Fire in lichen-rich subarctic tundra changes carbon and nitrogen cycling between ecosystem compartments but has minor effects on stocks

Fires are predicted to increase in Arctic regions due to ongoing climate change. Tundra fires can alter carbon and nutrient cycling and release a substantial quantity of greenhouse gases with global consequences. Yet, the long-term effects of tundra fires on carbon (C) and nitrogen (N) stocks and cycling are still unclear. Here we used a space-for-time approach to investigate the long-term fire effects on C and N stocks and cycling in soil and aboveground living biomass. We collected data from three large fire scars (>44, 28, and 12 years old) and corresponding control areas and used linear mixed-effect models in a Bayesian framework to analyse long-term development of C and N stocks and cycling after fire.We found that tundra fires had no long-term effect on total C and N stocks because a major part of the stocks was located belowground in soils which were largely unaltered by fire. However, fire had a strong long-term effect on stocks in the aboveground vegetation, mainly due to the reduction in the lichen layer. Fire reduced N concentrations in graminoids and herbs on the younger fire scars, which affected respective C/N ratios and may indicate an increased post-fire competition between vascular plants. Aboveground plant biomass was depleted in C-13 in all three fire scars. In soil, the relative abundance of C-13 changed with time after fire.Our results indicate that in lichen-rich subarctic tundra ecosystems, the contribution of fires to the release of additional carbon to the atmosphere might be relatively small as soil stocks appear to be resilient within the observed time frame

Depletion of intracellular Ca(2+) stores enhances flow-induced vascular dilatation in rat small mesenteric artery

1. The effect of depleting intracellular Ca(2+) stores on flow-induced vascular dilatation and the mechanism responsible for the vasodilatation were examined in rat isolated small mesenteric arteries. 2. The arteries were pressurized to 50 mmHg and preconstricted with phenylephrine. Intraluminal flow reversed the effect of phenylephrine, resulting in vasodilatation. Flow dilatation consisted of an initial transient peak followed by a sustained plateau phase. The magnitude of dilatation was markedly reduced by removing Ca(2+) from the intraluminal flow medium. 3. Depletion of intracellular Ca(2+) stores with either cyclopiazonic acid (CPA, 2 μM) or 1,4-dihydroxy-2,5-di-tert-butylbenzene (BHQ, 10 μM) significantly augmented the magnitude of flow dilatation. Flow-induced endothelial cell Ca(2+) influx was also markedly enhanced in arteries pretreated with CPA or BHQ. 4. Flow-induced dilatation was insensitive to N(w)-nitro-L-arginine methyl ester (100 μM) plus indomethacin (3 μM) or to oxyhemoglobin (3 μM), but was markedly reduced by 30 mM extracellular K(+) or 2 mM tetrabutylammonium (TBA), suggesting an involvement of EDHF. 5. Catalase at 1200 U ml(−1) abolished the flow-induced dilatation, while the application of exogenous H(2)O(2) (90–220 μM) induced relaxation in phenylephrine-preconstricted arteries. Relaxation to exogenous H(2)O(2) was blocked in the presence of 30 mM extracellular K(+), and H(2)O(2) (90 μM) hyperpolarized the smooth muscle cells, indicating that H(2)O(2) can act as an EDHF. 6. In conclusion, flow-induced dilatation in rat mesenteric arteries can be markedly enhanced by prior depletion of intracellular Ca(2+) stores. Furthermore, these data are consistent with a role for H(2)O(2) as the vasodilator involved

Spreading dilatation in rat mesenteric arteries associated with calcium-independent endothelial cell hyperpolarization

Both ACh and levcromakalim evoke smooth muscle cell hyperpolarization and associated relaxation in rat mesenteric resistance arteries. We investigated if they could evoke conducted vasodilatation along isolated arteries, whether this reflected spreading hyperpolarization and the possible mechanism involved. Focal micropipette application of either ACh, to stimulate endothelial cell muscarinic receptors, or levcromakalim, to activate smooth muscle K(ATP) channels, each evoked a local dilatation (88 ± 14%, n= 6 and 92 ± 6% reversal of phenylephrine-induced tone, n= 11, respectively) that rapidly spread upstream (at 1.5 mm 46 ± 19%, n= 6 and 57 ± 13%, n= 9) to dilate the entire isolated artery. The local dilatation to ACh was associated with a rise in endothelial cell [Ca(2+)](i) (F/F(t = 0)= 1.22 ± 0.33, n= 14) which did not spread beyond 0.5 mm (F/F(t = 0)= 1.01 ± 0.01, n= 14), while the local dilatation to levcromakalim was not associated with any change in endothelial cell [Ca(2+)](i). In contrast, ACh and levcromakalim both stimulated local (12.7 ± 1.2 mV, n= 10 and 13.5 ± 4.7 mV, n= 10) and spreading (at 2 mm: 3.0 ± 1.1 mV, n= 5 and 4.1 ± 0.7 mV, n= 5) smooth muscle hyperpolarization. The spread of hyperpolarization could be prevented by cutting the artery, so was not due to a diffusible agent. Both the spreading dilatation and hyperpolarization were endothelium dependent. The injection of propidium iodide into either endothelial or smooth muscle cells revealed extensive dye coupling between the endothelial cells, but limited coupling between the smooth muscle cells. Some evidence for heterocellular spread of dye was also evident. Together, these data show that vasodilatation can spread over significant distances in mesenteric resistance arteries, and suggest this reflects an effective coupling between the endothelial cells to facilitate [Ca(2+)](i)-independent spread of hyperpolarization

An evaluation of potassium ions as endothelium-derived hyperpolarizing factor in porcine coronary arteries

1. In the rat hepatic artery, the endothelium-derived hyperpolarizing factor (EDHF) was identified as potassium. Potassium hyperpolarizes the smooth muscles by gating inward rectified potassium channels and by activating the sodium-potassium adenosine triphosphatase (Na(+)-K(+)ATPase). Our goal was to examine whether potassium could explain the EDHF in porcine coronary arteries. 2. On coronary strips, the inhibition of calcium-dependent potassium channels with 100 nM apamin plus 100 μM charibdotoxin inhibited the endothelium-dependent relaxations, produced by 10 nM substance P and 300 nM bradykinin and resistant to nitro-L-arginine and indomethacin. 3. The scavenging of potassium with 2 mM Kryptofix 2.2.2 abolished the endothelium-dependent relaxations produced by the kinins and resistant to nitro-L-arginine and indomethacin. 4. Forty μM 18α glycyrrethinic acid or 50 μM palmitoleic acid, both uncoupling agents, did not inhibit these kinin relaxations. Therefore, EDHF does not result from an electrotonic spreading of an endothelial hyperpolarization. 5. Barium (0.3 nM) did not inhibit the kinin relaxations resistant to nitro-L-arginine and indomethacin. Therefore, EDHF does not result from the activation of inward rectified potassium channels. 6. Five hundred nM ouabain abolished the endothelium-dependent relaxations resistant to nitro-L-arginine and indomethacin without inhibiting the endothelium-derived NO relaxation. 7. The perifusion of a medium supplemented with potassium depolarized and contracted a coronary strip; however, the short application of potassium hyperpolarized the smooth muscles. 8. These results are compatible with the concept that, in porcine coronary artery, the EDHF is potassium released by the endothelial cells and that this ion hyperpolarizes and relaxes the smooth muscles by activating the Na(+)-K(+)ATPase