Some aspects of the phytotoxic action of fusaric acid on primary Ricinus roots

Fusaric acid, at a concentration of 1mM induced at pH 5.5 an early hyperpolarisation was followed by a marked depolarisation of membrane potential difference. During this time increased electrolyte leakage from the primary Ricinus roots was determined. At higher pH values (6.5 and 8) the depolarisation caused by fusaric acid was immediate without hyperpolarisation observed at pH 5.5. Simultaneous exposure of the roots to P-ATPase activator fusicoccin and fusaric acid (pH 6.5) diminished the hyperpolarising effect of fusicoccin. The present results suggest that the dissociated form of fusaric acid does directly affect particular cell targets (plasmalemma, mitochondria) and viability of root cells decreased with the time of exposure and concentration of fusaric acid.

Relation of membrane potential to basolateral TEA transport in isolated snake proximal renal tubules

We measured the effects of changes in bath K+ concentration ([K+]) on basolateral membrane potential difference (PD) and [3H]tetraethylammonium (TEA) transport in isolated snake (Thamnophis) proximal renal tubules (25 degrees C; pH 7.4). Increasing bath [K+] from 3 to 65 mM decreased PD from -60 mV (inside of cells negative) to -20 mV and 2-min uptake of [3H]TEA by approximately 25%, indicating that PD influences TEA entry into the cells. Uptake of [3H]TEA was inhibited similarly at both K+ concentrations by unlabeled TEA, indicating that uptake is carrier mediated. Kt (approximately 18 microM) for 2-min uptake of [3H]TEA in 3 mM K+ increased significantly in 65 mM K+, suggesting that the decrease in PD or the increase in [K+] alters the affinity of the transporter for TEA. The steady-state cell-to-bath ratio for [3H]TEA with 3 mM K+ (-60 mV PD) was approximately 16, significantly above the ratio of 10 predicted for passive distribution at electrochemical equilibrium. With 65 mM K+ (-20 mV PD) this ratio decreased to approximately 6, again significantly above the predicted ratio of 2. These data suggest that the PD can account for much, but not all, of the steady-state uptake of TEA. Efflux of [3H]TEA across the basolateral membrane was identical with either 3 or 65 mM K+ in the bath but was almost completely inhibited in either case by tetrapentylammonium, a potent inhibitor of TEA uptake. These data indicate that virtually all TEA transport across the basolateral membrane is carrier mediated and that transport out of the cells is unaffected by PD.

Influence of the Mesophyll on Stomatal Opening

Some studies have shown that stomata in detached epidennis behave differently, both quantitatively and qualitatively, from those in the intact leaf. Stomata in the intact leaf are very sensitive to environmental factors such as light, CO2 and osmotic stress, but stomata in detached epidermis are less sensitive to these factors than those in the intact leaf. Stomata in the intact leaf open in the light and close in the dark, whereas previously opened stomata in detached epidermis do not close on transfer to darkness and they are dependent on the KCl concentration in the incubation medium. Electrophysiological results also demonstrate different responses of guard cells in the intact leaf and detached epidennis. The electrical potential across the membrane of the guard cell in the intact leaf was hyperpolarised in response to light and CO2. However, there were no changes in the membrane potential difference in response to light and CO2 in detached epidermis. In CCCP-infiltrated leaf discs, the guard cell membrane was conversely depolarised by light, indicating that the guard cell membrane hyperpolarisation was related to the mesophyll cells. These results suggest the participation of the mesophyll in stomatal control. It is possible that stomatal opening in the intact leaf, to a greater or lesser extent. is dependent on an electrical signal or a chemical propagated from the mesophyll.

Effect of norepinephrine on cellular sodium transport in Ambystoma kidney proximal tubule

The effect of norepinephrine (NE) on mechanisms of cellular Na+ transport in the isolated, perfused proximal tubule of Ambystoma tigrinum was examined. Single-barreled voltage and ion-selective microelectrodes were used to determine basolateral (V1), luminal (V2), and transepithelial (V3) membrane potentials and intracellular Na+ activity (alpha Nai). In CO2/HCO3- control solution, addition of NE (10(-6) M) to the bath caused depolarizations of V1, V2, and V3 are decreased alpha Nai. These effects were mimicked by isoproterenol and inhibited by propranolol. Addition of NE in the absence of luminal Na+ and substrates did not cause any changes in V1, V2, V3, or alpha Nai. NE did not affect the changes in membrane potential difference (PD) or alpha Nai caused by removal and readdition of luminal substrates and/or Na+. To study the effect of NE on Na-K-adenosinetriphosphatase (Na-K-ATPase), the pump was inhibited by external K+ removal and then reactivated by readdition of 12 mM K+ to the bath in the presence and absence of NE. Reactivation of the pump caused hyperpolarization of membrane PDs, and alpha Nai recovered monotonically in 3-5 min. The peak hyperpolarizations of V1 and V2 (approximately 1 min) were significantly larger in the presence of NE. During the first 3 min, and also at the same alpha Nai, the rate of decrease of alpha Nai was significantly faster in the presence of NE. In conclusion, these results show a direct effect of NE on cell membrane PDs and alpha Nai in the kidney proximal tubule. Most likely, beta-receptors are involved in mediating the action of NE. Neither Na/H exchange nor Na-substrate cotransport at the luminal membrane are affected by NE. On the other hand, NE activates Na-K-ATPase.