Abstract
1. 1. In this study, we compared G-protein-mediated contractile responses of rat aorta and mesenteric artery rings induced by the α-adrenoceptor agonist, norepinephrine (NE) and by the direct G-protein activator, sodium fluoride, using various probes. 2. 2. Activator of the stimulatory G-protein (Gs), cholera toxin (CT), attenuated the sensitivity and maximum contractile response of both aorta and mesenteric artery to NE and sodium fluoride. The effect of the toxin on the NE-sensitivity was greater in mesenteric artery. 3. 3. Pretreatment of tissues with the inhibitor of Gi-protein, pertussis toxin (PT), reduced the sensitivity as well as maximum contraction of both the aorta and mesenteric artery to sodium fluoride, and of the mesenteric artery to NE. PT attenuated only the sensitivity but not the maximum contraction of the aorta to NE. The inhibitory effect of PT on sensitivity to NE or sodium fluoride was greater in the aorta. 4. 4. NE and sodium fluoride-induced contractions were reduced by the sulfhydryl G-protein inhibitor, N-ethylmaleimide (NEM) in both blood vessels. NEM produced greater inhibitory effect on the sensitivity of the aorta to both contractile agents. 5. 5. These data demonstrate that CT, PT and NEM-sensitive G-proteins are involved in NE- and sodium fluoride-induced contractile responses of the rat aorta and mesenteric artery. The differential effects of the G-protein probes indicate that certain variations in G-protein-mediated contractile responses exist among the two blood vessels, suggesting that G-protein involvement in functional responses may vary with the type of blood vessel investigated.
| Original language | English |
|---|---|
| Pages (from-to) | 75-83 |
| Number of pages | 9 |
| Journal | General Pharmacology |
| Volume | 26 |
| Issue number | 1 |
| DOIs | |
| State | Published - 1995 |
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All Science Journal Classification (ASJC) codes
- Pharmacology
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G-proteins in rat blood vessels-II. Assessment of functional involvement. / Abebe, Worku; Edwards, John D.; Agrawal, Devendra K.
In: General Pharmacology, Vol. 26, No. 1, 1995, p. 75-83.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - G-proteins in rat blood vessels-II. Assessment of functional involvement
AU - Abebe, Worku
AU - Edwards, John D.
AU - Agrawal, Devendra K.
PY - 1995
Y1 - 1995
N2 - 1. 1. In this study, we compared G-protein-mediated contractile responses of rat aorta and mesenteric artery rings induced by the α-adrenoceptor agonist, norepinephrine (NE) and by the direct G-protein activator, sodium fluoride, using various probes. 2. 2. Activator of the stimulatory G-protein (Gs), cholera toxin (CT), attenuated the sensitivity and maximum contractile response of both aorta and mesenteric artery to NE and sodium fluoride. The effect of the toxin on the NE-sensitivity was greater in mesenteric artery. 3. 3. Pretreatment of tissues with the inhibitor of Gi-protein, pertussis toxin (PT), reduced the sensitivity as well as maximum contraction of both the aorta and mesenteric artery to sodium fluoride, and of the mesenteric artery to NE. PT attenuated only the sensitivity but not the maximum contraction of the aorta to NE. The inhibitory effect of PT on sensitivity to NE or sodium fluoride was greater in the aorta. 4. 4. NE and sodium fluoride-induced contractions were reduced by the sulfhydryl G-protein inhibitor, N-ethylmaleimide (NEM) in both blood vessels. NEM produced greater inhibitory effect on the sensitivity of the aorta to both contractile agents. 5. 5. These data demonstrate that CT, PT and NEM-sensitive G-proteins are involved in NE- and sodium fluoride-induced contractile responses of the rat aorta and mesenteric artery. The differential effects of the G-protein probes indicate that certain variations in G-protein-mediated contractile responses exist among the two blood vessels, suggesting that G-protein involvement in functional responses may vary with the type of blood vessel investigated.
AB - 1. 1. In this study, we compared G-protein-mediated contractile responses of rat aorta and mesenteric artery rings induced by the α-adrenoceptor agonist, norepinephrine (NE) and by the direct G-protein activator, sodium fluoride, using various probes. 2. 2. Activator of the stimulatory G-protein (Gs), cholera toxin (CT), attenuated the sensitivity and maximum contractile response of both aorta and mesenteric artery to NE and sodium fluoride. The effect of the toxin on the NE-sensitivity was greater in mesenteric artery. 3. 3. Pretreatment of tissues with the inhibitor of Gi-protein, pertussis toxin (PT), reduced the sensitivity as well as maximum contraction of both the aorta and mesenteric artery to sodium fluoride, and of the mesenteric artery to NE. PT attenuated only the sensitivity but not the maximum contraction of the aorta to NE. The inhibitory effect of PT on sensitivity to NE or sodium fluoride was greater in the aorta. 4. 4. NE and sodium fluoride-induced contractions were reduced by the sulfhydryl G-protein inhibitor, N-ethylmaleimide (NEM) in both blood vessels. NEM produced greater inhibitory effect on the sensitivity of the aorta to both contractile agents. 5. 5. These data demonstrate that CT, PT and NEM-sensitive G-proteins are involved in NE- and sodium fluoride-induced contractile responses of the rat aorta and mesenteric artery. The differential effects of the G-protein probes indicate that certain variations in G-protein-mediated contractile responses exist among the two blood vessels, suggesting that G-protein involvement in functional responses may vary with the type of blood vessel investigated.
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U2 - 10.1016/0306-3623(94)00174-L
DO - 10.1016/0306-3623(94)00174-L
M3 - Article
VL - 26
SP - 75
EP - 83
JO - Vascular Pharmacology
JF - Vascular Pharmacology
SN - 1537-1891
IS - 1
ER -