Abstract
The effect of glucagon on chloride transport was studied in the rat medullary thick ascending limb (MTAL) perfused in vitro. In the bath, 10(-6) M glucagon increased the efflux coefficient of Cl (KeCl) from 6.88 +/- 0.21 x 10(5) to 9.65 +/- 0.38 x 10(-5) cm.sec -1 (P less than 0.01) without changing the influx coefficient (KiCl; 2.87 +/- 0.54 x 10(-5) in control vs. 2.83 +/- 0.57 x 10(-5) cm.sec-1 with glucagon) or transepithelial potential difference (4.8 +/- 0.76 in control vs. 5.0 +/- 0.71 mV with glucagon). A physiological concentration of glucagon (10(-8), (10(-10) M) also increased chloride efflux significantly. Pretreatment of tubules with luminal furosemide (10(-5) M) and/or basolateral ouabain (10(-4) M) completely abolished the effect of glucagon. In isolated MTALs incubated in the same medium as that used in the microperfusion study, 10(-6) M glucagon stimulated cAMP production by 255.2 +/- 33.7% (P less than 0.01). However, neither dibutyryl cAMP (10(-3), 10(-4) M) nor forskolin (10(-4), 10(-6) M) increased the chloride efflux. It is concluded that: 1) Glucagon stimulates net Cl reabsorption by increasing Cl efflux in the rat MTAL; and 2) cyclic AMP is not responsible for this effect of glucagon.
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