ライフサイエンスコーパス: NOS-I

1 NOS-I significantly decreased %CVC(max) in both groups b

2 sed in the O at COX-I sites (COX-I 16 +/- 1, NOS-I + COX-I 16 +/- 2 versus C 10 +/- 1%CVC(max); P < 0

3 In middle cerebral arteries, all adventitial NOS-I bundles and fine fibers were coincident with NADPH

4 ibers originate in the SPG, although not all NOS-I ganglionic cells in the SPG send fibers to pial ve

5 NADPH diaphorase histochemical and NOS I immunohistochemical studies were done in the adult

6 s calculated as the difference between C and NOS-I sites.

7 The Delta%CVC(max) between the control and NOS-I site was calculated as the difference between C an

8 The Delta%CVC(max) between the control and NOS-I sites was attenuated at DeltaT(or) > 0.5 degrees C

9 COX-I and NOS-I + COX-I attenuated the peak CVC response to ACh in

10 enase inhibited (COX-I, 10 mm ketorolac) and NOS-I + COX-I.

11 and [11C]AR-R 18512 was assayed in rats and NOS-I knockout mice, and PET was performed in baboons.

12 In forebrain, the distribution of sGC and NOS-I was complementary, with only occasional colocaliza

13 In the presence of L-arginine, NOS I produces nitric oxide (NO.).

14 principal cells were immunopositive for both NOS-I and sGCbeta; these cells could be seen at times re

15 o different enzyme preparations, H(4)B-bound NOS I and H(4)B-free NOS I, were used.

16 o be considerably greater in the H(4)B-bound NOS I preparation than in the H(4)B-free NOS I preparati

17 ter than that measured using the H(4)B-bound NOS I preparation.

18 l rate of H(2)O(2) production by H(4)B-bound NOS I was considerably greater than that for H(4)B-free

19 ge groups, and the response was unchanged by NOS-I (O: NOS-I 35 +/- 5 versus C 38 +/- 5%CVC(max); P =

20 and a subset of these spines also contained NOS-I.

21 )2 were found to inhibit, to a small degree, NOS I activity with a greater effect observed with Fe(MG

22 ckers correlated with increased macula densa NOS-I immunoreactivity.

23 in, small cells that were immunopositive for NOS-I rarely corresponded to those that were immunoposit

24 dal cells exhibit clear immunoreactivity for NOS-I.

25 /NK1-positive neurons were also positive for NOS-I, and 94% of NOS-positive neurons were also positiv

26 l generation of O(2)(-.) from the H(4)B-free NOS I preparation was found to be substantially greater

27 und NOS I preparation than in the H(4)B-free NOS I preparation.

28 eparations, H(4)B-bound NOS I and H(4)B-free NOS I, were used.

29 onsiderably greater than that for H(4)B-free NOS I.

30 uld be seen at times receiving contacts from NOS-I-positive fibers.

31 2%CVC(max) versus C; P < 0.001 both groups; NOS-I + COX-I O: 32 +/- 3 versus Y: 29 +/- 2%CVC(max); v

32 Nitric oxide synthase-I (NOS-I), the synthetic enzyme for NO, was found almost ex

33 lar uptake of [11C]AR-R 18512 was present in NOS-I knockout mice compared with control mice.

34 control (C, Ringer solution), NOS inhibited (NOS-I, 10 mM L-NAME), A-I (5 mM BEC + 5 mM nor-NOHA), L-

35 (C, Ringer solution), NO synthase inhibited (NOS-I, 10 mm l-NAME), cyclooxygenase inhibited (COX-I, 1

36 The spin trapping of NO* from isolated NOS I oxidation of L-arginine by ferro-N-dithiocarboxysa

37 We hypothesized that neuronal NOS (nNOS, NOS I) effects cutaneous vasodilatation during whole-bod

38 PAH lungs had normal NOS I-III expression, but substrate arginine levels were

39 Sensitization to type I NOS (NOS-I) blockers correlated with increased macula densa N

40 and the response was unchanged by NOS-I (O: NOS-I 35 +/- 5 versus C 38 +/- 5%CVC(max); P = 0.84) (Y:

41 with the sum of AAT repeats in intron 20 of NOS I gene alleles.

42 nd the number of AAT repeats in intron 20 of NOS I in subjects with sickle cell disease (SCD) and a h

43 significantly correlated with the number of NOS I AAT repeats.

44 However, the majority of NOS-I-positive synaptic puncta was associated with sGC a

45 Of these, only NOS I (neuronal nitric-oxide synthase; nNOS) is expresse

46 Neuronal nitric-oxide synthase (nNOS or NOS I) and endothelial NOS (eNOS or NOS III) differ wide

47 At variance with this pattern, NOS-I was concentrated mainly in somata.

48 R-R 18512 showed little evidence of specific NOS-I binding.

49 Neuronal nitric-oxide synthase (NOS I) in the absence of L-arginine has previously been

50 stained for neuronal nitric oxide synthase (NOS-I) but not for sGCbeta.

51 lure to find neuronal nitric oxide synthase (NOS-I) in the dendritic spines of these cells has cast d

52 o synthesize neuronal nitric oxide synthase (NOS-I)-selective imaging agents based on the 2 potent, s

53 of sGC with neuronal nitric oxide synthase (NOS-I, the NO-producing enzyme in neurons).

54 The nitric oxide synthases (NOS-I, neuronal, NOS-II, inducible, and NOS-III, endothe

55 Taken together these data demonstrate that NOS I generates O-2 and the formation of this free radic

56 Our light microscopic results show that NOS I, as defined mainly by the presence of NADPH diapho

57 We hypothesized that NOS-I may be in spines but in a form inaccessible to ant

58 g immunogold electron microscopy showed that NOS-I concentrates just inside the postsynaptic plasma m

59 Finally, by spin trapping nearly all of the NOS I produced O(2)(-.), we found that the initial rate

60 block tracer uptake by pretreatment with the NOS-I-selective inhibitor 7-nitroindazole or the corresp

61 L-citrulline was restricted to NOS-I-positive elements, and the large majority of NOS-e

62 nic cells that were VIP-I and/or ChAT-I were NOS-I and NADPHd-reactive.

63 To assess whether NOS-I and sGC immunoreactivities colocalize with their r

64 synaptophysin staining) were associated with NOS-I, and approximately 9% contained the beta subunit o

65 5 versus C 38 +/- 5%CVC(max); P = 0.84) (Y: NOS-I 41 +/- 4 versus C 39 +/- 4%CVC(max); P = 0.67).