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Table 3. Effect of cGMP 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) 100 μm 8-Br-cGMP (cGMP analog), (3) no agent (washout); protocol 2: (1) no agent (denervated control), (2) 2.5 μm Rp-8-pCPT-cGMPS (protein kinase G inhibitor), (3) 2.5 μm Rp-8-pCPT-cGMPS plus 100 μm 8-Br-cGMP; protocol 3: (1) no agent (denervated control), (2) 0.6 mm isoflurane (ISO), (3) 2.5 μm Rp-8-pCPT-cGMPS (after washout of isoflurane), (4) 2.5 μm Rp-8-pCPT-cGMPS plus 0.6 mm isoflurane; protocol 4: (1) no agent (denervated control), (2) 0.6 mm isoflurane, (3) 15 μm ODQ (inhibitor of cGMP synthesis; after washout of isoflurane), (4) 15 μm ODQ plus isoflurane.

* Different from control and washout,

† different from control,

‡ different from isoflurane and Rp-8-pCPT-cGMPS + isoflurane or isoflurane and ODQ + isoflurane;P ≤ 0.05; n = 8–15 for ODQ, and n = 8 for all other protocols.

WKY = Wistar Kyoto; SHR = spontaneously hypertensive rat.

Table 3. Effect of cGMP Pathway Analogs and Inhibitors on Isoflurane-induced Hyperpolarization of Vascular Smooth Muscle (VSM)
Table 3. Effect of cGMP Pathway Analogs and Inhibitors on Isoflurane-induced Hyperpolarization of Vascular Smooth Muscle (VSM)
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