Human | Uterine artery rings partially contracted with phenylephrine | AngII (4 × 10−8 M) | Transient contraction (3.1 ± 0.6%) followed by relaxation (40.8 ± 6.5%) | Indomethacin (10−6 M) | ↑ Contraction and abolished relaxation | Kimura et al., 2001 |
Pulmonary artery rings precontracted with U46619 | ACh (1 nM–3 μM) | Relaxation (Emax 45.1 ± 12.1%) | Flurbiprofen (1 μM) | Partly attenuated relaxation (33.4 ± 13.5%) | Lawrence et al., 1998 |
Middle cerebral artery blood flow by ultrasonography | Hypercapnia (8% CO2) | Vasodilation (87.7% of baseline velocity) | Indomethacin | Insignificant reduction in vasodilation (61%) | Markus et al., 1994 |
Hypocapnia Hyperventilation | Vasoconstriction (37.5%) | | ↓ Vasoconstrictor response (20.7%*) | |
Placentofetal resistance arteries from the placental villus stem | Bradykinin (10−6 – 10−9 M) | Vasoconstriction through release of vasoconstrictor PGs | Meclofenamate (10−7 M) | ↓ Vasoconstriction at bradykinin concentrations >3 × 10−7 M) | Tulenko, 1981 |
Dog | Coronary artery (in vivo measurement of coronary blood flow) | ACh (10–300 ng) | Increased coronary blood flow by ∼10 ml/min | Naproxen (10 mg/kg) | No effect | Gross and Moore, 2004 |
AA (30–1000 μg) | Increased coronary blood flow by ∼7 ml/min | | ↓ Blood flow by 10–20 ml/min | |
Pulmonary arterial and venous vascular resistance in perfused lung lobe | Serotonin (100 μg) | Increased lobar vascular resistance (both lobar arterial and venous resistance) | Meclofenamate (45 μM) | ↑ Lobar arterial resistance by ∼26 and venous resistance by ∼6 cm H2O/l/min | Hofman et al., 1991 |
Lobar intrapulmonary artery rings | Serotonin (10−7 M) | Contraction (1 g active tension) | Indomethacin (10 μM) | No change | |
Mesenteric Artery (in vitro isolated rings) | AngII (2 × 10−8 M) | ∼60% contraction compared with KCl | Indomethacin (10−6 M) | ∼60% increase in contraction | Yamazaki and Toda, 1991 |
Retinal artery rings precontracted with U46619 | Bradykinin (10−10 – 10−6 M) | Relaxation (max 94.2 ± 2.5% of maximum relaxation diameter to papaverine) | Indomethacin (10 μM) | No significant effect (92.5 ± 3.4%) | Jeppesen et al., 2002 |
Middle cerebral artery rings | AA (10 μg/ml) | Contraction (maximum 1.8 g) | Indomethacin (10−5 M) | Insignificant ↑ in contraction by ∼9% | Jancar et al., 1987 |
Rabbit | Celiac artery rings | NE (5 × 10−8 M) | Contraction (1.62 mN) | Indomethacin (0.8 μM) | 160 ± 15% Increase in contraction | Hadházy et al., 1984 |
Pulmonary artery | Contraction (2.4 mN) | 26 ± 6% ↑ Contraction | |
Femoral artery | Contraction (9.3 mN) | 15 ± 3% ↓ Contraction | |
Aorta | Contraction (4.58 mN) | 7 ± 3% ↑ Contraction | |
Aortic rings precontracted with NE 10−7 M | AA (10−8 – 10−5 M) | Relaxation (max 31 ± 2%) | Indomethacin (10−5 M) | Increased relaxation (42 ± 2%) | Pfister and Campbell, 1992 |
ACh (10−8 – 10−5 M) | Relaxation (max 43 ± 3%) | | No effect (41 ± 3%) | |
Rat | Cerebral pial arteriole (in vivo measurement of arteriolar diameter) | ACh (4 × 10−4 M) | Relaxation (111 ± 2% of baseline diameter) | Indomethacin (6 × 10−5 M) | No significant effect (107 ± 1% of baseline diameter) | Rosenblum et al., 1989 |
A-23187, calcium ionophore (10−5 M) | Relaxation (107 ± 1% of baseline diameter) | Indomethacin (6 × 10−5 M) | ↓ Relaxation (101 ± 1% of baseline diameter) | |
| Uterine arterioles (in vivo measurement of arteriolar diameter) | ACh (10−8 – 10−4 M) | Dilation | Ibuprofen (10−4 M) | ↓ Dilation at higher ACh concentrations (>1 μM) | Saha et al., 1998 |
AngII (10−11 – 10−7 M) | Constriction | Enhanced constriction | |
Phe (10−8 – 10−4 M) | Constriction | No effect | |
Renal arcuate artery rings | ACh (0.01–100 μM) | Relaxation (maximum response 17.2 ± 1.7%) | Indomethacin (14 μM) | ↑ Relaxation (maximum response 36.5 ± 3.3%) | Wu et al., 1994 |
NE (0.01–10 μM) | Contraction (maximum 1.84 ± 0.27 mN/mm) | ↓ Contraction (max 1.48 ± 0.21 mN/mm) | |