Table 1. Modulation of intracellular pH by STa in T₈₄ cells.

	pHi	dpHi/dt
Control	7.170 ± 0.028	0.133 ± 0.009
STa	7.144 ± 0.019	0.046 ± 0.009 *
HOE-694	7.172 ± 0.034	0.051 ± 0.010 *
HOE-694 + STa	7.130 ± 0.046	0.014 ± 0.001 * †
Forskolin	7.156 ± 0.021	0.051 ± 0.010 *
Forskolin + STa	7.171 ± 0.030	0.048 ± 0.009 *
Forskolin + HOE-694	7.161 ± 0.050	0.017 ± 0.003 * ‡
Forskolin + HOE-694 + STa	7.125 ± 0.061	0.016 ± 0.002 * ‡
H89 + HOE-694 + STa	7.143 ± 0.038	0.046 ± 0.008 *
db-cGMP	7.21 ± 0.054	0.110 ± 0.012
db-cGMP + STa	7.10 ± 0.021	0.050 ± 0.012 * §
db-cGMP + HOE-694	7.19 ± 0.053	0.057 ± 0.002 * §
db-cGMP + HOE-694 + STa	7.14 ± 0.051	0.015 ± 0.001 * § ¶
SNP	7.16 ± 0.026	0.123 ± 0.009
SNP + STa	7.15 ± 0.021	0.045 ± 0.011 *&
SNP + HOE-694	7.11 ± 0.024	0.047 ± 0.009 *&
SNP + HOE-694 + STa	7.14 ± 0.052	0.015 ± 0.012 *&$

The intracellular pH (pHi) was measured in BCECF-AM–preloaded T₈₄ cells as described in Methods. Cells were also subjected to an acid pulse (NH₄Cl assay) and the initial rates of pH_i recovery (dpHi/dt) was measured in cells in the absence (Control) or presence (30 minutes) of 0.25 μmol/L heat-stable (STa) enterotoxin, 25 μmol/L HOE-694 (Na⁺/H⁺ exchangers inhibitor), 10 μmol/L forskolin, 100 nmol/L H89 (protein kinase A inhibitor), 100 μmol/L dibutyryl cyclic GMP (db-cGMP), or 500 μmol/L sodium nitroprusside (SNP). STa at 0.1 and 0.75 μmol/L did not alter pHi values (7.121 ± 0.011 and 7.160 ± 0.014, respectively; P>0.05, n = 4). STa at 0.1 μmol/L partially reduced dpHi/dt value (0.098 ± 0.005 pHi units/minute, P<0.05, n = 4), and inhibition at 0.75 μmol/L (0.056 ± 0.007 pHi units/minute) was similar (P>0.05, n = 4) to 0.25 μmol/L STa (see also Fig 2B).

*P<0.04 versus Control

^† P<0.03 versus STa or HOE-694

^‡ P<0.03 versus Forskolin, Forskolin + STa, and H89 + HOE-694 + STa,

^§ P<0.05 versus db-cGMP

^¶ P<0.05 versus db-cGMP + STa and db-cGMP + HOE-694, &P<0.05 versus db-cGMP

^$ P<0.03 versus SNP + STa and SNP + HOE-694