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Table 4. Effect of cAMP Pathway Analogs and Inhibitors on Isoflurane-induced Hyperpolarization of Vascular Smooth Muscle (VSM)

Values are mean mV ± SD. For sequential measurements of in situ  VSM transmembrane potential, physiologic salt solution superfusate contained the following: protocol 1: (1) no agent (denervated control), (2) 0.15 μm Sp-5,6-DCl-cBimps (protein kinase A [PKA] activator), (3) no agent (washout); protocol 2: (1) no agent (denervated control), (2) 24.5 μm Rp cAMPS (PKA inhibitor), (3) 24.5 μm Rp cAMPS plus 0.15 μm Sp-5,6-DCl-cBimps; protocol 3: (1) no agent (denervated control), (2) 0.6 mm isoflurane (ISO), (3) 24.5 μm Rp cAMPS (after washout of isoflurane), (4) 24.5 μm Rp cAMPS plus 0.6 mm isoflurane; protocol 4: (1) no agent (denervated control), (2) 0.6 mm isoflurane, (3) 410 μm SQ22536 (inhibitor of cAMP synthesis; after washout of isoflurane), (4) 410 μm SQ22536 plus 0.6 mm isoflurane.

* Different from control and washout,

† different from all other conditions in the Rp cAMPS or the SQ22536 protocol;P ≤ 0.05; n = 8.

WKY = Wistar Kyoto; SHR = spontaneously hypertensive rat.

Table 4. Effect of cAMP Pathway Analogs and Inhibitors on Isoflurane-induced Hyperpolarization of Vascular Smooth Muscle (VSM)
Table 4. Effect of cAMP Pathway Analogs and Inhibitors on Isoflurane-induced Hyperpolarization of Vascular Smooth Muscle (VSM)
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