Abstract
Abstract Introduction Hyperchloraemic acidosis is known to be associated with impaired renal function in post-operative patients. We have experimentally investigated whether elevation in chloride and hydrogen ions have the potential to negatively impact the porcine renal vasculature. Methods Porcine renal (RA) and mesenteric (MA) arteries were placed in Krebs-Henseleit solution (K-H), gassed with 95%O2/5%CO2, and prepared for isometric tension recordings. 60mM KCl was used for standardized contractions and preparations were then exposed to the thromboxane-mimetic U46619, followed 6-18mM of either NaCl or Na Gluconate (NaGlu). Preparations were also exposed to increasing concentrations of noradrenaline in normal K-H (pH 7.4) and K-H pH 7.2. Results U46619 (10-20nM) produced stable contractions in RA and MA equivalent to 50% of that to 60mM KCl. 18mM NaCl caused a further contraction in RA (19.8±4.2%, n=9, p < 0.01), while 18mM NaGlu (3.8±4.4%, n=9) did not. Neither 6-18mM NaCl nor 6-18mM NaGlu caused responses in MA (< 4%, n=6). Noradrenaline produced concentration-dependent contractions in MA in normal K-H solution (logEC50 5.43±0.11: Max’ 226.8±24.6% 60mM KCl, n=6) that were significantly reduced (p < 0.05) in K-H pH 7.2 (logEC50 5.13±0.02: Max’ 174.4.8±3.3%, 60mM KCl, n=6). In contrast, in the RA noradrenaline contractions (logEC50 5.80±0.08: Max’ 162.8±12.0% 60mM KCl, n=11) were not affected (p > 0.05) by K-H solution pH 7.2 (logEC50 5.71±0.07: Max’ 177.8±15.3% 60mM KCl, n=11). Conclusion Elevation of chloride ions (experimental hyperchloraemia) selectively constricts porcine renal blood vessels, while corresponding elevation in hydrogen ions (acidosis) selectively dilates the mesenteric vasculature.
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