect of light pressure effleurage on salivary cortisol levels, heart rate and blood pressure was studied. DESIGN: Single centre, prospective, randomized and controlled study. METHODS: Thirty women, aged 50 to 75 years (mean 61 sd=7.2) with breast cancer undergoing radiation therapy in a hospital in southwestern Sweden were enrolled in the study. They were allocated to either receive massage in the form of a full-body light pressure effleurage treatment, or a control visit where they were given an equal amount of attention. Blood samples, saliva, notation of heart rate and blood pressure were collected before and after massage/control visit. Differences in change over time between groups were analyzed by Student's t-test. RESULTS: Light pressure effleurage massage decreased the deterioration of NK cell activity occurring during radiation therapy. Furthermore it lowered heart rate and systolic blood pressure. No effects were demonstrated on cortisol and diastolic pressure. CONCLUSIONS: A single full-body light pressure effleurage massage has a short-term effect on NK cell activity, systolic blood pressure and heart rate in patients with breast cancer. However, the long-term clinical importance of these findings needs to be further investigated.
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5. |
- Delbro, Dick S.
(författare)
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Expression of the non-neuronal cholinergic system in rat beta-cells
- 2012
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Ingår i: Autonomic Neuroscience. - : Elsevier. - 1566-0702 .- 1872-7484. ; 167:1-2, s. 75-77
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Tidskriftsartikel (refereegranskat)abstract
- Various markers of the cholinergic system (like e.g. choline acetyltransferase) were demonstrated by immunohistochemistry in, seemingly, beta-cells of rat pancreas. The findings may suggest an autocrine role of acetylcholine for the beta-cells. (C) 2011 Elsevier B.V. All rights reserved.
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6. |
- Elawa, Sherif, et al.
(författare)
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Sympathetic and vagal interaction in the control of cardiac pacemaker rhythm in the guinea-pig heart: Importance of expressing heart rhythm using an appropriate metric
- 2022
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Ingår i: Autonomic Neuroscience. - : ELSEVIER. - 1566-0702 .- 1872-7484. ; 243
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Tidskriftsartikel (refereegranskat)abstract
- There are many reports that, through pre-and post-junctional mechanisms, sympathetic and parasympathetic (vagal) nerves can interact in the control of heart rate. The predominant interaction is accentuated antagonism (AA), where the bradycardia produced by vagal stimulation (VNS) is amplified when heart rate has been increased by sympathetic stimulation (SNS) or beta-adrenergic agonists. The acetylcholine-activated potassium current (IK,Ach), is the primary driver of vagal bradycardia. To examine the participation of IK,Ach in AA, a series of experiments was performed on isolated, double innervated, guinea-pig atrial preparations. Vagal bradycardia was elicited by 10-s trains (1, 2, 5 and 7.5 Hz) or single bursts of VNS (3 stimuli at 50 Hz) before and during acceleration of HR by either SNS (1-3 Hz) or isoprenaline (ISO), in both absence and presence of tertiapin-Q (TQ-IK,Ach blocker). When expressed as an absolute change in HR (beats/min), bradycardia produced by VNS trains was amplified (AA) at all frequencies of VNS in ISO, and at 5 and 7.5 Hz during SNS. Bradycardia in response to 1 and 2 Hz VNS was reduced during SNS. In TQ, only the bradycardia produced by 5 and 7.5 Hz VNS in ISO was amplified. The bradycardia produced by a single burst of VNS was amplified in both ISO and SNS. After TQ the bradycardia in response to a VNS burst was unchanged in ISO, while it was reduced during SNS. When these data were adjusted to account for the increase in baseline HR brought about by SNS and ISO, there was no longer evidence of AA. Diminished responses to low frequencies of VNS (1 and 2 Hz) persisted, and were also seen during IK,Ach block by TQ. We applied the same adjustment to data from 20 published studies. In 8 studies all data indicated AA; 3 studies provided no evidence for AA, and in 9 studies evidence was mixed. There is no doubt that AA can occur in the control of heart rhythm during simultaneous SNS and VNS, but conditions which determine its occurrence, and the mechanisms involved in this interaction remain unclear.
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7. |
- Erelund, Sofia, et al.
(författare)
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Heart rate variability and cardiovascular risk factors in patients with rheumatoid arthritis : a longitudinal study
- 2023
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Ingår i: Autonomic Neuroscience. - : Elsevier. - 1566-0702 .- 1872-7484. ; 249
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Tidskriftsartikel (refereegranskat)abstract
- Background: It is established that the risk of cardiovascular disease (CVD) is increased in patients with Rheumatoid Arthritis (RA). Heart rate variability (HRV) is a method for evaluating the activity in the cardiac autonomic nervous system. Our aim was to assess the longitudinal development of HRV in patients with RA and compare with healthy controls. Furthermore, we wanted to investigate associations between HRV, inflammatory disease activity and cardiovascular complications in patients with RA over time.Method: HRV was assessed with frequency-domain analysis at baseline and after five years in 50 patients with early RA, all being younger than 60 years. HRV indices were age-adjusted based on the estimated age-dependency in 100 age and sex matched healthy controls. Additionally, clinical data including serological markers, disease activity, and blood pressure were collected from the patients. Eleven years after inclusion CVD was assessed.Results: At baseline, patients with RA presented with lower HRV compared to controls during deep breathing (6 breaths/min), paced normal breathing (12 breaths/min) and after passive tilt to the upright position. No significant change in HRV was observed at the five-year follow-up. A significant negative correlation was found between HRV parameters and systolic blood pressure (SBP) at baseline. A significant positive correlation was found between heart rate and inflammatory markers at baseline but not after five years. Nine patients had developed CVD after 11 years, but no significant association was found with baseline HRV data.Conclusion: This study showed that patients with RA have autonomic imbalance both at an early stage of the disease and after five years, despite anti-rheumatic medication, but no correlation between HRV and inflammation markers were observed. Reduced HRV was also significantly negatively correlated with increased SBP. Hypertension is a common finding in patients with RA. Thus, significant decline of HRV could be a useful early marker for development of hypertension in patients with RA.
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8. |
- Hidestål, Joakim, et al.
(författare)
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Hypersensitivity to noradrenaline in human omental vein but not artery isolated from a patient with idiopathic orthostatic hypotension.
- 2002
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Ingår i: Autonomic Neuroscience: Basic & Clinical. - 1872-7484. ; 97:1, s. 55-58
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Tidskriftsartikel (refereegranskat)abstract
- We investigated the smooth muscle contraction in response to noradrenaline (NA), endothelin-1 (ET) and 5-hydroxytryptamine (5-HT) in the omental artery and vein segments from a 67-year-old woman with idiopathic orthostatic hypotension. The blood vessels were obtained during the abdominal surgery and investigated in vitro. Noradrenaline, endothelin-1 and 5-hydroxytryptamine all induced a contraction in the artery and vein segments. Compared to the literature, the sensitivity to noradrenaline was 10 times higher than expected in the vein. In the artery, the sensitivity to noradrenaline and in both the artery and vein, the sensitivity to endothelin-1 and 5-hydroxytryptamine was similar to that reported in the literature. These results suggest that the patient had developed an isolated hypersensitivity to noradrenaline in the veins, probably due to an impairment of the sympathetic activity.
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9. |
- Klausner, A P, et al.
(författare)
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The role of corticotropin releasing factor and its antagonist, astressin, on micturition in the rat
- 2005
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Ingår i: Autonomic Neuroscience: Basic & Clinical. - : Elsevier BV. - 1872-7484. ; 123:1-2, s. 26-35
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Tidskriftsartikel (refereegranskat)abstract
- The purpose of this investigation was to evaluate the role of corticotropin releasing factor (CRF) on micturition. CRF is involved in the endocrine and central nervous system responses to stress and is also expressed in sites responsible for the control of micturition. In this investigation, cystometric experiments were performed in awake and unrestrained Wistar rats and on Spontaneous Hypertensive Rats, which are used as a rodent model of detrusor overactivity and anxiety. In vitro effects of CRF were evaluated using strips of detrusor muscle in an organ bath preparation. CRF (6.0 mu g) administered via intrathecal and intraperitoneal routes, but not intracerebroventricularly, lowered the micturition threshold. CRF reduced the intercontraction interval by 28% and 26% after intrathecal or intraperitoneal administration, respectively, and reduced micturition volume by 34.7% and 30.2%, respectively. In Wistar-Kyoto rats, 6.0 mu g intrathecal CRF significantly reduced intercontraction interval (423 +/- 79 vs. 669 +/- 59s) and micturition volume (0.30 +/- 0.04 vs. 0.69 +/- 0.07 ml) compared to controls that received saline vehicle. These effects were blocked by pretreatment with 6.0 mu g intrathecal astressin, a potent CRF antagonist, demonstrating that the effects are CRF receptor mediated. In Spontaneous Hypertensive Rats, 6.0 mu G intrathecal CRF was found to have minimal stimulatory effects on the bladder, whereas astressin reduced baseline detrusor overactivity. CRF had no direct contractile effects on detrusor muscle strips. These results demonstrate that in the absence of detrusor overactivity, CRE stimulates micturition when administered via the intrathecal or intraperitoneal routes. Further studies are needed to explore the possibility whether CRF antagonists are effective for detrusor overactivity and the overactive bladder syndrome.
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10. |
- Lin, Z, et al.
(författare)
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Increased expression of nitric oxide synthase in cultured neurons from adult rat colonic submucous ganglia
- 2004
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Ingår i: Autonomic Neuroscience: Basic & Clinical. - : Elsevier BV. - 1872-7484. ; 114:1-2, s. 29-38
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Tidskriftsartikel (refereegranskat)abstract
- Neuronal plasticity in the enteric nervous system (ENS) is probably a key step in intestinal adaptation during growth, maturation and ageing as well as in several pathophysiological situations. Studies on cultured myenteric neurons have revealed an increased vasoactive intestinal peptide (VIP) expression in neuronal nitric oxide synthase (NOS)-expressing neurons. In addition, both VIP and nitric oxide (NO) promote survival of cultured myenteric neurons. The aim of the present study was to investigate possible changes in the expression of VIP and NOS in cultured submucous neurons from adult rat large intestine. Submucous neurons were cultured as explants or as dissociated neurons for 3 and 8 days. Immunocytochemistry was used to determine the proportions of neurons containing VIP or NOS in preparations of uncultured controls (reflects the conditions in vivo) and in cultured explants of submucosa and dissociated submucous neurons. In situ hybridization was used to determine changes in the expressions of NOS and VIP mRNA. The relative number of NOS-expressing neurons increased significantly during culturing. The percentage of all neurons expressing NOS was 22% in controls, while approximately 50% of the cultured submucous neurons expressed NOS. VIP-expressing neurons constituted approximately 80% of all submucous neurons in controls as well as in cultured explants or dissociated neurons. Studies on coexistence revealed that the VIP-containing neurons were the ones that started to express NOS during culture. The induced expression of NOS in cultured adult submucous neurons indicates that nitric oxide, possibly in cooperation with VIP, is important for neuronal adaptation, maintenance and survival. (C) 2004 Elsevier B.V. All rights reserved.
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