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. Author manuscript; available in PMC: 2014 Sep 1.
Published in final edited form as: Curr Vasc Pharmacol. 2013 Sep;11(5):655–711. doi: 10.2174/1570161111311050008

Table 4.

Cerebrovascular Relaxation Pathways with Development

Variable Fetus Newborn Adult Reference
Intrinsic tone at 40 mmHg with endothelium intact (Mouse; %) 21±3 (210) 10±1 [106]
A-23187-Induced Relaxation (%) 35 (35) 100 [245]
Constriction to indomethacin at 40 mmHg (Mouse) 12±1 (46) 26±1 [106]
Constriction to L-NAME at 40 mmHg (Mouse) 17±1 (49) 35±2 [106]
pD2 of SNAP-Induced Relaxation 6.3±0.1 5.9±0.1 [246]
eNOS Relative Abundance 3.1±0.2 (135) 2.3±0.2 [247]
eNOS abundance (ng eNOS · mg protein−1)* 29±3 (263) 11±2 [248]
Maximum eNOS Specific Activity Slope NO (10−12 M)·eNOS (10−6 g)·min−1 3.8±0.5b (67) 5.7±1.0 [248]
eNOS abundance in microvessels (% newborn value)++ 100 (36) 280±30 [249]
eNOS specific activity (nmol NO · μg eNOS−1 · min−1)* 97±36 (55) 177±44 [248]
Slope of relation of eNOS specific activity to fluid shear stress (nmol NO · μg eNOS−1 · min−1 · dyne−1·cm2 −1)* 2.9±0.1 (43) 6.8±0.1 [248]
Basal eNOS activity in microvessels (14C-citriline incorporation, cpm · mg protein−1)++ ~3,500±200 (47) ~7,500±400 [249]
sGC abundance (% that in adult kidney) 0.37±0.6 (276) 0.17±0.03 [250]
sGC abundance (ng · mg protein−1) 7.1±0.9 (132) 5.4±1.5 [251]
sGC specific activity (pmol · μg sCG−1 · min−1) 60±2c (35) 171±19 [251]
sGC specific activity (pmol · cGMP−1 · mg−1 · min−1) 3.1±0.31 (214) 1.45±0.08 [250]
sGC activity, Vmax as determined by cGMP formation (pmol cGMP · mg protein−1 · min−1) 4.48±1.13 (954) 0.47±0.13 [252]
sGC abundance (ng sGC · mg protein−1) 17.6± 1.6a (1036) 1.7±0.3 [252]
Basal cGMP (10−9 M·10−3 protein−1) 3.3±0.5b (194) 1.7±0.2 [253]
Basal cGMP (10−6 M)* 0.59±0.11 (536) 0.11±0.02 [254]
cGMP Synthesis rate (10−6 M·1 cell water−1·min−1)* 0.31 ±0.06b (207) 0.15 ±0.04 [254]
cGMP synthesis rate (pmol cGMP · mg protein−1 · min−1) 29.5±5.6b (356) 8.3±1.4 [251]
cGMP-induced relaxation with 8-pCPT-cGMP (% maximal) 99.2±0.8 (111) 89.3±4.6 [251]
cGMP Degradation (10−6 M·1 cell water−1·min−1)* 106±6c (136) 78±6 [254]
cGMP (pm · mg protein−1) 1.0±0.1 (333) 0.3±0.1 [253]
cGMP (10−9 M·10−3 g Soluble Protein) 0.35±0.1 [250]
cGMP (10−9 M·sGC (10−6 g)·min 145±20 (−) [250]
ΔpD2 for 5-HT-induced contraction with 8-pCPT-cGMP* To 6.30±0.08 from 6.72±0.02 NSC [47]
Δ pD2 for 5-HT calcium sensitivity ΔTension · Δ [Ca2+]i (%)* To 176±27 from 128±17b NSC [47]
Δ pD2 for K+-induced contraction with 8-pCPT-cGMP in α-toxin permeabilized vessels* −0.4±0.1b NSC [47]
Δ maximum 5-HT-induced rise in [Ca2+]i with 8-pCPT-cGMP (%)* To 64±9 (150) from 88±6c To 82±7 from 98±14 [47]
Basal ratio of cGMP to cAMP ~6 ~3 [255]
Prostaglandin I2
NO
>
<
[154, 155]
COX-2 in microvessels (% newborn value)++ 100 128±10 [249]
Basal COX activity in microvessels (PG production, pg · μg protein−1)++ 2.2±0.4 2.2+-0.5 [249]
COX activity in microvessels (PGE2 production, pg · μg protein−1)++ 1.6±0.3 (133) 1.2±0.3 [249]
Hypoxic-Induced CBF (% Control) +43 [256]
Hypoxic-Induced CBF (% Control) +50 [257]
Above with L-NAME inhibition + [256]
Carbon Monoxide as measured by [HbCO] 2 to 3 (200 to 300) 1 [258]

Values are mean ± SE of 5 or more in each group;

Values in parentheses represent % of adult values;

Significantly different from adult value:

a

P<0.001;

b

P<0.01;

c

P<.05;

Basilar artery;

*

CCA;

++

Pigs; NSC, no significant change