TY - JOUR
T1 - Cardiovascular responses to static exercise in conscious cats
T2 - Effects of intracerebroventricular injection of clonidine
AU - Ally, Ahmmed
AU - Hand, Gregory A.
AU - Mitchell, Jere H.
PY - 1996/3/1
Y1 - 1996/3/1
N2 - 1. Static exercise elicits increases in arterial blood pressure and heart rate (HR) in humans and conscious animals. In this study, the effects of intracerebroventricular (I.C.V.) administration of clonidine, an α-adrenergic agonist, on these cardiovascular responses were investigated using conscious cats. Four cats were operantly trained to extend a forelimb and press a bar (200-650 g) for 15-60 s. A stainless-steel cannula was inserted into the right lateral ventricle for I.C.V. injection of drugs, and a common carotid artery was catheterized to measure mean arterial pressure (MAP) and HR. The number of exercise trials and changes in MAP, HR and force were pooled for 30 min periods. After the cats exercised for 30 min, either artificial cerebrospinal fluid (CSF) or clonidine (2 or 5 μg) were administered intracerebroventricularly. 2. Before clonidine injection, fifty-two exercise trials increased MAP and HR by 15 ± 3 mmHg and 41 ± 5 beats min-1, respectively. Administration of clonidine (2 μg) did not alter the resting MAP and HR, but attenuated the increases in MAP and HR in response to exercise (0-30 min post-clonidine: n = 81; ΔMAP, 6 ± 3 mmHg; ΔHR, 20 ± 6 beats min-1 30-60 min post-clonidine: n = 71; MAP, 4 ± 4 mmHg; ΔHR, 17 ± 8 beats min-1). Administration of artificial CSF I.C.V. had no effect on the cardiovascular responses to static exercise. 3. An increased dose of clonidine (5 μg) decreased resting MAP and HR by 31 ± 7 mmHg and 37 ± 7 beats min-1, respectively, and markedly blunted the cardiovascular responses to exercise (pre-clonidine: n = 52; ΔMAP, 17 ± 3 mmHg; ΔHR, 38 ± 5 beats min-1; post-clonidine 0-30 min: n = 66; ΔMAP, 4 ± 2 mmHg; ΔHR, 15 ± 5 beats min-1; post-clonidine 30-60 min: n = 60; ΔMAP, 4 ± 2 mmHg; ΔHR, 14 ± 6 beats min-1). Pretreatment with the α-adrenergic antagonist, yohimbine (8 μg, I.C.V.), blocked the attenuating effects of I.C.V. administration of clonidine (5 μg). 4. These results show that stimulation of central α-adrenoceptors by clonidine attenuates the cardiovascular responses to static exercise in conscious cats. In addition, this study suggests that α-adrenoceptors blocked by yohimbine injected I.C.V. do not appear to have a tonic influence on HR and blood pressure.
AB - 1. Static exercise elicits increases in arterial blood pressure and heart rate (HR) in humans and conscious animals. In this study, the effects of intracerebroventricular (I.C.V.) administration of clonidine, an α-adrenergic agonist, on these cardiovascular responses were investigated using conscious cats. Four cats were operantly trained to extend a forelimb and press a bar (200-650 g) for 15-60 s. A stainless-steel cannula was inserted into the right lateral ventricle for I.C.V. injection of drugs, and a common carotid artery was catheterized to measure mean arterial pressure (MAP) and HR. The number of exercise trials and changes in MAP, HR and force were pooled for 30 min periods. After the cats exercised for 30 min, either artificial cerebrospinal fluid (CSF) or clonidine (2 or 5 μg) were administered intracerebroventricularly. 2. Before clonidine injection, fifty-two exercise trials increased MAP and HR by 15 ± 3 mmHg and 41 ± 5 beats min-1, respectively. Administration of clonidine (2 μg) did not alter the resting MAP and HR, but attenuated the increases in MAP and HR in response to exercise (0-30 min post-clonidine: n = 81; ΔMAP, 6 ± 3 mmHg; ΔHR, 20 ± 6 beats min-1 30-60 min post-clonidine: n = 71; MAP, 4 ± 4 mmHg; ΔHR, 17 ± 8 beats min-1). Administration of artificial CSF I.C.V. had no effect on the cardiovascular responses to static exercise. 3. An increased dose of clonidine (5 μg) decreased resting MAP and HR by 31 ± 7 mmHg and 37 ± 7 beats min-1, respectively, and markedly blunted the cardiovascular responses to exercise (pre-clonidine: n = 52; ΔMAP, 17 ± 3 mmHg; ΔHR, 38 ± 5 beats min-1; post-clonidine 0-30 min: n = 66; ΔMAP, 4 ± 2 mmHg; ΔHR, 15 ± 5 beats min-1; post-clonidine 30-60 min: n = 60; ΔMAP, 4 ± 2 mmHg; ΔHR, 14 ± 6 beats min-1). Pretreatment with the α-adrenergic antagonist, yohimbine (8 μg, I.C.V.), blocked the attenuating effects of I.C.V. administration of clonidine (5 μg). 4. These results show that stimulation of central α-adrenoceptors by clonidine attenuates the cardiovascular responses to static exercise in conscious cats. In addition, this study suggests that α-adrenoceptors blocked by yohimbine injected I.C.V. do not appear to have a tonic influence on HR and blood pressure.
UR - http://www.scopus.com/inward/record.url?scp=0029921185&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0029921185&partnerID=8YFLogxK
U2 - 10.1113/jphysiol.1996.sp021236
DO - 10.1113/jphysiol.1996.sp021236
M3 - Article
C2 - 8866875
AN - SCOPUS:0029921185
SN - 0022-3751
VL - 491
SP - 519
EP - 527
JO - Journal of Physiology
JF - Journal of Physiology
IS - 2
ER -