Bradykinin contributes to the exercise pressor reflex: mechanism of action

1993 ◽  
Vol 75 (5) ◽  
pp. 2061-2068 ◽  
Author(s):  
H. L. Pan ◽  
C. L. Stebbins ◽  
J. C. Longhurst
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Left Ventricular Pressure ◽  
Muscle Afferents ◽  
Left Ventricular ◽  
Receptor Blockade ◽  
Exercise Pressor Reflex ◽  
Pressor Reflex ◽  
Over Time

This study determined the receptors responsible for mediating bradykinin's effect on skeletal muscle afferents that cause the pressor reflex in anesthetized cats. In eight cats, 1 microgram of bradykinin was injected intra-arterially into the gracilis muscle before and after intravenous injection of a kinin B2-receptor antagonist (NPC 17731, 20 micrograms/kg). Initial injection of bradykinin reflexly increased mean arterial pressure by 23 +/- 7 mmHg, maximal change in pressure over time by 439 +/- 272 mmHg/s, and heart rate by 11 +/- 4 beats/min. The hemodynamic response to bradykinin was abolished by kinin B2-receptor blockade. Similar injection of the kinin B1-receptor agonist des-Arg9-bradykinin caused no cardiovascular responses (n = 6). In eight different animals, mean arterial pressure, maximal change in left ventricular pressure over time, and heart rate responses to 30 s of electrically stimulated hindlimb contraction were attenuated by 50 +/- 6, 55 +/- 7, and 41 +/- 8%, respectively, after kinin B2-receptor blockade. In eight other animals, mean arterial pressure, maximal change in left ventricular pressure over time, and heart rate responses were reduced by 58 +/- 8, 66 +/- 6, and 40 +/- 12%, respectively, after inhibition of prostaglandin synthesis with indomethacin (2.5–3 mg/kg iv) and were then abolished by subsequent B2-receptor blockade. These data suggest that bradykinin contributes to the exercise pressor reflex through its action on kinin B2 receptors located on the nerve endings of the muscle afferents.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Identifying the role of group III/IV muscle afferents in the carotid baroreflex control of mean arterial pressure and heart rate during exercise

2018 ◽  
Vol 596 (8) ◽  
pp. 1373-1384 ◽  
Author(s):  
Thomas J. Hureau ◽  
Joshua C. Weavil ◽  
Taylor S. Thurston ◽  
Ryan M. Broxterman ◽  
Ashley D. Nelson ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Muscle Afferents ◽  
Baroreflex Control ◽  
Group Iii ◽  
Carotid Baroreflex

Endogenous bradykinin in the thoracic spinal cord contributes to the exercise pressor reflex

1996 ◽  
Vol 81 (3) ◽  
pp. 1288-1294 ◽  
Author(s):  
C. L. Stebbins ◽  
S. Bonigut
Keyword(s):  
Spinal Cord ◽  
Heart Rate ◽  
Intrathecal Injection ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Thoracic Spinal Cord ◽  
Exercise Pressor Reflex ◽  
Thoracic Spinal ◽  
Pressor Reflex ◽  
Hoe 140

This investigation tested the hypothesis that bradykinin causes excitatory effects in the thoracic spinal cord that augment the exercise pressor reflex. Thus we performed 30 s of electrically stimulated static contraction of the hindlimb in the anesthetized cat (alpha-chloralose) to provoke reflex-induced increases in mean arterial pressure, maximal rate of rise of left ventricular pressure (dP/dt), and heart rate (i.e., the exercise pressor reflex). These three responses were compared before and 15 min after intrathecal injection of 2 micrograms (n = 3), 10 micrograms (n = 6), or 50 micrograms (n = 3) of the selective bradykinin B2- receptor antagonist HOE-140 into the thoracic spinal cord or 10 micrograms of this antagonist into the lumbar (n = 3) spinal cord. In three of the six cats in which 10 micrograms of HOE-140 were injected into the thoracic spinal cord, an additional contraction was performed 60-90 min after treatment. The 2-microgram dose of HOE-140 had no effect on the exercise pressor reflex. Injection of 10 micrograms of this antagonist into the thoracic spinal cord reduced the contraction-evoked pressor, maximal dP/dt, and heart rate responses by 49 +/-7, 58 +/- 4, and 64 +/- 13%, respectively (P < 0.05). Fifty micrograms of HOE-140 failed to attenuate these responses further. In the three cats in which an additional contraction was performed 60-90 min after treatment with 10 micrograms of the antagonist, blood pressure and dP/dt responses had returned, in part, toward initial values. Neither intravenous (n = 3) nor intrathecal injection of 10 micrograms of HOE-140 into the lumbar spinal cord had any effect on the contraction-induced cardiovascular responses. Thoracic injection of 50-200 ng of bradykinin provoked a pressor response of 26 +/- 5 mmHg that was abolished by a similar injection of 10 micrograms of HOE-140. These data suggest that endogenous bradykinin contributes to the exercise pressor reflex by an excitatory action in the thoracic spinal cord.

Augmented catecholamine uptake by the heart during hemorrhage in the conscious dog

1986 ◽  
Vol 250 (1) ◽  
pp. H76-H81 ◽  
Author(s):  
O. L. Woodman ◽  
J. Amano ◽  
T. H. Hintze ◽  
S. F. Vatner
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Nerve Stimulation ◽  
Left Ventricular ◽  
Sympathetic Nerve Stimulation ◽  
Net Release

Changes in arterial and coronary sinus concentrations of norepinephrine (NE) and epinephrine (E) in response to hemorrhage were examined in conscious dogs. Hemorrhage (45 +/- 3.2 ml/kg) decreased mean arterial pressure by 47 +/- 6%, left ventricular (LV) dP/dt by 38 +/- 6%, and mean left circumflex coronary blood flow by 47 +/- 6%, while heart rate increased by 44 +/- 13%. Increases in concentrations of arterial NE (5,050 +/- 1,080 from 190 +/- 20 pg/ml) and E (12,700 +/- 3,280 from 110 +/- 20 pg/ml) were far greater than increases in coronary sinus NE (1,700 +/- 780 from 270 +/- 50 pg/ml) and E (4,300 +/- 2,590 from 90 +/- 10 pg/ml). Net release of NE from the heart at rest was converted to a fractional extraction of 66 +/- 9% after hemorrhage. Fractional extraction of E increased from 16 +/- 6% at rest to 73 +/- 8% after hemorrhage. In cardiac-denervated dogs, hemorrhage (46 +/- 2.8 ml/kg) decreased mean arterial pressure by 39 +/- 15%, LV dP/dt by 36 +/- 10%, and mean left circumflex coronary blood flow by 36 +/- 13%, while heart rate increased by 24 +/- 10%. Hemorrhage increased arterial NE (1,740 +/- 150 from 210 +/- 30 pg/ml) and E (3,050 +/- 880 from 140 +/- 20 pg/ml) more than it increased coronary sinus NE (460 +/- 50 from 150 +/- 30 pg/ml) and E (660 +/- 160 from 90 +/- 20 pg/ml) but significantly less (P less than 0.05) than observed in intact dogs. These experiments indicate that hemorrhage, unlike exercise and sympathetic nerve stimulation, does not induce net overflow of NE from the heart.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Effect of Levosimendan Compared to Conventional Inotropic Agents on Hemodynamics and Outcome in Patient with Poor LV Function Undergoing Cardiac Surgery

2019 ◽  
Vol 7 (19) ◽  
pp. 3205-3210
Author(s):  
Mahmoud Khaled ◽  
Ahmad Naem Almogy ◽  
Mohamed Shehata ◽  
Fahim Ragab ◽  
Khaled Zeineldein
Keyword(s):  
Heart Rate ◽  
Cardiac Surgery ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Venous Pressure ◽  
Left Ventricular ◽  
Base Deficit ◽  
Inotropic Agents ◽  
Poor Left Ventricular Function ◽  
Mixed Venous

BACKGROUND: Patients undergoing heart surgery involving cardiopulmonary bypass (CPB) experience global myocardial ischemia with subsequent reperfusion which, despite cardioplegic protection, may result in different degrees of transient ventricular dysfunction. Levosimendan is a “calcium sensitisers”, it improves myocardial contractility by sensitising troponin C to calcium without increasing myocardial oxygen consumption and without impairing relaxation and diastolic function. AIM: To evaluate the adding effect of a calcium sensitiser (levosimendan) compared to the conventional inotropic and vasoactive agent used in the patient with poor left ventricular function undergoing cardiac surgery on different measured hemodynamic variables and the effect on the outcome. METHODS: It is prospective observational studies were patients were divided into 2 groups of 30 patients each. The first Group received conventional inotropic and vasoactive treatment at different doses, while the other group received levosimendan additionally at a loading dose of 6-12mic/kg according to mean arterial pressure over 0.5 hr followed by 24 hrs infusion at 0.05 to 0.2 mic/kg/min. Hemodynamic data were collected at the end and 30 minutes after CPB, after that at 6, 12, 24, and 36 hours post CPB. Mean arterial pressure (MAP), central venous pressure (CVP), heart rate (HR), mixed venous saturation (Svo2), and base deficit (BD) were measured. RESULTS: Levosimendan had significantly improved postoperative hemodynamic values as in the mixed venous pressure at different times postoperative (p < 0.05), also the base deficit at different times postoperative (p < 0.05), while there was a significant reduction in systemic vascular resistance as decreased mean arterial pressure in levosimendan group compared to conventional group at 6hrs postoperative mean 77.50 ± 10.81 vs 83.73 ± 10.81 with (p = 0.029), and at 12 hrs postoperative mean 77.37 ± 10.10vs 84.23 ± 13.81 with (p = 0.032), and there was no significant difference in heart rate at different times postoperative between both groups (p > 0.05), while there was no significant effect on mortality between both groups (p = 0.781). CONCLUSION: Levosimendan had improved hemodynamic parameters significantly with no effect on mortality compared to conventional inotropic agents in a patient with poor left ventricular function undergoing cardiac surgery.

The Exercise Pressor Reflex and Changes in Radial Arterial Pressure and Heart Rate During Walking in Patients with Arteriosclerosis Obliterans

Angiology ◽  
1999 ◽  
Vol 50 (5) ◽  
pp. 361-374 ◽  
Author(s):  
Paolo Reggiani ◽  
Alessandro Mattioli ◽  
Ezio Corbellini ◽  
Stefano Garducci ◽  
Michele Catalano ◽  
...  
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Arteriosclerosis Obliterans ◽  
Exercise Pressor Reflex ◽  
Pressor Reflex

Clonidine Modulation of Hemodynamic and Catecholamine Responses Associated with Hypoxia or Hypercapnia in Dogs

1996 ◽  
Vol 84 (3) ◽  
pp. 672-685 ◽  
Author(s):  
Toshiaki Nishikawa ◽  
Hiroshi Naito
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Bolus Injection ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Control Group ◽  
Plasma Norepinephrine ◽  
Plasma Catecholamine ◽  
Anesthetized Dogs ◽  
Plasma Catecholamine Concentrations

Background Hypoxia or hypercapnia elicits cardiovascular responses associated with increased plasma catecholamine concentrations, whereas clonidine, an alpha(2)- adrenergic agonist, decreases plasma catecholamine concentrations. The authors examined whether systemic clonidine administration would alter the hemodynamic and catecholamine responses to hypoxia or hypercapnia in anesthetized dogs. Methods Pentobarbital-anesthetized dogs whose lungs were mechanically ventilated were instrumented for measurement of mean arterial pressure, heart rate, mean pulmonary artery pressure, right atrial pressure, cardiac output, left ventricular end-diastolic pressure, and the peak of first derivative of left ventricular pressure. The dogs were randomly assigned to receive an intravenous bolus injection of 10 microg/kg clonidine followed by continous infusion at a rate of 1 microg. kg (-1). min (-1)(clonidine-10 group, n = 7), an intravenous bolus injection of microg/kg clonidine followed by continuous infusion at a rate of 0.5 micro.kg(-).min(-1)(clonidine-5 group, n = 7), or an equivalent volume of 0.9% saline (control group = 7). Each dog underwent random challenges of hypoxia (PaO2 30, 40, and 50 mmHg) and hypercapnia (PaCO2 60, 80, and 120 mmHg). Measurements of hemodynamic and plasma norepinephrine and epinephrine concentrations were made after the loading dose of clonidine and the first and the second exposure of hypoxia or hypercapnia. Results Although significant increases from prehypoxic values in mean arterial pressure (39 +/- 10 mmHg) and plasma norepinephrine (291 +/- 66 pg/ml) and epinephrine (45 +/- 22 pg/ml) concentrations were noted during hypoxia of PaO2 30, mmHg in the control group (P&lt;0.05), such changes were absent in both clonidine groups. During hypercapnia of PaCo2 120 mmHg, changes from prehypercapnic values in mean arterial pressure, mean pulmonary artery pressure, the peak of first derivative of left ventricular pressure, and plasma norepinephrine and epinephrine concentrations in the clonidine-10 and clonidine-5 groups were significantly less than those in the control group. Plasma clonidine concentrations in the clonidine-10 and clonidine-5 groups were 16.8 +/- 1.7 and 8.9 =/- 1.0, 42.5 =/- 2.9 and 21.5 +/- 1.5, and 51.1 +/- 3.2 and 26.7 +/- 1.0 ng/ml after the loading dose of clonidine and the first and the second exposure of hypoxia or hypercapnia, respectively. Conclusions Systemic clonidine administration alter the hemodynamic changes associated with hypoxia or hypercapnia and suppresses plasma catecholamine responses in anesthetized dogs when a larger dose of clonidine is administered. catecholamines: epinephrine; norepinephrine.)

Baroreflex mechanisms buffering alpha-adrenergic agonists in conscious dogs

1987 ◽  
Vol 253 (4) ◽  
pp. H728-H736
Author(s):  
A. M. Fujii ◽  
S. F. Vatner
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Adrenergic Receptor ◽  
Peripheral Resistance ◽  
Conscious Dogs ◽  
Receptor Blockade ◽  
Receptor Agonists ◽  
Alpha Adrenergic Receptor

To determine the relative importance of the mechanisms utilized by the arterial baroreflex in buffering the pressor and vasoconstrictor responses to alpha-adrenergic receptor agonists, we studied responses to norepinephrine and phenylephrine in conscious dogs. The dogs were studied 2-8 wk after instrumentation with aortic catheters and aortic electromagnetic flow probes to measure arterial pressure and cardiac output. Total peripheral resistance was calculated on-line by a digital computer. The dogs were studied after beta-adrenergic receptor blockade (propranolol 1.0 mg/kg) to eliminate the complicating inotropic effects of the agonists studied. Norepinephrine (0.2 microgram/kg bolus) increased mean arterial pressure by 30 +/- 3 mmHg, total peripheral resistance by 51 +/- 4 mmHg . l-1 . min-1, and decreased heart rate by 26 +/- 3 beats/min. After arterial baroreceptor denervation, norepinephrine increased mean arterial pressure by 69 +/- 8 mmHg, total peripheral resistance by 48 +/- 6 mmHg . l-1 . min-1, and heart rate did not change. After ganglionic blockade (hexamethonium 40 mg/kg), norepinephrine increased mean arterial pressure by 76 +/- 3 mmHg, total peripheral resistance by 47 +/- 4 mmHg X l-1 X min-1, and heart rate did not change. Only after elimination of the buffering by heart rate by use of cholinergic receptor blockade (atropine 0.1 mg/kg) or ventricular pacing could buffering of the vasoconstrictor responses to alpha-adrenergic receptor agonists be demonstrated. Thus in conscious dogs the primary mechanism for buffering increases in arterial pressure induced by alpha-adrenergic receptor agonists is compensatory changes in heart rate and cardiac output with little buffering of total peripheral resistance.

Forearm training reduces the exercise pressor reflex during ischemic rhythmic handgrip

1998 ◽  
Vol 84 (1) ◽  
pp. 277-283 ◽  
Author(s):  
Sogol Mostoufi-Moab ◽  
Eric J. Widmaier ◽  
Jacob A. Cornett ◽  
Kristen Gray ◽  
Lawrence I. Sinoway
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Venous Blood ◽  
Voluntary Contraction ◽  
Positive Pressure ◽  
Ph Response ◽  
Exercise Pressor Reflex ◽  
Pressure Threshold ◽  
Pressor Reflex

Mostoufi-Moab, Sogol, Eric J. Widmaier, Jacob A. Cornett, Kristen Gray, and Lawrence I. Sinoway. Forearm training reduces the exercise pressor reflex during ischemic rhythmic handgrip. J. Appl. Physiol. 84(1): 277–283, 1998.—We examined the effects of unilateral, nondominant forearm training (4 wk) on blood pressure and forearm metabolites during ischemic and nonischemic rhythmic handgrip (30 1-s contractions/min at 25% maximal voluntary contraction). Contractions were performed by 10 subjects with the forearm enclosed in a pressurized Plexiglas tank to induce ischemic conditions. Training increased the endurance time in the nondominant arm by 102% ( protocol 1). In protocol 2, tank pressure was increased in increments of 10 mmHg/min to +50 mmHg. Training raised the positive-pressure threshold necessary to engage the pressor response. In protocol 3, handgrip was performed at +50 mmHg and venous blood samples were analyzed. Training attenuated mean arterial pressure (109 ± 5 and 98 ± 4 mmHg pre- and posttraining, respectively, P < 0.01), venous lactate (2.9 ± 0.4 and 1.8 ± 0.3 mmol/l pre- and posttraining, respectively, P < 0.01), and the pH response (7.21 ± 0.02 and 7.25 ± 0.01, pre- and posttraining, respectively, P < 0.01). However, deep venous O2 saturation was unchanged. Training increased the positive-pressure threshold for metaboreceptor engagement, reduced metabolite concentrations, and reduced mean arterial pressure during ischemic exercise.

Reflex sympathetic augmentation of left-ventricular inotropic state in the conscious dog

1981 ◽  
Vol 241 (6) ◽  
pp. H857-H863
Author(s):  
C. Yoran ◽  
L. Higginson ◽  
M. A. Romero ◽  
J. W. Covell ◽  
J. Ross
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Pressure Rise ◽  
Left Ventricular Pressure ◽  
Systemic Arterial Pressure ◽  
Left Ventricular ◽  
Adrenergic Blockade ◽  
Conscious Dog ◽  
Inotropic State ◽  
Simultaneous Decrease

Cardiac reflex responses to a series of partial inferior vena caval occlusions were studied in conscious previously instrumented dogs. Heart rate responses during the fall of systemic arterial pressure were mediated both by increased sympathetic tone and withdrawal of parasympathetic tone. Responses of the left-ventricular inotropic state, estimated from changes in left ventricular pressure rise (LV dP/dt), were studied early after release of a series of partial vena caval occlusions, and a positive linear relation between the prior fall in the systemic arterial pressure and the increase in LV dP/dt was demonstrated. Serial studies showed this effect of persist for at least 12 s beyond the reflex slowing of heart rate early after release of vena caval occlusion. The positive inotropic response was markedly attenuated by beta-adrenergic blockade and also occurred at a constant heart rate. It was present after adrenalectomy. These studies suggest that the integrated baroreceptor responses that are activated by a simultaneous decrease in the venous return and systemic arterial pressure play an important role in the regulation of left-ventricular inotropic state in the conscious dog.

Enkephalin lowers vascular resistance in dog hindlimb via a peripheral nonlimb site

1991 ◽  
Vol 260 (2) ◽  
pp. H386-H392 ◽  
Author(s):  
J. L. Caffrey ◽  
H. Gu ◽  
B. A. Barron ◽  
J. F. Gaugl
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Opiate Receptors ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Sharp Decline ◽  
Descending Aorta ◽  
A Site

The intravenous administration of methionine enkephalin in anesthetized dogs produces an abrupt decline in mean arterial pressure, left ventricular pressure, and the maximal rate of left ventricular pressure development. All of these changes are prevented by receptor blockade with the opiate antagonist, naloxone. To evaluate peripheral vascular contributions to these responses, experiments were conducted in a constant pressure-isolated perfused hindlimb. In this model, the sharp decline in mean arterial pressure associated with enkephalin injection (5 micrograms/kg iv) coincided with an equally sharp decline in vascular resistance (rise in blood flow) in the hindlimb. Both were blocked by naloxone pretreatment (1 mg/kg). When equal doses of enkephalin were administered directly into the femoral inflow (external iliac artery), both arterial pressure and hindlimb flow responses were all but eliminated. This observation ruled out significant direct vascular interactions in the response and indicated a site of action outside the hindlimb. Additional catheters were placed in the bracheocephalic artery and descending aorta to permit the comparison of arterial injections conducted, respectively, into the cerebral or abdominal circulations. Injections introduced into the descending aorta consistently produced the greatest response, followed by injections (in descending order of effectiveness) into the jugular, the brachiocephalic, and external iliac. The response in the hindlimb vasculature was initiated at a site somewhere between the diaphragm and terminal aorta. The vascular response to enkephalin was subsequently eliminated by blocking ganglionic transmission with the nicotinic antagonist mecamylamine. These observations suggest that the opioids probably interrupt local vasomotor traffic via opiate receptors in regional sympathetic ganglia or in the spinal cord.

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