When carbonic anhydrase activity decreases, the regional blood flow (rBF) in organs increases as hypercapnia develops. However, the effects of acetazolamide (AZ)-induced vasodilation have not been estimated with respect to vessel size and organs. The aim of this study was to determine the diameter of the capillaries in various organs that respond to inhibition of carbonic anhydrase activity by AZ. White rabbits were anesthetized with urethane and ketamine and infused with AZ. While the systolic blood pressure (SBP), pH, hemoglobin concen tration, and base excess did not change, the partial pressure of arterial oxygen (PaO2) increased significantly and the partial pressure of arterial carbon dioxide (PaCO2) decreased significantly with AZ. The rBF was calculated by using 3 different sizes (15, 25, and 50 μm) of colored microspheres (CM). The rBF measured with 15μm CM in the brain, kidneys, and liver increased in response to AZ, and the rBF in these organs was different with the different sizes of CM. However, the rBF calculated by using the different sizes of CM in the stomach and abdominal muscle did not change after the administration of AZ. The AZ-induced vasodilation occurred in all sizes of vessels in the liver, in the small and medium-sized vessels in kidneys, and in the larger capillaries in the brain.
1. al-Adrenoceptor-mediated inhibition of the fi-adrenoceptor-dependent Cl-current was investigated in guinea-pig ventricular myocytes using the patch clamp technique. The Clconductance activated by noradrenaline (0-1-10 #M) with an a1-blocker (prazosin, 5 #m) was significantly greater than that activated by noradrenaline alone. Phenylephrine and methoxamine, al-agonists, exerted an inhibitory effect on the Cl-conductance activated by isoprenaline. The dose-response relationship for isoprenaline and the Cl-current activation was shifted to higher doses in the presence of phenylephrine (30 /M).2. The interaction of al-and ,8-agonists on Cl-current was also observed on the single channel level; in some of the outside-out membrane patches, phenylephrine (50 /M) depressed the activity of the single Cl-channel which was induced by 5/M adrenaline. 3. Phenylephrine had no effect on the Cl-conductance induced by forskolin (0 5-5 uM), an activator of adenylate cyclase. The Cl-conductance activated persistently by isoprenaline in GTPyS-loaded cells was also insensitive to phenylephrine. The results suggest that the observed az-adrenergic attenuation of the /8-adrenergic response is not primarily due to inhibition of adenylate cyclase activity. The a1-adrenergic action may interfere with the processes leading to enzyme activation in the /-adrenergic pathway.
The effects of various [Mg2+]i, particularly low [Mg2+]i, on the delayed rectifier K+ current (IK) were studied in guinea pig ventricular myocytes with the patch clamp technique. The magnitude of IK was evaluated from the amplitude of its tail current elicited on repolarization following the depolarizing steps. The pipette-perfusion technique was also used. The initial variations of IK magnitude were dependent on [Mg2+]i in the internal solutions with which the whole-cell recording was begun. With 0.03 to 1 mM [Mg2+]i, IK was relatively stable after patch rupture, showing a minimal decay with time; with 3 mM [Mg2+]i, IK rapidly declined; with [Mg2+]i, less than 0.01 mM IK transiently increased after patch break, but declined progressively thereafter as the magnitude of IK decreased to about 30% of the initial magnitude in 10 min. The decline of IK at low [Mg2+]i showed the following features. The decline was accompanied little by changes in the voltage-activation relation or by changes in the kinetics of current deactivation. The decline was not related to changes in [Ca2+]i and was also observed in ATP gamma S-loaded, isoprenaline-stimulated cells, in which IK channels were presumed to be persistently phosphorylated. An application of okadaic acid did not prevent the decline of IK during Mg2+ depletion. It is suggested that a presence of [Mg2+]i higher than 0.01 mM is required to maintain IK in guinea pig ventricular cells. The depression of IK at low [Mg2+]i appears to involve a phosphorylation-dephosphorylation-independent mechanism.
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