The role of α2‐adrenoceptors in the vasculature of the rat tail
1 The effects of α2‐adrenoceptor agonists and antagonists on rat tail skin temperature (tts), an indicator of local cutaneous blood flow, were studied in conscious and anaesthetized rats and in the isolated, Krebs perfused, vascular bed of the rat tail. 2 In conscious rats, at an ambient temperature...
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| Veröffentlicht in: | British journal of pharmacology 1995-04, Vol.114 (8), p.1724-1730 |
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| description | 1
The effects of α2‐adrenoceptor agonists and antagonists on rat tail skin temperature (tts), an indicator of local cutaneous blood flow, were studied in conscious and anaesthetized rats and in the isolated, Krebs perfused, vascular bed of the rat tail.
2
In conscious rats, at an ambient temperature of 18.5–20°C, tts was 21.0 ± 0.2°C and core (rectal) temperature (tc) was 38.2 ± 0.04°C (n = 126). The α2‐adrenoceptor antagonist, delequamine (RS‐15385‐197; 1 mg kg−1, s.c., n = 6), produced a rapid elevation in t to 29.1 ± 0.7°C (P < 0.001 vs. saline‐treated control group), attained 10 min after injection. tc fell slightly, by 1.0 ± 0.1°C. The tts response was dose‐related over the dose‐range tested (0.01‐1 mg kg‐1, s.c.), with an ED50 of 17 μg kg1, s.c. (n =6 per dose).
3
The maximum increases in tts in response to a dose of 1 mg kg‐1, s.c. of α2‐adrenoceptor antagonists were as follows (n = 6 per drug): delequamine (+ 9.6 ± 0.8°C)> yohimbine (+ 9.0 ± 1.0°C)> WY‐26703 (+ 7.9 ± 1.3°C) > piperoxan (+ 5.6 ± 1 7°C) > idazoxan (+ 4.6 ± 1.3°C) > imiloxan (+ 4.1 ± 1.3°C) > SKF 104078 (+2.0 ± 1.9°C)>BDF‐6143 (+1.3 ± 0.8°C).
4
Prazosin (0.3mg kg‐1, s.c.), hydralazine (10mg kg‐1, s.c.) and nifedipine (3mg kg‐1, s.c.) did not increase tts, whereas propranolol (10mg kg‐1, s.c.) evoked a small increase in tts (+2.9 ± 1.0°C). Pentolinium (2–10 mg kg−1, s.c.) elicited a dose‐related increase in tts which was elevated by 4.4 ± 1.3°C after a dose of 10 mg kg−1; tc was reduced in a dose‐related manner. Drug vehicles (1 ml kg−1, s.c) had no effect on tte or tc.
5
In anaesthetized rats, idazoxan (300 μg, i.v.) produced a rapid increase in tts which was detectable 2 min after beginning the injection, reaching a peak after 7 min. When the same dose was administered i.c.v., tts also rose, but more slowly. The peak response (+ 3.6 ± 0.7°C, n = 5) was significantly smaller than when idazoxan was administered intravenously (+6.3± 1.2°C, n = 5), which suggests that the increase in tts following systemic administration of α2‐adrenoceptor antagonists is not due to a central effect. The change in tts was not secondary to changes in blood pressure.
6
In the isolated, Krebs perfused, tail vascular bed of the rat, at an ambient temperature of 20–21°C, under constant flow conditions (3.5‐4.0 ml min−1; n = 4), baseline perfusion pressure was 57 ± 4 mmHg. 5‐Hydroxytryptamine (5‐HT; 70–150 nm) increased perfusion pressure by 56 ± 9 mmHg. The α2‐adrenoceptor agonist, UK‐14,304 (10 nmol), elicite |
| doi_str_mv | 10.1111/j.1476-5381.1995.tb14963.x |
| format | Article |
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The effects of α2‐adrenoceptor agonists and antagonists on rat tail skin temperature (tts), an indicator of local cutaneous blood flow, were studied in conscious and anaesthetized rats and in the isolated, Krebs perfused, vascular bed of the rat tail.
2
In conscious rats, at an ambient temperature of 18.5–20°C, tts was 21.0 ± 0.2°C and core (rectal) temperature (tc) was 38.2 ± 0.04°C (n = 126). The α2‐adrenoceptor antagonist, delequamine (RS‐15385‐197; 1 mg kg−1, s.c., n = 6), produced a rapid elevation in t to 29.1 ± 0.7°C (P < 0.001 vs. saline‐treated control group), attained 10 min after injection. tc fell slightly, by 1.0 ± 0.1°C. The tts response was dose‐related over the dose‐range tested (0.01‐1 mg kg‐1, s.c.), with an ED50 of 17 μg kg1, s.c. (n =6 per dose).
3
The maximum increases in tts in response to a dose of 1 mg kg‐1, s.c. of α2‐adrenoceptor antagonists were as follows (n = 6 per drug): delequamine (+ 9.6 ± 0.8°C)> yohimbine (+ 9.0 ± 1.0°C)> WY‐26703 (+ 7.9 ± 1.3°C) > piperoxan (+ 5.6 ± 1 7°C) > idazoxan (+ 4.6 ± 1.3°C) > imiloxan (+ 4.1 ± 1.3°C) > SKF 104078 (+2.0 ± 1.9°C)>BDF‐6143 (+1.3 ± 0.8°C).
4
Prazosin (0.3mg kg‐1, s.c.), hydralazine (10mg kg‐1, s.c.) and nifedipine (3mg kg‐1, s.c.) did not increase tts, whereas propranolol (10mg kg‐1, s.c.) evoked a small increase in tts (+2.9 ± 1.0°C). Pentolinium (2–10 mg kg−1, s.c.) elicited a dose‐related increase in tts which was elevated by 4.4 ± 1.3°C after a dose of 10 mg kg−1; tc was reduced in a dose‐related manner. Drug vehicles (1 ml kg−1, s.c) had no effect on tte or tc.
5
In anaesthetized rats, idazoxan (300 μg, i.v.) produced a rapid increase in tts which was detectable 2 min after beginning the injection, reaching a peak after 7 min. When the same dose was administered i.c.v., tts also rose, but more slowly. The peak response (+ 3.6 ± 0.7°C, n = 5) was significantly smaller than when idazoxan was administered intravenously (+6.3± 1.2°C, n = 5), which suggests that the increase in tts following systemic administration of α2‐adrenoceptor antagonists is not due to a central effect. The change in tts was not secondary to changes in blood pressure.
6
In the isolated, Krebs perfused, tail vascular bed of the rat, at an ambient temperature of 20–21°C, under constant flow conditions (3.5‐4.0 ml min−1; n = 4), baseline perfusion pressure was 57 ± 4 mmHg. 5‐Hydroxytryptamine (5‐HT; 70–150 nm) increased perfusion pressure by 56 ± 9 mmHg. The α2‐adrenoceptor agonist, UK‐14,304 (10 nmol), elicited a further increase in perfusion pressure by 27.5 ± 15 mmHg but had no effect in the absence of 5‐HT; this response to UK‐14,304 was abolished by rauwolscine (1 μm).
7
Under constant pressure conditions (∼100 mmHg; n = 9), baseline mean perfusion flow was 2.1 ± 0.2 ml min−1, and mean tail skin temperature was 31.6 ± 0.6°C. 5‐HT (119 ± 28 nM) decreased. tts by 3.3 ± 2.0°C and reduced flow by 1.2 ± 0.3 ml min−1. UK‐14,304 (10 nmol) further reduced tts by 3.0 ± 0.3°C without significant effect on flow; this effect was also abolished by 1 μm rauwolscine.
8
We conclude that post‐junctional α2‐adrenoceptors in the vasculature of the rat tail have a major vasoconstrictor role, controlling both the flow and distribution of blood within the tail and thereby thermoregulatory heat loss from its surface.</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1111/j.1476-5381.1995.tb14963.x</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Biological and medical sciences ; cutaneous vasoconstriction ; delequamine ; Fundamental and applied biological sciences. Psychology ; Hemodynamics. Rheology ; rat tail ; RS‐15385‐197 ; thermoregulation ; Vertebrates: cardiovascular system ; α2‐Adrenoceptors</subject><ispartof>British journal of pharmacology, 1995-04, Vol.114 (8), p.1724-1730</ispartof><rights>1995 British Pharmacological Society</rights><rights>1995 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3504741$$DView record in Pascal Francis$$Hfree_for_read</backlink></links><search><creatorcontrib>Redfern, William S.</creatorcontrib><creatorcontrib>MacLean, Margaret R.</creatorcontrib><creatorcontrib>Clague, Ruth U.</creatorcontrib><creatorcontrib>McGrath, John C.</creatorcontrib><title>The role of α2‐adrenoceptors in the vasculature of the rat tail</title><title>British journal of pharmacology</title><description>1
The effects of α2‐adrenoceptor agonists and antagonists on rat tail skin temperature (tts), an indicator of local cutaneous blood flow, were studied in conscious and anaesthetized rats and in the isolated, Krebs perfused, vascular bed of the rat tail.
2
In conscious rats, at an ambient temperature of 18.5–20°C, tts was 21.0 ± 0.2°C and core (rectal) temperature (tc) was 38.2 ± 0.04°C (n = 126). The α2‐adrenoceptor antagonist, delequamine (RS‐15385‐197; 1 mg kg−1, s.c., n = 6), produced a rapid elevation in t to 29.1 ± 0.7°C (P < 0.001 vs. saline‐treated control group), attained 10 min after injection. tc fell slightly, by 1.0 ± 0.1°C. The tts response was dose‐related over the dose‐range tested (0.01‐1 mg kg‐1, s.c.), with an ED50 of 17 μg kg1, s.c. (n =6 per dose).
3
The maximum increases in tts in response to a dose of 1 mg kg‐1, s.c. of α2‐adrenoceptor antagonists were as follows (n = 6 per drug): delequamine (+ 9.6 ± 0.8°C)> yohimbine (+ 9.0 ± 1.0°C)> WY‐26703 (+ 7.9 ± 1.3°C) > piperoxan (+ 5.6 ± 1 7°C) > idazoxan (+ 4.6 ± 1.3°C) > imiloxan (+ 4.1 ± 1.3°C) > SKF 104078 (+2.0 ± 1.9°C)>BDF‐6143 (+1.3 ± 0.8°C).
4
Prazosin (0.3mg kg‐1, s.c.), hydralazine (10mg kg‐1, s.c.) and nifedipine (3mg kg‐1, s.c.) did not increase tts, whereas propranolol (10mg kg‐1, s.c.) evoked a small increase in tts (+2.9 ± 1.0°C). Pentolinium (2–10 mg kg−1, s.c.) elicited a dose‐related increase in tts which was elevated by 4.4 ± 1.3°C after a dose of 10 mg kg−1; tc was reduced in a dose‐related manner. Drug vehicles (1 ml kg−1, s.c) had no effect on tte or tc.
5
In anaesthetized rats, idazoxan (300 μg, i.v.) produced a rapid increase in tts which was detectable 2 min after beginning the injection, reaching a peak after 7 min. When the same dose was administered i.c.v., tts also rose, but more slowly. The peak response (+ 3.6 ± 0.7°C, n = 5) was significantly smaller than when idazoxan was administered intravenously (+6.3± 1.2°C, n = 5), which suggests that the increase in tts following systemic administration of α2‐adrenoceptor antagonists is not due to a central effect. The change in tts was not secondary to changes in blood pressure.
6
In the isolated, Krebs perfused, tail vascular bed of the rat, at an ambient temperature of 20–21°C, under constant flow conditions (3.5‐4.0 ml min−1; n = 4), baseline perfusion pressure was 57 ± 4 mmHg. 5‐Hydroxytryptamine (5‐HT; 70–150 nm) increased perfusion pressure by 56 ± 9 mmHg. The α2‐adrenoceptor agonist, UK‐14,304 (10 nmol), elicited a further increase in perfusion pressure by 27.5 ± 15 mmHg but had no effect in the absence of 5‐HT; this response to UK‐14,304 was abolished by rauwolscine (1 μm).
7
Under constant pressure conditions (∼100 mmHg; n = 9), baseline mean perfusion flow was 2.1 ± 0.2 ml min−1, and mean tail skin temperature was 31.6 ± 0.6°C. 5‐HT (119 ± 28 nM) decreased. tts by 3.3 ± 2.0°C and reduced flow by 1.2 ± 0.3 ml min−1. UK‐14,304 (10 nmol) further reduced tts by 3.0 ± 0.3°C without significant effect on flow; this effect was also abolished by 1 μm rauwolscine.
8
We conclude that post‐junctional α2‐adrenoceptors in the vasculature of the rat tail have a major vasoconstrictor role, controlling both the flow and distribution of blood within the tail and thereby thermoregulatory heat loss from its surface.</description><subject>Biological and medical sciences</subject><subject>cutaneous vasoconstriction</subject><subject>delequamine</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hemodynamics. Rheology</subject><subject>rat tail</subject><subject>RS‐15385‐197</subject><subject>thermoregulation</subject><subject>Vertebrates: cardiovascular system</subject><subject>α2‐Adrenoceptors</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><recordid>eNo9kE1OwzAQhS0EEqVwhwixTZiJndjZQStKkSrBoqytSeKIRCGpnBTaHUfgKlyEQ3ASnLbqbObnPY1mPsauEQJ0cVsFKGTsR1xhgEkSBX2KIol5sDlho6N0ykYAIH1Epc7ZRddVAE6U0YhNlm_Gs21tvLbwfn_Cv69vyq1p2sys-tZ2Xtl4vbN8UJeta-rXduccRpZ6r6eyvmRnBdWduTrkMXudPSync3_x_Pg0vV_4VShD7ocCKCeSEYhYKSFQRIWChLsDBYdUGqCQUGWKuw7yRKUmhsT9UuQpISg-Zjf7vSt3C9WFpSYrO72y5TvZreZusRTobHd722dZm-1RRtADMV3pAYsesOiBmD4Q0xs9eZnvSv4Pml1iVg</recordid><startdate>199504</startdate><enddate>199504</enddate><creator>Redfern, William S.</creator><creator>MacLean, Margaret R.</creator><creator>Clague, Ruth U.</creator><creator>McGrath, John C.</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing</general><scope>IQODW</scope></search><sort><creationdate>199504</creationdate><title>The role of α2‐adrenoceptors in the vasculature of the rat tail</title><author>Redfern, William S. ; MacLean, Margaret R. ; Clague, Ruth U. ; McGrath, John C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-j2723-240adaa750468844145f8093538430b7e0a2a18c8330b0d98be609963fdba1083</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Biological and medical sciences</topic><topic>cutaneous vasoconstriction</topic><topic>delequamine</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hemodynamics. Rheology</topic><topic>rat tail</topic><topic>RS‐15385‐197</topic><topic>thermoregulation</topic><topic>Vertebrates: cardiovascular system</topic><topic>α2‐Adrenoceptors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Redfern, William S.</creatorcontrib><creatorcontrib>MacLean, Margaret R.</creatorcontrib><creatorcontrib>Clague, Ruth U.</creatorcontrib><creatorcontrib>McGrath, John C.</creatorcontrib><collection>Pascal-Francis</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Redfern, William S.</au><au>MacLean, Margaret R.</au><au>Clague, Ruth U.</au><au>McGrath, John C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The role of α2‐adrenoceptors in the vasculature of the rat tail</atitle><jtitle>British journal of pharmacology</jtitle><date>1995-04</date><risdate>1995</risdate><volume>114</volume><issue>8</issue><spage>1724</spage><epage>1730</epage><pages>1724-1730</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>1
The effects of α2‐adrenoceptor agonists and antagonists on rat tail skin temperature (tts), an indicator of local cutaneous blood flow, were studied in conscious and anaesthetized rats and in the isolated, Krebs perfused, vascular bed of the rat tail.
2
In conscious rats, at an ambient temperature of 18.5–20°C, tts was 21.0 ± 0.2°C and core (rectal) temperature (tc) was 38.2 ± 0.04°C (n = 126). The α2‐adrenoceptor antagonist, delequamine (RS‐15385‐197; 1 mg kg−1, s.c., n = 6), produced a rapid elevation in t to 29.1 ± 0.7°C (P < 0.001 vs. saline‐treated control group), attained 10 min after injection. tc fell slightly, by 1.0 ± 0.1°C. The tts response was dose‐related over the dose‐range tested (0.01‐1 mg kg‐1, s.c.), with an ED50 of 17 μg kg1, s.c. (n =6 per dose).
3
The maximum increases in tts in response to a dose of 1 mg kg‐1, s.c. of α2‐adrenoceptor antagonists were as follows (n = 6 per drug): delequamine (+ 9.6 ± 0.8°C)> yohimbine (+ 9.0 ± 1.0°C)> WY‐26703 (+ 7.9 ± 1.3°C) > piperoxan (+ 5.6 ± 1 7°C) > idazoxan (+ 4.6 ± 1.3°C) > imiloxan (+ 4.1 ± 1.3°C) > SKF 104078 (+2.0 ± 1.9°C)>BDF‐6143 (+1.3 ± 0.8°C).
4
Prazosin (0.3mg kg‐1, s.c.), hydralazine (10mg kg‐1, s.c.) and nifedipine (3mg kg‐1, s.c.) did not increase tts, whereas propranolol (10mg kg‐1, s.c.) evoked a small increase in tts (+2.9 ± 1.0°C). Pentolinium (2–10 mg kg−1, s.c.) elicited a dose‐related increase in tts which was elevated by 4.4 ± 1.3°C after a dose of 10 mg kg−1; tc was reduced in a dose‐related manner. Drug vehicles (1 ml kg−1, s.c) had no effect on tte or tc.
5
In anaesthetized rats, idazoxan (300 μg, i.v.) produced a rapid increase in tts which was detectable 2 min after beginning the injection, reaching a peak after 7 min. When the same dose was administered i.c.v., tts also rose, but more slowly. The peak response (+ 3.6 ± 0.7°C, n = 5) was significantly smaller than when idazoxan was administered intravenously (+6.3± 1.2°C, n = 5), which suggests that the increase in tts following systemic administration of α2‐adrenoceptor antagonists is not due to a central effect. The change in tts was not secondary to changes in blood pressure.
6
In the isolated, Krebs perfused, tail vascular bed of the rat, at an ambient temperature of 20–21°C, under constant flow conditions (3.5‐4.0 ml min−1; n = 4), baseline perfusion pressure was 57 ± 4 mmHg. 5‐Hydroxytryptamine (5‐HT; 70–150 nm) increased perfusion pressure by 56 ± 9 mmHg. The α2‐adrenoceptor agonist, UK‐14,304 (10 nmol), elicited a further increase in perfusion pressure by 27.5 ± 15 mmHg but had no effect in the absence of 5‐HT; this response to UK‐14,304 was abolished by rauwolscine (1 μm).
7
Under constant pressure conditions (∼100 mmHg; n = 9), baseline mean perfusion flow was 2.1 ± 0.2 ml min−1, and mean tail skin temperature was 31.6 ± 0.6°C. 5‐HT (119 ± 28 nM) decreased. tts by 3.3 ± 2.0°C and reduced flow by 1.2 ± 0.3 ml min−1. UK‐14,304 (10 nmol) further reduced tts by 3.0 ± 0.3°C without significant effect on flow; this effect was also abolished by 1 μm rauwolscine.
8
We conclude that post‐junctional α2‐adrenoceptors in the vasculature of the rat tail have a major vasoconstrictor role, controlling both the flow and distribution of blood within the tail and thereby thermoregulatory heat loss from its surface.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><doi>10.1111/j.1476-5381.1995.tb14963.x</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Biological and medical sciences cutaneous vasoconstriction delequamine Fundamental and applied biological sciences. Psychology Hemodynamics. Rheology rat tail RS‐15385‐197 thermoregulation Vertebrates: cardiovascular system α2‐Adrenoceptors |
| title | The role of α2‐adrenoceptors in the vasculature of the rat tail |
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