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The effects of GTP, with or without polyethylene glycol (PEG), on the release and uptake of Ca2+ were examined by using saponin-treated macrophages and sarcoplasmic reticulum isolated from skeletal muscles. The application of GTP in concentrations in the range 0.1-10 microM induced a gradual, small but sustained release of Ca2+ from the saponin-treated macrophages. The addition of PEG to GTP markedly enhanced the GTP-mediated Ca2+ release. GTP at the same concentration ranges used for Ca2+ release decreased the amount of Ca2+ uptake, at a steady state, but stimulated the rate of Ca2+ accumulation in the presence of oxalate, the Ca2+-precipitating anion. The addition of PEG abolished the GTP-evoked stimulation of Ca2+ accumulation in the presence of oxalate. The stimulating effect on the rate of Ca2+ accumulation by GTP and its elimination by PEG were not due to changes in the permeability of oxalate by either GTP or PEG, or both. The Ca2+-releasing effect of GTP without PEG was enhanced by eliminating the uptake activity by decreasing the content of ATP. These results indicate that GTP has an inherent activity to release Ca2+ from non-mitochondrial intracellular stores of saponin-treated macrophages, and PEG enhances the GTP-mediated Ca2+ release, partly owing to its eliminating effect on GTP-stimulated Ca2+ uptake activity. These effects of GTP observed with saponin-permeabilized macrophages were not apparent in the isolated skeletal-muscle sarcoplasmic reticulum.

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SUMMARY1. Effects of a-human atrial natriuretic polypeptide (a-HANP) on electrical and mechanical properties of smooth muscle cells of the guinea-pig and rabbit renal arteries and of the guinea-pig mesenteric artery were investigated.2. a-HANP (up to 10 nM) modified neither the membrane potential nor resistance of smooth muscle cells of the guinea-pig and rabbit renal arteries. In the guinea-pig mesenteric and renal arteries, a-HANP (up to 10 nm) had no effect on the amplitude and facilitation (mesenteric artery) or depression (renal artery) ofexcitatory junction potentials nor on action potentials.3. In the guinea-pig renal artery, a-HANP (up to 10 ni) had no effect on the depolarizations induced by noradrenaline (NA) (up to 10 FM) but markedly inhibited NA-induced contraction. a-HANP (10 nM) slightly inhibited the K-induced contraction. In the rabbit renal artery, a-HANP (10 nM) inhibited the NA-induced contraction and to a lesser extent the K-induced contraction. 4. In the rabbit renal artery, the effects of a-HANP on the release of Ca from the cellular storage by two applications of NA, and its re-storage, were investigated in Ca-free solution containing 2 mM-EGTA. When 5 nm-a-HANP was applied before and during the first application of0-5 ,uM-NA, the contraction was markedly inhibited but the contraction to a second application of 10,uM-NA was potentiated. If the first dose of NA was 10 /M the effect was very small. Under the same experimental procedures, nitroglycerine (10 /M) showed almost the same effects as o-HANP on the NA-induced contractions. When both the first (3 mM) and second (10 mM) contractions were evoked by caffeine in Ca-free solution, a-HANP (5 nM) and nitroglycerine (10 ,M) inhibited both contractions to the same extent.5. In the rabbit renal artery, applications of a-HANP or nitroglycerine increased the amount of guanosine 3',5'-phosphate (cyclic GMP) in a dose-dependent manner. However, a much higher concentration of nitroglycerine was required (2 x 103 times).6. In the rabbit renal artery, hydrolysis of phosphatidyl inositol 4,5-bisphosphate (PI-P2) activated by 0 5 1sM-NA was inhibited by a-HANP, in a dose-dependent manner, but activation by 10 /sM-NA was not inhibited by a-HANP (up to 100 nm).