Abstract
1. Local modulation of adrenergic responses was examined in the hindlimb vasculature of chronically instrumented intact conscious rats. Sprague-Dawley rats (n = 22) were instrumented with a Doppler flow probe around the right common iliac artery, a polyethylene catheter inserted just distal to the flow probe and a left carotid arterial catheter. 2. The effects of various concentrations of the α1-adrenergic receptor agonist phenylephrine (0.005-0.075 μg kg-1), the α2-adrenergic receptor agonist clonidine (0.1-0.7 μg kg-1), and the endogenous adrenergic receptor agonist adrenaline (0.02-0.08 μg kg-1), were investigated under control conditions, and in the presence of the nitric oxide (NO) synthase inhibitor N(ω)-nitro-L-arginane methyl ester hydrochoride (L-NAME) (NO-X, 0.2 mg kg-1) and the cyclo-oxygenase inhibitor indomethacin (CO-X, 10 mg kg-1). Results were presented as dose-response curves. 3. Heart rate and arterial pressure were not altered by any of the agents because all were locally injected into the hindlimb vasculature and the selected doses were lower than those which elicited systemic responses. 4. Maximal vasoconstrictor responses to phenylephrine were enhanced in the presence of NO-X (50 ± 6%) and CO-X (70 ± 9%). Maximal vasoconstrictor responses to clonidine were also enhanced in the presence of NO-X (75.3 ± 4.8%) and CO-X (50.6 ± 5.7%). 5. The responses to adrenaline were biphasic; NO-X significantly attenuated the vasodilator response (87 ± 6%), and enhanced the vasoconstrictor response (51 ± 7%). CO-X attenuated the vasoconstrictor response (71 ± 6%). 6. These results demonstrate local modulation of responses to α1- and β-adrenergic receptor agonists by receptor-mediated dose-dependent release of NO and prostaglandins.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 817-825 |
| Number of pages | 9 |
| Journal | Journal of Physiology |
| Volume | 485 |
| Issue number | 3 |
| State | Published - 1995 |
| Externally published | Yes |
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Local modulation of adrenergic responses in the hindlimb vasculature of the intact conscious rat. / DiCarlo, S. E.; Patil, R. D.; Collins, H. L.; Chen, Chao-Yin.
In: Journal of Physiology, Vol. 485, No. 3, 1995, p. 817-825.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Local modulation of adrenergic responses in the hindlimb vasculature of the intact conscious rat
AU - DiCarlo, S. E.
AU - Patil, R. D.
AU - Collins, H. L.
AU - Chen, Chao-Yin
PY - 1995
Y1 - 1995
N2 - 1. Local modulation of adrenergic responses was examined in the hindlimb vasculature of chronically instrumented intact conscious rats. Sprague-Dawley rats (n = 22) were instrumented with a Doppler flow probe around the right common iliac artery, a polyethylene catheter inserted just distal to the flow probe and a left carotid arterial catheter. 2. The effects of various concentrations of the α1-adrenergic receptor agonist phenylephrine (0.005-0.075 μg kg-1), the α2-adrenergic receptor agonist clonidine (0.1-0.7 μg kg-1), and the endogenous adrenergic receptor agonist adrenaline (0.02-0.08 μg kg-1), were investigated under control conditions, and in the presence of the nitric oxide (NO) synthase inhibitor N(ω)-nitro-L-arginane methyl ester hydrochoride (L-NAME) (NO-X, 0.2 mg kg-1) and the cyclo-oxygenase inhibitor indomethacin (CO-X, 10 mg kg-1). Results were presented as dose-response curves. 3. Heart rate and arterial pressure were not altered by any of the agents because all were locally injected into the hindlimb vasculature and the selected doses were lower than those which elicited systemic responses. 4. Maximal vasoconstrictor responses to phenylephrine were enhanced in the presence of NO-X (50 ± 6%) and CO-X (70 ± 9%). Maximal vasoconstrictor responses to clonidine were also enhanced in the presence of NO-X (75.3 ± 4.8%) and CO-X (50.6 ± 5.7%). 5. The responses to adrenaline were biphasic; NO-X significantly attenuated the vasodilator response (87 ± 6%), and enhanced the vasoconstrictor response (51 ± 7%). CO-X attenuated the vasoconstrictor response (71 ± 6%). 6. These results demonstrate local modulation of responses to α1- and β-adrenergic receptor agonists by receptor-mediated dose-dependent release of NO and prostaglandins.
AB - 1. Local modulation of adrenergic responses was examined in the hindlimb vasculature of chronically instrumented intact conscious rats. Sprague-Dawley rats (n = 22) were instrumented with a Doppler flow probe around the right common iliac artery, a polyethylene catheter inserted just distal to the flow probe and a left carotid arterial catheter. 2. The effects of various concentrations of the α1-adrenergic receptor agonist phenylephrine (0.005-0.075 μg kg-1), the α2-adrenergic receptor agonist clonidine (0.1-0.7 μg kg-1), and the endogenous adrenergic receptor agonist adrenaline (0.02-0.08 μg kg-1), were investigated under control conditions, and in the presence of the nitric oxide (NO) synthase inhibitor N(ω)-nitro-L-arginane methyl ester hydrochoride (L-NAME) (NO-X, 0.2 mg kg-1) and the cyclo-oxygenase inhibitor indomethacin (CO-X, 10 mg kg-1). Results were presented as dose-response curves. 3. Heart rate and arterial pressure were not altered by any of the agents because all were locally injected into the hindlimb vasculature and the selected doses were lower than those which elicited systemic responses. 4. Maximal vasoconstrictor responses to phenylephrine were enhanced in the presence of NO-X (50 ± 6%) and CO-X (70 ± 9%). Maximal vasoconstrictor responses to clonidine were also enhanced in the presence of NO-X (75.3 ± 4.8%) and CO-X (50.6 ± 5.7%). 5. The responses to adrenaline were biphasic; NO-X significantly attenuated the vasodilator response (87 ± 6%), and enhanced the vasoconstrictor response (51 ± 7%). CO-X attenuated the vasoconstrictor response (71 ± 6%). 6. These results demonstrate local modulation of responses to α1- and β-adrenergic receptor agonists by receptor-mediated dose-dependent release of NO and prostaglandins.
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UR - http://www.scopus.com/inward/citedby.url?scp=0028998809&partnerID=8YFLogxK
M3 - Article
C2 - 7562619
AN - SCOPUS:0028998809
VL - 485
SP - 817
EP - 825
JO - Journal of Physiology
JF - Journal of Physiology
SN - 0022-3751
IS - 3
ER -