Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “RELAXATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,135 records · Page 63Linked to original sources
PubMed1994

Relaxation of retinal pericyte contractile tone through the nitric oxide-cyclic guanosine monophosphate pathway.

PURPOSE: Pericytes are contractile cells outside the endothelial lining of capillaries. The study investigated whether nitric oxide, known to cause relaxation of vascular smooth muscle cells, also relaxes pericytes. METHODS: Cultured bovine pericytes were exposed to a nitric oxide donor, sodium nitroprusside, and to 8-bromoguanosine 3':5'-cyclic monophosphate (8-bromo cGMP) in the presence and in the absence of methylene blue, an inhibitor of guanylate cyclase. Relaxation was assessed by counting the loss of wrinkles induced by pericytes when they are cultured on thin sheets of silicone. Intracellular cyclic guanosine monophosphate (cGMP) was measured by radioimmunoassay. RESULTS: Pericytes relaxed to sodium nitroprusside (3 x 10(-8) to 10(-4) M) in a concentration-dependent manner (ED50: 10(-6) M). The maximal response was characterized by the loss of almost all the wrinkles. The half-maximal relaxation was strongly inhibited by methylene blue (3 x 10(-7) M). Sodium nitroprusside (3 x 10(-6) M) caused a 14-fold increase in the intracellular concentration of cGMP, an effect inhibited by methylene blue (3 x 10(-7) M). The cGMP analogue, 8-bromo-cGMP (10(-5) and 3 x 10(-5) M) strongly relaxed the cells in a concentration-dependent manner, but the relaxation was not reduced by methylene blue (3 x 10(-7) M). CONCLUSIONS: Sodium nitroprusside, which releases nitric oxide, strongly relaxes pericytes through an increase of cGMP. Therefore, the presence of the endothelium-derived relaxing factor nitric oxide in the microcirculation can modulate the tone of pericytes, and it thus has the potential to influence blood flow in capillaries.

Animals↗
PubMed1994

Rapid protein synthesis and turnover is involved in interleukin-1-induced relaxation of the rabbit isolated mesenteric artery. Analysis of the arachidonate cascade.

The rabbit isolated superior mesenteric artery, when precontracted with phenylephrine, relaxes in a sustained manner in less than 30 min when exposed to recombinant interleukin-1 (IL-1), and this is a prostaglandin (PG)-dependent, endothelium- and 5-lipoxygenase-independent process. We have studied the dependency of IL-1-induced relaxation on protein synthesis and trafficking using isolated rings of rabbit mesenteric arteries. Three chemically unrelated protein synthesis inhibitors (PSIs) (cycloheximide, anisomycin and puromycin) completely prevented the response to IL-1. Moreover, the PSIs reversed IL-1-induced relaxations within 15 to 30 min of application. The amplitude and/or the duration of the relaxation induced by arachidonic acid and iloprost (a PGI2 mimetic) were partially inhibited by cycloheximide treatment, but not those induced by nitroglycerin or by cromakalim. However, tissues initially relaxed by IL-1 and then recontracted by a PSI are still able to relax when challenged with either arachidonic acid or iloprost, suggesting that cyclooxygenase is not depleted and that the responsiveness to PGs is intact under these conditions. Manoalide, thioether amide glycerophosphocholine (type II phospholipase A2 inhibitors) or brefeldin A (an inhibitor of intracellular protein trafficking) did not inhibit IL-1-induced relaxation. The data suggest the involvement of newly synthesized protein(s) with a very rapid turnover in the vascular response to IL-1. PSIs probably act at several levels to inhibit the relaxant response to IL-1, but depletion of tissue cyclooxygenase does not appear to be the limiting mechanism for the PSI effect on IL-1-induced relaxations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Effect of some products of protein catabolism on the endothelium-dependent and -independent relaxation of rabbit thoracic aorta rings.

We have investigated the effect that some products of protein catabolism have on endothelium-dependent and -independent relaxation of rabbit aorta rings precontracted with phenylephrine (PE). All the products tested, i.e., creatinine (CRT), guanidinosuccinic acid (GSA), urea (UR), guanidine (GND) and methylguanidine (MG), are structurally related to L-arginine (L-ARG), the substrate for nitric oxide (NO) biosynthesis which accounts for the biological properties of endothelium-derived relaxing factor (EDRF). Endothelium-derived NO (EDNO) release was induced by agents acting via a receptor- [acetylcholine (ACh)] or a nonreceptor-mediated mechanism (calcium ionophore A23187), and the endothelial-independent relaxation was induced by the NO donor glyceryl trinitrate (GTN). CRT (0.1-10 mM) did not modify the endothelium-dependent relaxation caused by ACh or A23187 but produced a small increase in the response to the endothelium-independent vasorelaxant GTN. Concentrations of GSA up to 1 mM did not affect the relaxation of rabbit aortic rings induced by either ACh or A23187, but at 10 mM, GSA enhanced the relaxation produced by these agents. UR (1-100 mM) inhibited, in a concentration-dependent manner, the relaxation induced by ACh, but not that caused by A23187 or GTN. By comparison, GND and MG (0.1-10 mM) produced a concentration-related inhibition of both ACh- and A23187-induced relaxation. The inhibition by these compounds was either completely or partially reversed by L-ARG. In contrast, the relaxation induced by GTN was inhibited only by higher concentrations (10 mM) of GND or MG. These results indicate that some products of protein catabolism can reduce EDNO formation in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

The potent relaxant effect of adenosine in rabbit corpora cavernosa is nitric oxide independent and mediated by A2 receptors.

In the present study the effect of adenosine and adenosine analogues on rabbit isolated cavernosal smooth muscle has been evaluated in comparison with the effect of acetylcholine and electrical field stimulation. In the presence of guanethidine and indomethacin, acetylcholine and electrical field stimulation relaxed the rabbit corpus cavernosum, which was precontracted with phenylephrine. The nitric oxide synthesis inhibitor, N omega-nitro-L-arginine-methylester (L-NAME), greatly reduced the relaxation induced by electrical stimulation and completely abolished the relaxant effect of acetylcholine. A concentration-dependent relaxation of the rabbit corpus cavernosum was produced by adenosine; this effect was not modified by L-NAME, but was reduced by adenosine deaminase. On the other hand, the adenosine-induced relaxation was potentiated by the inhibitor of adenosine deaminase, erythro-9-(2-hydroxy-3-nonyl)adenine and by the adenosine uptake inhibitor dipyridamole. Moreover, the effect of adenosine was antagonized by the unspecific adenosine receptor antagonist 8-phenyltheophylline. The receptor subtypes involved in cavernosal relaxation were characterized by using selective receptor antagonists: 1,3-dipropyl-8-cyclopentylxanthine, a blocker of A, receptors, did not modify adenosine-induced relaxation. This effect was, however, antagonized by the A2-receptor antagonist CGS15943. A relaxant effect was also obtained with nanomolar concentrations of two synthetic adenosine analogues, the preferential A2 receptor agonist 5'-N-ethylcarboxamidoadenosine and the A2a selective agonist CGS21680. These results demonstrated that adenosine has potent relaxant activity on the corpus cavernosum, acting through a mechanism different from the nitric oxide pathway, and that receptors involved in the effect of adenosine belong to the A2a subtype.

Acetylcholine↗
PubMed1996

Novel guanylyl cyclase inhibitor potently inhibits cyclic GMP accumulation in endothelial cells and relaxation of bovine pulmonary artery.

The aim of the present study was: 1) to determine the effects of the novel selective inhibitor of guanylyl cyclase, ODQ (1H-[1,2,4]oxadiazolo[4,3,-a]quinoxaline-1-one) on basal and agonist-stimulated cyclic GMP levels in cultured porcine aortic endothelial cells and bovine pulmonary artery strips; 2) to determine its effects on agonist-induced relaxations of bovine pulmonary artery strips; and 3) to compare pulmonary artery cyclic GMP levels with vessel relaxation. ODQ (1 nM-30 microM) inhibited cyclic GMP accumulation in endothelial cells stimulated with S-nitrosoglutathione, nitroprusside and 3-morpholine-sydnonimine at IC50 values of 40 to 100 nM. Complete suppression of cyclic GMP generation was observed at approximately 10 microM. Relaxation of pulmonary artery strips induced by S-nitrosoglutathione, nitroprusside, glycerol trinitrate, nitrite (all endothelium-independent), bradykinin and the Ca++ ionophore A23187 (endothelium-dependent) were antagonized by ODQ (1-10 microM) in a concentration-dependent way. A consistent feature of the inhibitor was that maximal relaxant effects also were reduced. Basal levels and agonist-induced increases in arterial tissue cyclic GMP were inhibited in the same concentration range. However, tissue cyclic GMP production correlated poorly with pulmonary artery relaxation in that relaxations induced by S-nitrosoglutathione were only inhibited in part (50%), whereas rises in cyclic GMP were abolished completely by ODQ (10 microM). Furthermore, at 1 microM, ODQ had no effect on relaxation induced by endothelium-dependent agonists, but prevented entirely stimulation of cyclic GMP accumulation in arterial tissue. These results suggest that ODQ inhibits nitrovasodilator-induced and endothelium-dependent relaxation through inhibition of guanylyl cyclase activation, but also point to the presence of a cyclic GMP-independent component of relaxation in bovine pulmonary artery.

Animals↗
PubMed1996

Ventricular relaxation in the stage 24 chick embryo following changes in volume and blockade of Na+ and Ca2+ channels.

OBJECTIVE: Early in cardiac development, regulation of cytosolic Ca2+ has been thought to depend primarily on sarcolemmal Ca2+ transport. We hypothesized that perturbation of cytosolic Ca2+ in the embryonic ventricle would result in a change in ventricular relaxation which could be quantified by a monoexponential model. We reasoned that since it has been difficult to selectively block the Na(+)-Ca2+ exchanger in vivo, that blockade of Na+ (lidocaine) or Ca2+ (verapamil) channels in the embryonic heart may perturb cytosolic Ca2+ and thereby alter ventricular relaxation. METHODS: All studies were performed in ovo in Hamilton-Hamburger stage 24 chick embryos. Isovolumic relaxation time (mean +/- standard deviation, 58 +/- 19 ms) was derived from dorsal aortic flow and atrioventricular inflow during 61 cardiac cycles in 4 embryos. Ventricular pressure was digitally recorded from 13 embryos during 188 cycles following intravenous injection of chick Ringer's solution (5 embryos), verapamil (4 embryos) or lidocaine (4 embryos). Ventricular relaxation was characterized by a monoexponential model: P(t) = P infinity + Poe-1/tau where P(t) = pressure at time (t), P infinity = pressure asymptote, Po = pressure at the onset of relaxation and tau = the isovolumic relaxation constant. Non-linear least-squares regression was used to estimate tau and P infinity during isovolumic relaxation at baseline and at 30 s and 60 s post-injection. RESULTS: Ventricular end-diastolic pressure was increased by all three interventions. Both lidocaine and verapamil prolonged cycle length. Lidocaine prolonged tau while chick Ringer's solution and verapamil did not. No significant change in P chi was observed. CONCLUSIONS: This study demonstrates that blockade of Na+ channels with lidocaine slows ventricular relaxation presumably by perturbing cytosolic Ca2+ via the Na(+)-Ca2+ exchange system. Changes following Ca2+ channel blockade with verapamil are less evident in the stage 24 chick embryo. Evaluation of ventricular relaxation may provide a useful way to study developmental aspects of Ca2+ transport.

Animals↗
PubMedDate not supplied

Relaxant effect of nicorandil on the tonic contraction of the canine large coronary artery induced by phorbol 12,13-dibutylate.

The contractile response to a protein kinase C activator, phorbol 12,13-dibutylate, and the relaxant effect of nicorandil on this contraction were studied in the canine isolated coronary artery. Phorbol 12,13-dibutylate (10(-9)-3 x 10(-6) M) elicited slowly developing, dose-dependent and sustained contractions which were antagonized by a putative protein kinase C inhibitor, staurosporine. Removal of Ca2+ from the medium or pretreatment with nifedipine (10(-6) M) partly inhibited the response to phorbol 12,13-dibutylate. Nicorandil (10(-7)-3 x 10(-4) M) produced full relaxation at its maximum effect in rings precontracted with phorbol 12,13-dibutylate (10(-7) M). Nitroglycerin (10(-9)-3 x 10(-5) M) caused only a partial relaxation (to about 30%), but subsequent addition of cromakalim (10(-5) M) to the nitroglycerin-treated rings (cromakalim alone inducing a partial relaxation of about 35%) caused nearly full relaxation. Methylene blue (5 x 10(-6) M) inhibited the relaxant response to lower (< or = 10(-5) M) but not to higher concentrations of nicorandil, while it antagonized the nitroglycerin-induced relaxation at all concentrations used. The relaxant response at higher concentrations of nicorandil (> or = 3 x 10(-5) M) was antagonized by 10(-6) M of glibenclamide. These results suggest that the contraction induced by phorbol 12,13-dibutylate may be related to an activation of protein kinase C and, in part, to increases in the Ca2+ influx via voltage-dependent Ca2+ channels. It appears that nicorandil relaxes the contraction induced by phorbol 12,13-dibutylate through a nitrate-like mode of action, combined with a potassium channel-opening activity.

Animals↗
PubMed1997

Differential effect of nitric oxide synthase inhibitors on acetylcholine-induced relaxation of rat pulmonary and celiac artery rings.

The effect of NG-monomethyl-L-arginine (L-NMMA) and N omega-nitro-L-arginine methyl ester (L-NAME) on acetylcholine (ACh) induced relaxation of rat intrapulmonary artery and celiac artery ring segments was studied in vitro with and without meclofenamate pretreatment. L-NMMA, and to a lesser extent L-NAME, raised baseline tone more in pulmonary than celiac arteries. Pretreatment of pulmonary and celiac artery rings with meclofenamate did not alter this contractile effect. Pulmonary artery and celiac artery ring segments were precontracted with phenylephrine, and cumulative concentration-relaxation curves to ACh were obtained before and after incubation of the rings with L-NAME or L-NMMA. L-NAME inhibited the ACh-induced relaxation of pulmonary arterial rings at 10000 fold lower concentrations than those needed to only partly inhibit the ACh-induced relaxation of celiac artery rings. L-NMMA (10-300 microM) inhibited the ACh-induced relaxation of pulmonary arterial rings in a concentration-dependent manner, whereas L-NMMA (300 microM) only partially inhibited the ACh-induced relaxation of celiac artery rings. The inhibition of ACh-induced relaxation by L-NAME and to a lesser extent by L-NMMA was more when pulmonary and celiac artery rings were pretreated with meclofenamate (1.0 microM). These results suggest that in the pulmonary artery nitric oxide plays a greater role in the modulation of baseline vascular tone and ACh-induced relaxation than in the celiac artery. In addition, cyclooxygenase products do not contribute to the direct contractile responses to L-NAME and L-NMMA in both the pulmonary and celiac artery rings but do modulate the ACh-induced relaxation of these vessels.

Acetylcholine↗
PubMed1997

The hemodynamic manifestation of normal myocardial relaxation. A framework for experimental and clinical evaluation.

Myocardial relaxation clinically manifests itself as left ventricular pressure (LVP) fall. The transition from contraction to relaxation is the precise moment at which 81-84% of peak isometric force has developed or the equivalent timing early during ejection. Defining the completion of relaxation and distinguishing relaxation from diastole appears merely semantic. Diastole is not a passive phase of the cardiac cycle. During diastole mechanical left ventricular properties still change due to incomplete relaxation, due to creep and stress relaxation, and due to autoregulation by preload and by nitric oxide. Description of timing and rate of LVP fall may provide useful information on underlying cardiac diseases such as ischaemia and hypertrophy. This information will however only be reliable if systolic cardiac function and systolic load are normal, and in the absence of a significant degree of nonuniformity, such as induced by conduction disturbances or by regional myocardial ischemia. The various effects of load and of nonuniformity on myocardial relaxation in the normal heart are reviewed. Coupling of timing and rate of LVP fall are explained in terms of cross-bridge mechanics. Specific effects of systolic pressure on LVP fall and their relation to systolic cardiac function are emphasized. These data constitute a conceptual framework for the analysis of myocardial relaxation in cardiovascular research and in the cardiac patient. Comparison of clinical and experimental data during manipulation of afterload should lead to an improved understanding of clinical relaxation disturbances and to a therapeutic approach, which is relevant from the physiopathological point of view. LVP fall may provide useful and quantitative information on systolic LV function if measurements are performed under different conditions of systolic load. This information is similar to systolic pressure-volume relations, but can be performed with the sole use of a micromanometer in the LV cavity.

Animals↗
PubMed1998

Effect of loading conditions on myocardial relaxation velocities determined by Doppler tissue imaging in heart transplant recipients.

BACKGROUND: Cardiac allograft rejection is accompanied by cellular infiltration and tissue edema resulting in myocardial relaxation abnormalities. Doppler tissue imaging is capable of measuring myocardial relaxation velocities and is useful in the detection of heart rejection. However, the influence of ventricular loading conditions on myocardial relaxation velocities has not been studied. This study is performed to determine whether myocardial relaxation velocities are affected by left ventricular loading conditions. METHODS: Twenty heart transplant recipients without evidence of rejection by endomyocardial biopsy underwent preload and afterload reduction with nitroglycerin. The pulmonary wedge pressure was reduced from 18.2+/-0.9 to 12.0+/-0.9 mm Hg 9 (p=0.001) and the mean blood pressure from 130.0+/-5.6 to 116.1+/-7.0 mm Hg (p=0.001). Pulsed-wave Doppler tissue imaging was performed before and after administration of nitroglycerin, and the peak myocardial relaxation velocities of the inferior wall were measured. RESULTS: Myocardial relaxation velocities did not change with the administration of nitroglycerin; 0.188+/-0.009 to 0.178+/- 0.006 m/sec (p=0.4) in spite of a significant reduction in pulmonary capillary wedge pressure. Furthermore, there was no correlation between pulmonary capillary wedge pressure, mean arterial pressure, wall stress, and myocardial relaxation velocities. CONCLUSIONS: Loading conditions on the left ventricle have no influence on myocardial relaxation velocities. Therefore in heart transplant recipients changes in myocardial relaxation velocities by Doppler tissue imaging may be useful in the diagnosis of rejection, in spite of diverse loading conditions.

Echocardiography, Doppler, Color↗
PubMed1977

Relaxation therapy in the treatment of hypertension. A review.

The literature on the use of relaxation or relaxation-like procedures (relaxation therapy) in the treatment of hypertension was critically reviewed. Relaxation therapy resulted in greater reduction of blood pressure than placebo or other control procedures. A positive relationship was found between the average blood pressure decrease and the average pretreatment pressure. Relaxation-like therapies shared the features of muscular relaxation, regular practice, mental focusing, and task awareness. Research on the relative contributions of these components indicated that task awareness adds to the treatment effect in the laboratory setting, and that regular practice is necessary for optimal results in the clinical setting. The role of muscular relaxation and mental focusing is unclear. We concluded that relaxation therapy may become a useful adjunct to medication in the clinical management of hypertension, especially for individuals whose blood pressures remain high despite pharmacological treatment.

Antihypertensive Agents↗
PubMed1993

A "fair" comparison of progressive and imaginal relaxation.

Progressive and imaginal relaxation-training procedures are difficult to compare because the latter takes many forms. In this study, an imaginal procedure was used that closely followed progressive operations except that muscle tension was imagined rather than experienced. The dependent variable was the total score on the Relaxation Inventory. College students were placed in groups (ns = 50) high and low on suggestibility based on scores on the Creative Imagination Scale, assigned in equal numbers to the imaginal and progressive relaxation conditions and given four sessions of relaxation training. The pre- and posttrials effects were significant within each of the four training sessions. There were no significant differences in reports of relaxation by the progressive and imaginal treatments. The expected cumulative effect of relaxation training across the four sessions was not found; in fact, the imaginal condition showed a significant decrease. The only significant suggestibility effect was an interaction between suggestibility and trials in which highly suggestible subjects reported less pre-session relaxation. These results are consistent with reports of no differences between progressive and imaginal relaxation training.

Adult↗
PubMed1986

Relaxation therapy for hypertension. Comparison of effects with concomitant placebo, diuretic, and beta-blocker.

We compared the effects of relaxation therapy in hypertensive patients taking placebo, a beta-blocker (atenolol, 100 mg/d), or a diuretic (chlorthalidone, 50 mg/d), and we also compared the effects of relaxation therapy with the effects of the latter two drugs alone. Blood pressures were measured not only in the relaxation therapists' office and at a hypertension clinic, but also in the patient's environment by means of 24-hour ambulatory blood pressure recordings. The effect of relaxation therapy, while statistically significant, was modest. There was no generalization of effect to ambulatory blood pressure. Atenolol was significantly more effective than relaxation in reducing both systolic and diastolic pressure. Chlorthalidone was significantly more effective than relaxation in reducing systolic but not diastolic pressure in the hypertension clinic only. The long-term effects of relaxation were independent of concomitant drug use, but within the actual relaxation sessions blood pressure dropped further during chlorthalidone than during placebo or atenolol treatment.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

The effectiveness of relaxation training in reducing treatment-related symptoms and improving emotional adjustment in acute non-surgical cancer treatment: a meta-analytical review.

Cancer patients often have to deal with severe side effects and psychological distress during cancer treatment, which have a substantial impact on their quality of life. Among psychosocial interventions for reducing treatment-related side effects, relaxation and imagery were most investigated in controlled trials. In this study, meta-analytic methods were used to synthesize published, randomized intervention-control studies aiming to improve patients' treatment-related symptoms and emotional adjustment by relaxation training. Mean weighted effect sizes were calculated for 12 categories, treatment-related symptoms (nausea, pain, blood pressure, pulse rate) and emotional adjustment (anxiety, depression, hostility, tension, fatigue, confusion, vigor, overall mood). Significant positive effects were found for the treatment-related symptoms. Relaxation training also proved to have a significant effect on the emotional adjustment variables depression, anxiety and hostility. Additionally, two studies point to a significant effect of relaxation on the reduction of tension and amelioration of the overall mood. Intervention features of the relaxation training, the time the professional spent with the patient overall (intervention intensity) and the schedule of the intervention (offered in conjunction with or independent of medical treatment to the cancer patient) were relevant to the effect of relaxation on anxiety. The interventions offered independently of medical treatment proved to be significantly more effective for the outcome variable anxiety. Relaxation seems to be equally effective for patients undergoing different medical procedures (chemotherapy, radiotherapy, bone marrow transplantation, hyperthermia). According to these results relaxation training should be implemented into clinical routine for cancer patients in acute medical treatment.

Blood Pressure↗
PubMed1998

Nitric oxide relaxes bovine ciliary muscle contracted by carbachol through elevation of cyclic GMP.

It is generally accepted that nitric oxide relaxes vascular smooth muscles by activating guanylyl cyclase, which in turn increases cyclic 3':5' guanosine monophosphate level. Despite the physiological significance of nitric oxide, very few studies have attempted to characterize the mode of action of this mediator in ciliary muscles. Therefore, the present experiments were designed to investigate whether or not the relaxation induced by sodium nitroprusside as a donor of nitric oxide is accompanied by the increase in cyclic 3':5' guanosine monophosphate level in the bovine ciliary muscle, and these responses are affected by methylene blue as an inhibitor of guanylyl cyclase and 3-isobutyl-1-methylxanthine as an inhibitor of phosphodiesterases. The relaxation activity of exogenous 8-bromo-cyclic 3':5' guanosine monophosphate was also determined. Sodium nitroprusside produced a concentration-dependent relaxation in the bovine ciliary muscle strips which had been contracted by carbachol as a cholinergic agonist. Relaxation in response to sodium nitroprusside was accompanied by a significant (P<0.05 and P<0.005) increase in cyclic 3':5' guanosine monophosphate level. The relaxation response and the increase in cyclic 3':5' guanosine monophosphate caused by sodium nitroprusside were significantly (P<0.01 and P<0.05) augmented by the pretreatment with 3-isobutyl-1-methylxanthine, and were significantly (P<0.005 and P<0.05) attenuated in the presence of methylene blue. The exogenously applied 8-bromo-cyclic 3':5' guanosine monophosphate relaxed the ciliary muscle strips in a concentration-dependent manner. These results suggest that nitric oxide causes relaxation of the bovine ciliary muscle through the activation of guanylyl cyclase and an increase in cyclic 3':5' guanosine monophosphate level.

1-Methyl-3-isobutylxanthine↗
PubMed2002

Changes in orcine muscle water characteristics during growth--an in vitro low-field NMR relaxation study.

This study investigates the effects of developmental stage and muscle type on the mobility and distribution of water within skeletal muscles, using low-field (1)H-NMR transverse relaxation measurements in vitro on four different porcine muscles (M. longissimus dorsi, M. semitendinosus, M. biceps femoris, M. vastus intermedius) from a total of 48 pigs slaughtered at various weight classes between 25 kg and 150 kg. Principal component analysis (PCA) revealed effects of both slaughter weight and muscle type on the transverse relaxation decay. Independent of developmental stage and muscle type, distributed exponential analysis of the NMR T(2) relaxation data imparted the existence of three distinct water populations, T(2b), T(21), and T(22), with relaxation times of approximately 1-10, 45-120, and 200-500 ms, respectively. The most profound change during muscle growth was a shift toward faster relaxation in the intermediate time constant, T(21). It decreased by approx. 24% in all four muscle types during the period from 25 to 150 kg live weight. Determination of dry matter, fat, and protein content in the muscles showed that the changes in relaxation time of the intermediate time constant, T(21), during growth should be ascribed mainly to a change in protein content, as the protein content explained 77% of the variation in the T(21) time constant. Partial least squares (PLS) regression revealed validated correlations in the region of 0.58 to 0.77 between NMR transverse relaxation data and muscle development for all the four muscle types, which indicates that NMR relaxation measurements may be used in the prediction of muscle developmental stage.

Animals↗
PubMed2000

Nitric oxide and prostanoid-dependent relaxation induced by angiotensin II in the isolated precontracted mouse tracheal muscle and the role of potassium channels.

In this study we examined the mechanism of the concentration-dependent relaxant effect of angiotensin II (A II) on mouse isolated tracheal rings precontracted by carbachol. The contractile effect of carbachol is increased while the relaxant effect of A II decreased by pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME). This finding suggests that the L-arginine nitric oxide (NO) pathway is activated by the peptide. The relaxing effect of A II was also mediated through the release of cyclo-oxygenase products of arachidonic acid, as evidenced by the inhibition of the response by lysine acetylsalicylic acid (ASA) pretreatment. A II also caused a relaxation in the isolated tracheal rings precontracted by K(+)(>60 m m). K(+)-channel blockers partially inhibited the relaxant effect of A II in carbachol-precontracted mouse tracheal rings. A non-selective blocker of K(+)channels, tetraethylammonium, completely abolished the relaxation induced by A II. Among the other channel blockers, the inhibitory effect of apamine and glibenclamide was higher than that of iberiotoxin, indicating the involvement of K(ATP)and small conductance K(Ca)channels in the relaxing response to the octapeptide. These results suggest that the mechanisms, involved in the relaxation induced by A II in the isolated mouse tracheal rings precontracted by carbachol, were firstly l -arginine NO and cyclo-oxygenase products of arachidonic acid, secondly K(+)channels.

Angiotensin II↗
PubMed2001

Involvement of nitric oxide in non-adrenergic non-cholinergic relaxation and action of vasoactive intestinal polypeptide in circular muscle strips of the rat gastric fundus.

We examined the characteristics of the non-adrenergic non-cholinergic (NANC) nerve induced relaxation and the possible interaction between nitric oxide (NO) and vasoactive intestinal polypeptide (VIP) on the basal tone of the circular muscle of the rat gastric fundus. Electrically induced NANC relaxations were partly inhibited by N(omega)-nitro-L-arginine (100 microM), whereas sodium nitroprusside (SNP; 10 microM) and VIP (5 nM) induced relaxations were not affected. 2-Amino-5,6-dihydro-6-methyl-4H-1,3-thiazine (AMT; 5 microM) also inhibited the responses to electrical stimuli to a similar extent as N(omega)-nitro-L-arginine but not VIP. However, AMT plus N(omega)-nitro-L-arginine did not give an additional inhibition above that of each drug alone on NANC relaxations, and dexamethasone (10 microM) had no effect on NANC nerve induced relaxations. 1H-[1,2,4,]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 10 microM), a selective inhibitor of guanylate cyclase, abolished the responses to NANC nerve stimulation and SNP, while VIP responses were not influenced. N-ethylmaleimide (100 microM), an adenylate cyclase inhibitor, attenuated relaxations to NANC nerve stimulation, VIP and isoproterenol (1 nM), while having no effect on those to SNP, but in combination with N(omega)-nitro-L-arginine, there was no additional inhibition on the responses to nerve stimulation. Alpha-chymotrypsin (10 u ml(-1)) severely diminished VIP induced relaxations, but did not reduce electrical responses. In conclusion, these results suggest that NO is involved in the relaxations induced by short-term electrical stimulation. However, another possible unidentified transmitter that can trigger the accumulation of cyclic GMP is not entirely ruled out and there is no interaction between NO and VIP in the circular muscle strip of the rat gastric fundus, even in the basal state of the tissue.

Adenylyl Cyclase Inhibitors↗