| 51. |
- Haus, Jacob M, et al.
(författare)
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Contractile and connective tissue protein content of human skeletal muscle: : effects of 35 and 90 days of simulated microgravity and exercise countermeasures.
- 2007
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Ingår i: American Journal of Physiology. Regulatory Integrative and Comparative Physiology. - : American Physiological Society. - 0363-6119 .- 1522-1490. ; 293:4, s. 1722-1727
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Tidskriftsartikel (refereegranskat)abstract
- We examined the effects of 35 and 90 days of simulated microgravity with or without resistance-exercise (RE) countermeasures on the content of the general skeletal muscle protein fractions (mixed, sarcoplasmic, and myofibrillar) and specific proteins that are critical for muscle function (myosin, actin, and collagen). Subjects from two studies, using either unilateral lower limb suspension (ULLS) or bed rest (BR), comprised four separate groups: 35 days ULLS (n =11), 35 days ULLS+RE (n = 10), 90 days BR (n = 9), and 90 days BR+RE (n = 8). RE consisted of four sets of seven maximal concentric and eccentric repetitions of the quadriceps femoris muscles that were performed 2 or 3 times per week. Pre- and post-simulated weightlessness muscle biopsies were analyzed from the vastus lateralis of all groups and the soleus of the 35-day ULLS and 90-day BR groups. The general protein fractions and the specific proteins myosin, actin, and collagen of the vastus lateralis were unchanged (P > 0.05) in both control and countermeasures groups over 35 and 90 days, despite large changes in quadriceps femoris muscle volume (35 days ULLS: -9%, 35 days ULLS+RE: +8%; and 90 days BR: -18%, 90 days BR+RE: -1%). The soleus demonstrated a decrease in mixed (35 days ULLS: -12%, P = 0.0001; 90 days BR: -12%, P = 0.004) and myofibrillar (35 days ULLS: -12%, P = 0.009; 90 days BR: -8%, P = 0.04) protein, along with large changes in triceps surae muscle volume (35 days ULLS: -11%; 90 days BR: -29%). Despite the loss of quadriceps femoris muscle volume or preservation with RE countermeasures during simulated microgravity, the quadriceps femoris muscles are able to maintain the concentrations of the general protein pools and the main contractile and connective tissue elements. Soleus muscle protein composition appears to be disproportionately altered during long-duration simulated weightlessness.
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| 52. |
- Hellström, Martin, et al.
(författare)
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Cardiac hypertrophy and decreased high-density lipoprotein cholesterol in Lrig3-deficient mice
- 2016
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Ingår i: American Journal of Physiology. Regulatory Integrative and Comparative Physiology. - : American Physiological Society. - 0363-6119 .- 1522-1490. ; 310:11, s. R1045-R1052
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Tidskriftsartikel (refereegranskat)abstract
- Genetic factors confer risk for cardiovascular disease. Recently, large genome-wide population studies have shown associations between genomic loci close to LRIG3 and heart failure and plasma high-density lipoprotein (HDL) cholesterol level. Here, we ablated Lrig3 in mice and investigated the importance of Lrig3 for heart function and plasma lipid levels. Quantitative reverse transcription-polymerase chain reaction (RT-PCR) was used to analyze Lrig3 expression in the hearts of wild-type and Lrig3-deficient mice. In addition, molecular, physiological, and functional parameters such as organ weights, heart rate, blood pressure, heart structure and function, gene expression in the heart, and plasma insulin, glucose, and lipid levels were evaluated. The Lrig3-deficient mice were smaller than the wild-type mice but otherwise appeared grossly normal. Lrig3 was expressed at detectable but relatively low levels in adult mouse hearts. At 9 mo of age, ad libitum-fed Lrig3-deficient mice had lower insulin levels than wildtype mice. At 12 mo of age, Lrig3-deficient mice exhibited increased blood pressure, and the Lrig3-deficient female mice displayed signs of cardiac hypertrophy as assessed by echocardiography, heart-to-body weight ratio, and expression of the cardiac hypertrophy marker gene Nppa. Additionally, Lrig3-deficient mice had reduced plasma HDL cholesterol and free glycerol. These findings in mice complement the human epidemiological results and suggest that Lrig3 may influence heart function and plasma lipid levels in mice and humans.
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| 53. |
- Hindle, Allyson G., et al.
(författare)
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Low guanylyl cyclase activity in Weddell seals : implications for peripheral vasoconstriction and perfusion of the brain during diving
- 2019
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Ingår i: American Journal of Physiology. Regulatory Integrative and Comparative Physiology. - : AMER PHYSIOLOGICAL SOC. - 0363-6119 .- 1522-1490. ; 316:6, s. R704-R715
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Tidskriftsartikel (refereegranskat)abstract
- Nitric oxide (NO) is a potent vasodilator, which improves perfusion and oxygen delivery during tissue hypoxia in terrestrial animals. The vertebrate dive response involves vasoconstriction in select tissues. which persists despite profound hypoxia. Using tissues collected from Weddell seals at necropsy, we investigated whether vasoconstriction is aided by downregulation of local hypoxia signaling mechanisms. We focused on NO-soluble guanylyl cyclasc (GC)-cGMP signaling, a well-known vasodilatory transduction pathway. Seals have a lower GC protein abundance. activity, and capacity to respond to NO stimulation than do terrestrial mammals. In seal lung homogenates, GC produced less cGMP (20.1 +/- 3.7 pmol.mg protein(-1).min(-1)) than the lungs of dogs (-80 +/- 144 pmol.mg protein(-1).min(-1) less than seals), sheep (-472 +/- 96), rats (-664 +/- 104) or mice ( -1,160 +/- 104, P < 0.0001). Amino acid sequences of the GC enzyme alpha-subunits differed between seals and terrestrial mammals, potentially affecting their structure and function. Vasoconstriction in diving Weddell seals is not consistent across tissues; perfusion is maintained in the brain and heart but decreased in other organs such as the kidney. A NO donor increased median GC activity 49.5-fold in the seal brain but only 27.4-fold in the kidney. consistent with the priority of cerebral perfusion during diving. Nos3 expression was high in the seal brain, which could improve NO production and vasodilatory potential. Conversely, Pde5a expression was high in the seal renal artery, which may increase cGMP breakdown and vasoconstriction in the kidney. Taken together, the results of this study suggest that alterations in the NO-cGMP pathway facilitate the diving response.
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| 54. |
- Holmlund, Petter, et al.
(författare)
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Venous collapse regulates intracranial pressure in upright body positions
- 2018
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Ingår i: American Journal of Physiology. Regulatory Integrative and Comparative Physiology. - : American Physiological Society. - 0363-6119 .- 1522-1490. ; 314:3, s. R377-R385
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Tidskriftsartikel (refereegranskat)abstract
- Recent interest in intracranial pressure (ICP) in the upright posture has revealed that the mechanisms regulating postural changes in ICP are not fully understood. We have suggested an explanatory model where the postural changes in ICP depend on well-established hydrostatic effects in the venous system and where these effects are interrupted by collapse of the internal jugular veins (IJVs) in more upright positions. The aim of this study was to investigate this relationship by simultaneous invasive measurements of ICP, venous pressure and IJV collapse in healthy volunteers. ICP (monitored via the lumbar route), central venous pressure (PICC-line) and IJV cross-sectional area (ultrasound) were measured in 11 healthy volunteers (47±10 years) in seven positions, from supine to sitting (0°-69°). Venous pressure and anatomical distances were used to predict ICP in accordance with the explanatory model, and IJV area was used to assess IJV collapse. The hypothesis was tested by comparing measured ICP to predicted ICP. Our model accurately described the general behavior of the observed postural ICP changes (mean difference: -0.03±2.7 mmHg). No difference was found between predicted and measured ICP for any tilt-angle (p-values: 0.65 - 0.94). The results support the hypothesis that postural ICP changes are governed by hydrostatic effects in the venous system and IJV collapse. This improved understanding of the postural ICP regulation may have important implications for the development of better treatments for neurological and neurosurgical conditions affecting ICP.
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| 55. |
- Hultström, Michael, et al.
(författare)
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Adenosine triphosphate increases the reactivity of the afferent arteriole to low concentrations of norepinephrine
- 2007
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Ingår i: American Journal of Physiology. Regulatory Integrative and Comparative Physiology. - : American Physiological Society. - 0363-6119 .- 1522-1490. ; 293:6, s. R2225-R2231
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Tidskriftsartikel (refereegranskat)abstract
- Adenosine triphosphate (ATP) and norepinephrine ( NE) interact in the control of blood flow in the kidney. A combined effect of NE and ATP has not been previously investigated at the level of the afferent arteriole (Af). We studied the effects of ATP on the contractile response of the Af to NE. Vascular reactivity to ATP, NE, and their combination was investigated in isolated perfused Af from mice. The roles of alpha-adrenoceptors and P2-ATP-receptors were investigated by use of specific agonists and antagonists. Cytosolic calcium was measured using the fluorescent calcium dye fura-2. ATP in concentrations from 10(-12) to 10(-4) mol/l induced transient contractions. NE constricted the Af in a dose-dependent manner and induced significant contractions at > 10(-7) mol/l. Treatment with ATP (10(-8) and 10(-6) mol/l) increased the NE response. Diameters were reduced by 20% already at 10(-11) mol/l NE during ATP treatment of 10(-6) mol/l. ATP increased the calcium response to NE significantly at 10(-8) and 10(-7)mol/l NE. The P2-type ATP receptor blocker pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS) (10(-5) mol/l) abolished the sensitization of the NE response by ATP. The alpha(1)-blocker prazosin (10(-7) mol/l) inhibited the ATP effect, as did the alpha(2)-blocker yohimbine (10(-7) mol/l). Neither the phenylephrine- nor clonidine-induced concentration response curves was affected by ATP in the bath solution. Costimulation with ATP enhances the response of the Af to NE. This effect is mediated by increased cytosolic calcium. The enhancing effect involves P2-type ATP receptors and both alpha(1)- and alpha(2)-adrenoceptors.
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| 56. |
- Hultström, Michael, et al.
(författare)
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Moderate hypothermia induces a preferential increase in pancreatic islet blood flow in anesthetized rats
- 2007
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Ingår i: American Journal of Physiology. Regulatory Integrative and Comparative Physiology. - : American Physiological Society. - 0363-6119 .- 1522-1490. ; 293:3, s. R1438-R1443
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Tidskriftsartikel (refereegranskat)abstract
- The aim of the study was to characterize the effects of induced moderate hypothermia on splanchnic blood flow, with particular reference to that of the pancreas and the islets of Langerhans. We also investigated how interference with the autonomic nervous system at different levels influenced the blood perfusion during hypothermia. For this purpose, hypothermia (body temperature of 28°C) was induced by external cooling, whereas normothermic (37.5°C) anesthetized Sprague-Dawley rats were used as controls. Some rats were pretreated with either propranolol, yohimbine, atropine, hexamethonium, or a bilateral abdominal vagotomy. Our findings suggest that moderate hypothermia elicits complex, organ-specific circulatory changes, with increased perfusion noted in the pylorus, as well as the whole pancreas and the pancreatic islets. The pancreatic islets maintain their high blood perfusion through mechanisms involving both sympathetic and parasympathetic mediators, whereas the increased pyloric blood flow is mediated through parasympathetic mechanisms. Renal blood flow was decreased, and this can be prevented by ganglionic blockade and is also influenced by β-adrenoceptors.
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| 57. |
- HYLLAND, Patrick, et al.
(författare)
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ANOXIC BRAIN FAILURE IN AN ECTOTHERMIC VERTEBRATE - RELEASE OF AMINO-ACIDS AND K+ IN RAINBOW-TROUT THALAMUS
- 1995
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Ingår i: AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY. - : AMER PHYSIOLOGICAL SOC. - 0363-6119. ; 38:5, s. R1077-R1084
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Tidskriftsartikel (refereegranskat)abstract
- The release of excitatory amino acids such as glutamate contributes greatly to anoxic and/or ischemic brain damage in mammals. However, for anoxia-intolerant ectothermic vertebrates, there has been no information on how anoxia affects extracellular amino
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| 58. |
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| 59. |
- Johansson, Maria E, 1977, et al.
(författare)
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Hyperinsulinemic rats are normotensive but sensitized to angiotensin II.
- 2008
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Ingår i: American Journal of Physiology. Regulatory Integrative and Comparative Physiology (USA). - : American Physiological Society. - 0363-6119 .- 0363-6119 .- 1522-1490. ; 294:4
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Tidskriftsartikel (refereegranskat)abstract
- The effect of insulin on blood pressure (BP) is debated, and an involvement of an activated renin-angiotensin aldosterone system (RAAS) has been suggested. We studied the effect of chronic insulin infusion on telemetry BP and assessed sympathetic activity and dependence of the RAAS. Female Sprague-Dawley rats received insulin (2 units/day, INS group, n = 12) or insulin combined with losartan (30 mg.kg(-1).day(-1), INS+LOS group, n = 10), the angiotensin II receptor antagonist, for 6 wk. Losartan-treated (LOS group, n = 10) and untreated rats served as controls (n = 11). We used telemetry to measure BP and heart rate (HR), and acute ganglion blockade and air-jet stress to investigate possible control of BP by the sympathetic nervous system. In addition, we used myograph technique to study vascular function ex vivo. The INS and INS+LOS groups developed euglycemic hyperinsulinemia. Insulin did not affect BP but increased HR (27 beats/min on average). Ganglion blockade reduced mean arterial pressure (MAP) similarly in all groups. Air-jet stress did not increase sympathetic reactivity but rather revealed possible blunting of the stress response in hyperinsulinemia. Chronic losartan markedly reduced 24-h-MAP in the INS+LOS group (-38 +/- 1 mmHg P < 0.001) compared with the LOS group (-18 +/- 1 mmHg, P
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| 60. |
- Johansson, Rebecka, et al.
(författare)
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Phenotypic modulation of cultured bladder smooth muscle cells and the expression of inducible nitric oxide synthase.
- 2004
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Ingår i: American Journal of Physiology: Regulatory, Integrative and Comparative Physiology. - : American Physiological Society. - 0363-6119 .- 1522-1490. ; 286:4, s. 642-648
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Tidskriftsartikel (refereegranskat)abstract
- Phenotypic modulation of smooth muscle is associated with various pathological conditions, including bladder dysfunction. Cytoskeletal dynamics modulate the cell phenotype and were recently shown to be involved in regulation of inducible nitric oxide synthase ( iNOS). We tested the hypothesis that the cell differentiation status affects iNOS expression, and that iNOS is preferentially expressed in immature dedifferentiated bladder smooth muscle cells (BSMC). Isolated rat BSMC were put into different stages of differentiation by serum deprivation on laminin-coated plates in the presence of IGF-I and by interaction with Rho signaling and actin polymerization. iNOS and smooth muscle-myosin heavy chain (SM-MHC) protein expression were investigated with Western blot analysis. Our results showed iNOS protein in BSMC exposed to interleukin-1beta ( 2 ng/ml) + TNF-alpha ( 50 ng/ml). Growth of BSMC in serum-free medium on laminin in the presence of IGF-I increased SM-MHC expression, whereas cytokine-induced iNOS was inhibited. Disruption of F-actin with latrunculin B ( 0.5 muM) potentiated iNOS expression and decreased SM-MHC expression. Rho inhibition with C3 (2.5 mug/ml) increased iNOS expression, whereas SM-MHC expression was slightly decreased. Rho-kinase inhibition with Y-27632 ( 10 muM) mediated a decrease in iNOS and a slight increase in SM-MHC expression. In conclusion, the capacity of BSMC to express iNOS was negatively correlated to differentiation status measured as SM-MHC expression. Actin cytoskeletal dynamics and Rho signaling are involved in regulation of cytokine-induced iNOS expression in BSMC. Phenotypic changes and impairment in actin cytoskeleton formation may potentiate cytokine activation and in turn increase nitric oxide production in the bladder during disease.
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