scholarly journals Intracoronary alpha 2-adrenergic receptor blockade attenuates ischemia in conscious dogs during exercise.

1988 ◽  
Vol 62 (3) ◽  
pp. 436-442 ◽  
Author(s):  
R Seitelberger ◽  
B D Guth ◽  
G Heusch ◽  
J D Lee ◽  
K Katayama ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Conscious Dogs ◽  
Receptor Blockade ◽  
Adrenergic Receptor Blockade

Reflex cardiovascular responses to chemoreceptor stimulation in conscious dogs with cardiac hypertrophy

1983 ◽  
Vol 245 (5) ◽  
pp. H871-H879
Author(s):  
P. A. Murray ◽  
S. F. Vatner
Keyword(s):  
Adrenergic Receptor ◽  
Cycle Length ◽  
Cardiac Cycle ◽  
Cardiovascular Responses ◽  
Conscious Dogs ◽  
Receptor Blockade ◽  
Coronary Resistance ◽  
Coronary Vasoconstriction ◽  
Reflex Activation ◽  
Adrenergic Receptor Blockade

Carotid chemoreceptor reflex activation (CCRA) has been previously shown to result in intense alpha-adrenergic peripheral vasoconstriction, a biphasic coronary vascular response characterized by an early vasodilation and a late alpha-adrenergic vasoconstriction, and a cholinergic increase in cardiac cycle length in normal conscious dogs. In the present study, we investigated the extent to which these reflex cardiovascular responses to CCRA are modified after the development of pressure-overload right ventricular (RV) hypertrophy induced by chronic (9-12 mo) pulmonary arterial stenosis. With heart rate constant and respiration allowed to vary spontaneously, the magnitude of the late CCRA-induced (intracarotid nicotine) increase (P less than 0.01) in right coronary resistance was markedly attenuated (P less than 0.01) in conscious dogs with RV hypertrophy [0.29 +/- 0.07 (SE) mmHg X ml-1 X min] compared with normal dogs (1.87 +/- 0.36). When respiration was controlled to eliminate pulmonary inflation reflex activation, the late CCRA-induced increase (P less than 0.01) in right coronary resistance was still found to be depressed (P less than 0.01) in the RV hypertrophy group (1.11 +/- 0.20 mmHg X ml-1 X min) compared with normal dogs (3.65 +/- 0.75). This late CCRA-induced right coronary vasoconstriction was not potentiated by beta-adrenergic receptor blockade but was abolished (P less than 0.01) by alpha-adrenergic receptor blockade. In contrast to the depressed right coronary vasoconstriction, the CCRA-induced alpha-adrenergic constriction (P less than 0.01) of the iliac arterial vascular bed was similar in both groups, and the cholinergic increase (P less than 0.01) in cardiac cycle length was enhanced (P less than 0.01) in the RV hypertrophy group compared with normal dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Neurally mediated cardiac effects of forskolin in conscious dogs

1996 ◽  
Vol 271 (4) ◽  
pp. H1473-H1482 ◽  
Author(s):  
M. Iwase ◽  
Y. Ishikawa ◽  
Y. T. Shen ◽  
R. P. Shannon ◽  
N. Sato ◽  
...  
Keyword(s):  
Heart Rate ◽  
Adenylyl Cyclase ◽  
Adrenergic Receptor ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Receptor Blockade ◽  
Beta Adrenergic Receptor ◽  
Beta Adrenergic ◽  
Ganglionic Blockade ◽  
Adrenergic Receptor Blockade

Because major cardiovascular disease states are characterized by defects in adenylyl cyclase regulation, it becomes important to understand the mechanisms by which adenylyl cyclase activators affect inotropy and chronotropy in intact conscious animals. Accordingly, we examined the inotropic and chronotropic responses to forskolin in 11 normal conscious, chronically instrumented dogs and 3 dogs with ventricular denervation (VD). Left ventricular first derivative of pressure (LV dP/dt) increased by 96 +/- 7%, P < 0.05, in response to forskolin (50 nmol.kg-1.min-1) in normal dogs and by significantly less, 52 +/- 14%, in VD dogs. Circulating norepinephrine (NE) levels increased similarly in both groups (from 226 +/- 18 to 389 +/- 33 pg/ml in normal dogs, from 177 +/- 23 to 329 +/- 71 pg/ml in VD dogs). In the presence of ganglionic blockade, the increase in LV dP/dt in response to forskolin was reduced (+62 +/- 4%) in normal dogs but was unchanged in VD dogs (+52 +/- 12%). Ganglionic blockade abolished the increase in circulating NE levels in both groups. Increases in heart rate in the presence of ganglionic blockade (+54 +/- 6 beats/min) were less than in the presence of atropine alone (+92 +/- 10 beats/min). Notably, the LV dP/dt and heart rate responses to forskolin were further attenuated by beta-adrenergic receptor blockade in the presence and absence of ganglionic blockade. Morphine also attenuated the increases in both LV dP/dt and plasma NE in response to forskolin. Increases in LV dP/dt in response to NKH-477 (30 micrograms/kg), a water-soluble forskolin derivative, were similar before and after ganglionic blockade (+63 +/- 8 and +51 +/- 10%, respectively). However, in vitro experiments in LV sarcolemmal membrane preparations demonstrated that stimulation of adenylyl cyclase by forskolin and NKH-477 was not affected by beta-adrenergic receptor blockade. These results indicate that in conscious dogs, inotropic and chronotropic effects of forskolin are not only due to direct activation of adenylyl cyclase, but the effects also are mediated by neural mechanisms and potentiated by the prevailing level of sympathetic tone.

Splenic contraction-induced increases in arterial O2 reduce requirement for CBF in conscious dogs

1995 ◽  
Vol 269 (2) ◽  
pp. H491-H503 ◽  
Author(s):  
N. Sato ◽  
Y. T. Shen ◽  
K. Kiuchi ◽  
R. P. Shannon ◽  
S. F. Vatner
Keyword(s):  
Adrenergic Receptor ◽  
Conscious State ◽  
Conscious Dogs ◽  
Receptor Blockade ◽  
Sympathomimetic Amines ◽  
Blood Flows ◽  
Before And After ◽  
Myocardial O2 Consumption ◽  
Consequent Increase ◽  
Adrenergic Receptor Blockade

We investigated the extent to which sympathomimetic amines induced splenic contraction and associated increases in arterial O2 content (CaO2) and how these mechanisms affected control of the coronary circulation by sympathomimetic amines in conscious dogs. Blood hemoglobin (Hb) and CaO2 increased by 16 +/- 2 and 18 +/- 2%, respectively, during norepinephrine (NE, 0.8 micrograms.kg-1.min-1 iv) in the intact, conscious state after splenic contraction. Phenylephrine (PE) induced similar effects. After either alpha 1-adrenergic-receptor blockade or splenectomy, these effects were abolished. Isoproterenol (Iso) also decreased splenic thickness, which was abolished after ganglionic, alpha-, or beta 1/beta 2-adrenergic-receptor blockade. Direct infusions of NE and PE into the splenic artery decreased splenic thickness and increased Hb and CaO2, whereas Iso had no effect. After splenectomy, NE did not increase CaO2, but coronary blood flow (CBF) increased more (73 +/- 6%) vs. before splenectomy (49 +/- 7%) without any differences before and after splenectomy in the responses of pressures, contractility, and myocardial O2 consumption (MVO2). In contrast, renal, mesenteric, and iliac artery blood flows were not significantly different in response to sympathomimetic amines before and after splenectomy. These data indicate that sympathomimetic amines induced splenic contraction either directly or reflexly via alpha-adrenergic-receptor stimulation. The consequent increase in Hb and CaO2 allows for equivalent increases in MVO2, but at a smaller increase in CBF.

Effects of alpha-adrenergic receptor blockade on coronary circulation in conscious dogs

1982 ◽  
Vol 243 (1) ◽  
pp. H94-H98
Author(s):  
P. Macho ◽  
T. H. Hintze ◽  
S. F. Vatner
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Adrenergic Receptor ◽  
Coronary Circulation ◽  
Conscious Dogs ◽  
Receptor Blockade ◽  
Receptor Blocking ◽  
Blocking Agents ◽  
Alpha Adrenergic Receptor ◽  
Adrenergic Receptor Blockade

The effects of three alpha-adrenergic-receptor blocking agents (phentolamine, prazosin, and trimazosin) were compared on the coronary circulation and left ventricular (LV) function in chronically instrumented conscious dogs. The three alpha-adrenergic-receptor blocking agents were administered in equidepressor doses (mean arterial pressure fell by approximately 20%) and in the presence of beta-adrenergic-receptor blockade and constant heart rate. LV systolic pressure, LV end-diastolic pressure, and LV end-diastolic diameter also fell similarly with the three drugs. Phentolamine decreased the time rate of change of LV pressure (LV dP/dt) by 21 +/- 3%, whereas trimazosin and prazosin decreased LV dP/dt only by 14 +/- 2 and 11 +/- 2%, respectively. LV velocity was not changed with trimazosin and prazosin but decreased with phentolamine by 12 +/- 4%. The three drugs exerted differential effects on the coronary circulation. Only trimazosin increased coronary blood flow (18 +/- 5%). Trimazosin decreased late diastolic coronary resistance (LDCR) by 35 +/- 2%, which was significantly more than reductions in LDCR induced by prazosin (22 +/- 2%) and by phentolamine (11 +/- 3%). A test dose of phenylephrine (5.0 micrograms/kg) increased mean arterial pressure by 53 +/- 3.5 mmHg. After trimazosin, prazosin, and phentolamine, the same dose of phenylephrine increased mean arterial pressure by 24 +/- 2.1, 14 +/- 1.6, and 1.9 +/- 0.6 mmHg, respectively. The response after phentolamine was significantly less than with trimazosin (P less than 0.01) and prazosin (P less than 0.02). Thus the capacity of these three alpha-adrenergic-receptor blocking drugs to dilate coronary vessels is inversely proportional to their capability to block exogenous alpha-adrenergic-receptor agonists.

Effect of β-Adrenergic Receptor Blockade on Blood Flow to Collateral-Dependent Myocardium During Exercise

Circulation ◽  
1995 ◽  
Vol 91 (5) ◽  
pp. 1560-1567 ◽  
Author(s):  
Jay H. Traverse ◽  
John D. Altman ◽  
James Kinn ◽  
Dirk J. Duncker ◽  
Robert J. Bache
Keyword(s):  
Blood Flow ◽  
Adrenergic Receptor ◽  
Receptor Blockade ◽  
Adrenergic Receptor Blockade

scholarly journals Alpha-adrenergic receptor blockade and hyperaemic response in patients with intermediate coronary stenoses

2004 ◽  
Vol 25 (22) ◽  
pp. 2034-2039 ◽  
Author(s):  
E BARBATO ◽  
J BARTUNEK ◽  
W AARNOUDSE ◽  
M VANDERHEYDEN ◽  
F STAELENS ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Receptor Blockade ◽  
Alpha Adrenergic Receptor ◽  
Hyperaemic Response ◽  
Coronary Stenoses ◽  
Adrenergic Receptor Blockade
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