{'fraction_non_alphanumeric': 0.0527369826435247, 'fraction_numerical': 0.01602136181575434, 'mean_word_length': 4.948412698412699, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Control of capillary hydraulic conductivity via membrane potential-dependent changes in Ca2+ influx.

Capillary permeability has been shown to be sensitive to the levels of intracellular calcium. We examined the role of membrane potential in the regulation of capillary water permeability by a Ca2+ leak mechanism. Repeated measures of Lp were taken in situ on individually perfused mesenteric capillaries of cerebrally pithed frogs (Rana pipiens). A rise in extracellular potassium ([K+]o) to 24 mM induced a 45% decrease in Lp (n = 20), whereas lowering [K+]o to 0.24 mM elevated Lp by twofold (n = 9). To investigate whether these changes in Lp were due specifically to changes in membrane potential and consequent changes in the driving force for Ca2+ influx, we performed the following experiments: 1) [K+]o was elevated while the product of [K+]o and extracellular chloride concentration [Cl-]o was kept constant, 2) [K+]o was elevated under nominally Ca(2+)-free conditions, 3) K+ leak was induced by addition of 10 microM valinomycin, and 4) Na(+)-K+ pump was blocked by 10 microM ouabain. A constant [K+]o [Cl-]o product did not prevent high K+ from lowering Lp. Nominally Ca(2+)-free conditions abolished the effect of high K+. Valinomycin mimicked the response to low K+, and ouabain failed to change Lp. The data from this study conform to the hypothesis that membrane potential is an important regulator of capillary barrier properties via changes in Ca2+ influx through leak channels.