Key result
Prostaglandin-induced pial vasodilation links to increased cGMP and is blunted by NOS inhibitor L-NNA.
Why the study?
Does nitric oxide synthase inhibition blunt prostaglandin-induced pial arterial vasodilation in newborn pigs?
Does nitric oxide synthase inhibition blunt prostaglandin-induced pial arterial vasodilation in newborn pigs?
Prostaglandin-induced pial arterial vasodilation in newborn pigs is mediated in part by nitric oxide and cGMP, but not cAMP.
Animal findings in pigs leave open NO-cGMP mediation of neonatal pial vasodilation; human studies needed before any clinical inference.
The present study was designed to investigate the role of nitric oxide (NO), guanosine 3',5'-cyclic monophosphate (cGMP), and adenosine 3',5'-cyclic monophosphate (cAMP) in the vasodilator response to prostaglandin (PG)I2 and PGE2 in newborn pigs equipped with a closed cranial window. PGI2 (1-100 ng/ml) produced pial arterial dilation that was blunted by nitro-L-arginine (L-NNA, 10(-6) M), an NO synthase inhibitor (9 +/- 1 vs. 2 +/- 1%, 21 +/- 1 vs. 5 +/- 3% for 1 and 100 ng/ml PGI2 respectively, n = 6; means +/- SE). PGI2-induced vasodilation was associated with increased cortical periarachnoid cerebrospinal fluid (CSF) cGMP, and these changes in cGMP were blocked by L-NNA (386 +/- 8 and 1,054 +/- 30 fmol/ml vs. 266 +/- 6 and 274 +/- 4 fmol/ml for control and PGI2 100 ng/ml before and after L-NNA respectively, n = 6). In contrast, PGI2-associated changes in CSF cAMP were unchanged by L-NNA (1,021 +/- 25 and 2,703 +/- 129 fmol/ml vs. 980 +/- 23 and 2,636 +/- 193 fmol/ml for control, PGI2 100 ng/ml before and after L-NNA, respectively, n = 6). PGE2 elicited similar changes in pial artery diameter and cyclic nucleotides; vasodilation and changes in CSF cGMP also being similarly inhibited by L-NNA. After L-NNA, topical administration of the NO donor sodium nitroprusside (SNP, 10(-9) M) increased pial artery diameter up to the resting level before L-NNA and partially restored the vasodilation elicited by PGI2 and PGE2.(ABSTRACT TRUNCATED AT 250 WORDS)
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William M. Armstead (1995) studied Animal model (newborn pigs) (n=6). Prostaglandin I2 (PGI2) and PGE2 with/without nitro-L-arginine (L-NNA) vs. Control (before L-NNA) was evaluated on Pial arterial dilation and changes in CSF cGMP/cAMP. In newborn pigs, prostaglandin-induced pial arterial vasodilation is associated with increased cGMP and is blunted by the nitric oxide synthase inhibitor L-NNA.