Bradykinin-induced chemoreflexes from skeletal muscle: implications for the exercise reflex

1985 ◽  
Vol 59 (1) ◽  
pp. 56-63 ◽  
Author(s):  
C. L. Stebbins ◽  
J. C. Longhurst
Keyword(s):  
Skeletal Muscle ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Diastolic Pressure ◽  
Cardiovascular Response ◽  
Muscle Afferents ◽  
Left Ventricular ◽  
Gracilis Muscle ◽  
Initial Increase

We examined the cardiovascular response to bradykinin stimulation of skeletal muscle afferents and the effect of prostaglandins on this response. Intra-arterial injection of 1 microgram bradykinin into the gracilis muscle of cats reflexly increased mean arterial pressure by 16 +/- 2 mmHg, left ventricular end-diastolic pressure by 1.6 +/- 0.6 mmHg, maximal dP/dt by 785 +/- 136 mmHg/s, heart rate by 11 +/- 2 beats/min, and mean aortic flow by 22 +/- 3 ml/min. The hemodynamic responses were abolished following denervation of the gracilis muscle. The increases in mean arterial pressure and maximal dP/dt were reduced by 68 and 45%, respectively, following inhibition of prostaglandin synthesis with indomethacin (2–8 mg/kg iv). Treatment with prostaglandin E2 (PGE2, 15–25 micrograms ia) restored the initial increase in mean arterial pressure, but not dP/dt, caused by bradykinin stimulation. Injection of PGE2 (15–30 micrograms ia) into the gracilis, without prior treatment with indomethacin, augmented the bradykinin-induced increases in mean arterial pressure and dP/dt. We conclude that small doses of bradykinin injected into skeletal muscle are capable of reflexly activating the cardiovascular system and that prostaglandins are necessary for the full manifestation of the corresponding hemodynamic response. The pattern of hemodynamic adjustment following bradykinin injection into skeletal muscle is very similar to that induced by static exercise. Therefore, it is possible that intense exercise provides a stimulus for this bradykinin-induced reflex in vivo.

scholarly journals Abnormal cardiovascular response to nitroglycerin in migraine

Cephalalgia ◽  
2019 ◽  
Vol 40 (3) ◽  
pp. 266-277
Author(s):  
Willebrordus PJ van Oosterhout ◽  
Guus G Schoonman ◽  
Dirk P Saal ◽  
Roland D Thijs ◽  
Michel D Ferrari ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Initial Increase

Introduction Migraine and vasovagal syncope are comorbid conditions that may share part of their pathophysiology through autonomic control of the systemic circulation. Nitroglycerin can trigger both syncope and migraine attacks, suggesting enhanced systemic sensitivity in migraine. We aimed to determine the cardiovascular responses to nitroglycerin in migraine. Methods In 16 women with migraine without aura and 10 age- and gender-matched controls without headache, intravenous nitroglycerin (0.5 µg·kg−1·min−1) was administered. Finger photoplethysmography continuously assessed cardiovascular parameters (mean arterial pressure, heart rate, cardiac output, stroke volume and total peripheral resistance) before, during and after nitroglycerin infusion. Results Nitroglycerin provoked a migraine-like attack in 13/16 (81.2%) migraineurs but not in controls ( p = .0001). No syncope was provoked. Migraineurs who later developed a migraine-like attack showed different responses in all parameters vs. controls (all p < .001): The decreases in cardiac output and stroke volume were more rapid and longer lasting, heart rate increased, mean arterial pressure and total peripheral resistance were higher and decreased steeply after an initial increase. Discussion Migraineurs who developed a migraine-like attack in response to nitroglycerin showed stronger systemic cardiovascular responses compared to non-headache controls. The stronger systemic cardiovascular responses in migraine suggest increased systemic sensitivity to vasodilators, possibly due to insufficient autonomic compensatory mechanisms.

Defense reaction alters the response to blood loss in the conscious rabbit

2001 ◽  
Vol 280 (4) ◽  
pp. R985-R993 ◽  
Author(s):  
James C. Schadt ◽  
Eileen M. Hasser
Keyword(s):  
Skeletal Muscle ◽  
Mean Arterial Pressure ◽  
Blood Loss ◽  
Arterial Pressure ◽  
Cardiovascular Response ◽  
Muscle Blood Flow ◽  
Venous Blood ◽  
Defense Reaction ◽  
Simultaneous Exposure ◽  
Air Jet

The interaction of sensory stressors with the cardiovascular response to blood loss has not been studied. The cardiovascular response to a stressor (i.e., the defense reaction) includes increased skeletal muscle blood flow and perhaps a reduction in arterial baroreflex function. Arterial pressure maintenance during blood loss requires baroreflex-mediated skeletal muscle vasoconstriction. Therefore, we hypothesized that the defense reaction would limit arterial pressure maintenance during blood loss. Male, New Zealand White rabbits were chronically prepared with arterial and venous catheters and Doppler flow probes. We removed venous blood in conscious rabbits until mean arterial pressure decreased to <40 mmHg. We repeated the experiment with (air) and without (sham) simultaneous exposure to an air jet stressor. Air resulted in a defense reaction (e.g., mean arterial pressure = 94 ± 1 and 67 ± 1 mmHg for air and sham, respectively). Contrary to our hypothesis, air increased the blood loss necessary to produce hypotension (19.3 ± 0.2 vs. 16.9 ± 0.2 ml/kg for sham). Air did not reduce skeletal muscle vasoconstriction during normotensive hemorrhage. However, air did enhance renal vasoconstriction (97 ± 3 and 59 ± 3% of baseline for sham and air, respectively) during the normotensive phase. Thus the defense reaction did not limit but rather extended defense of arterial pressure during hemorrhage.

scholarly journals Dietary nitrate supplementation: impact on skeletal muscle vascular control in exercising rats with chronic heart failure

2016 ◽  
Vol 121 (3) ◽  
pp. 661-669 ◽  
Author(s):  
Scott K. Ferguson ◽  
Clark T. Holdsworth ◽  
Trenton D. Colburn ◽  
Jennifer L. Wright ◽  
Jesse C. Craig ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Skeletal Muscle ◽  
Mean Arterial Pressure ◽  
Chronic Heart Failure ◽  
Arterial Pressure ◽  
Vascular Function ◽  
Left Ventricular ◽  
Male Rats ◽  
Dietary Nitrate

Chronic heart failure (CHF) results in central and peripheral derangements that ultimately reduce skeletal muscle O2 delivery and impair exercise tolerance. Dietary nitrate (NO3−) supplementation improves skeletal muscle vascular function and tolerance to exercise. We tested the hypothesis that NO3− supplementation would elevate exercising skeletal muscle blood flow (BF) and vascular conductance (VC) in CHF rats. Myocardial infarction (MI) was induced (coronary artery ligation) in young adult male rats. After 21 days of recovery, rats randomly received 5 days of NO3−-rich beetroot juice (CHF + BR, n = 10) or a placebo (CHF, n = 10). Mean arterial pressure (carotid artery catheter) and skeletal muscle BF (radiolabeled microspheres) were measured during treadmill exercise (20 m/min, 5% grade). CHF-induced dysfunction, as determined by myocardial infarction size (29 ± 3% and 33 ± 4% in CHF and CHF + BR, respectively) and left ventricular end-diastolic pressure (18 ± 2 and 18 ± 2 mmHg in CHF and CHF + BR, respectively), and exercising mean arterial pressure (131 ± 3 and 128 ± 4 mmHg in CHF and CHF + BR, respectively) were not different ( P > 0.05) between groups. Total exercising hindlimb skeletal muscle BF (95 ± 5 and 116 ± 9 ml·min−1·100 g−1 in CHF and CHF + BR, respectively) and VC (0.75 ± 0.05 and 0.90 ± 0.05 ml·min−1·100 g−1·mmHg−1 in CHF and CHF + BR, respectively) were 22% and 20% greater in BR-supplemented rats, respectively ( P < 0.05). During exercise, BF in 9 and VC in 10 hindlimb muscles and muscle portions were significantly greater in the CHF + BR group. These results provide strong evidence that dietary NO3− supplementation improves skeletal muscle vascular function during exercise in rats with CHF and, thus, support the use of BR as a novel therapeutic modality for the treatment of CHF.

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)

Hemodynamic effects of periodic obstructive apneas in sedated pigs with congestive heart failure

2000 ◽  
Vol 88 (3) ◽  
pp. 1051-1060 ◽  
Author(s):  
Ling Chen ◽  
Quihu Shi ◽  
Steven M. Scharf
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Air Breathing ◽  
Obstructive Sleep

Because of similar physiological changes such as increased left ventricular (LV) afterload and sympathetic tone, an exaggerated depression in cardiac output (CO) could be expected in patients with coexisting obstructive sleep apnea and congestive heart failure (CHF). To determine cardiovascular effects and mechanisms of periodic obstructive apnea in the presence of CHF, 11 sedated and chronically instrumented pigs with CHF (rapid pacing) were tested with upper airway occlusion under room air breathing (RA), O2 breathing (O2), and room air breathing after hexamethonium (Hex). All conditions led to large negative swings in intrathoracic pressure (−30 to −39 Torr) and hypercapnia ([Formula: see text] ∼60 Torr), and RA and Hex also caused hypoxia (to ∼42 Torr). Relative to baseline, RA increased mean arterial pressure (from 97.5 ± 5.0 to 107.3 ± 5.7 Torr, P < 0.01), systemic vascular resistance, LV end-diastolic pressure, and LV end-systolic length while it decreased CO (from 2.17 ± 0.27 to 1.52 ± 0.31 l/min, P < 0.01), stroke volume (SV; from 23.5 ± 2.4 to 16.0 ± 4.0 ml, P < 0.01), and LV end-diastolic length (LVEDL). O2 and Hex decreased mean arterial pressure [from 102.3 ± 4.1 to 16.0 ± 4.0 Torr ( P < 0.01) with O2 and from 86.0 ± 8.5 to 78.1 ± 8.7 Torr ( P < 0.05) with Hex] and blunted the reduction in CO [from 2.09 ± 0.15 to 1.78 ± 0.18 l/ml for O2 and from 2.91 ± 0.43 to 2.50 ± 0.35 l/ml for Hex (both P< 0.05)] and SV. However, the reduction in LVEDL and LV end-diastolic pressure was the same as with RA. There was no change in systemic vascular resistance and LVEDL during O2 and Hex relative to baseline. In the CHF pigs during apnea, there was an exaggerated reduction in CO and SV relative to our previously published data from normal sedated pigs under similar conditions. The primary difference between CHF (present study) and the normal animals is that, in addition to increased LV afterload, there was a decrease in LV preload in CHF contributing to SV depression not seen in normal animals. The decrease in LV preload during apneas in CHF may be related to effects of ventricular interdependence.

Cardiovascular reflexes elicited by passive gastric distension in anesthetized cats

1981 ◽  
Vol 240 (4) ◽  
pp. H539-H545 ◽  
Author(s):  
J. C. Longhurst ◽  
H. L. Spilker ◽  
G. A. Ordway
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Diastolic Pressure ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Reflex Response ◽  
Gastric Distension ◽  
Cardiovascular Reflexes ◽  
Myocardial Oxygen Demand ◽  
Before And After

Hemodynamic responses to passive gastric distension were examined in alpha-chloralose anesthetized cats. Gastric balloons were distended with 37 degrees C fluid at slow (50 ml/min) and rapid (250 ml/min) infusion rates before and after laparotomy. Passive gastric distension at the slow infusion rate significantly (P less than 0.05) increased mean arterial pressure (MAP) by 28%, dP/dt at 40 mmHg developed pressure by 29%, and systemic vascular resistance (SVR) by 35%. Likewise, the rapid distension rate significantly (P less than 0.05) increased MAP (20%), dP/dt (16%), and SVR (23%). Heart rate, aortic flow, and left ventricular end-diastolic pressure remained unchanged at both distension rates. Cardiovascular responses to passive gastric distension were similar before and after laparotomy. Section of the vagus nerve at the diaphragm did not alter the responses, whereas abdominal splanchnic nerve section significantly (P less than 0.05) reduced the changes in mean arterial pressure and dP/dt. These results indicate that passive gastric distension in the cat elicits cardiovascular reflexes sufficient to increase myocardial oxygen demand. Such a reflex response could potentially contribute to postprandial angina in humans.

Changes in protein kinase C in early cardiomyopathy and in gracilis muscle in the BB/Wor diabetic rat

1998 ◽  
Vol 274 (1) ◽  
pp. H295-H307 ◽  
Author(s):  
Thomas D. Giles ◽  
Jie Ouyang ◽  
E. Kenneth Kerut ◽  
Michael B. Given ◽  
Gayle Eileen Allen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Diabetic Cardiomyopathy ◽  
Left Ventricular ◽  
Gracilis Muscle ◽  
Rate Of Change ◽  
Kinase C ◽  
Septal Thickness

Hyperglycemia can upregulate protein kinase C (PKC), which may be an important mediator of the progression from normal heart and muscle function to diabetic myopathy in the myocardium and skeletal muscle in type 1 insulin-dependent diabetes mellitus (IDM). We evaluated this possibility during the early stage of IDM in BB/Wor diabetic (D) rats and age-matched BB/Wor diabetes-resistant (DR) rats. Interventricular septal thickness, E wave peak velocity of tricuspid inflow (both minimum and maximum), and left ventricular (LV) weight index were increased, and the rate of change in LV pressure (LV dP/d t) decreased in D rats subjected to M-mode and two-dimensional echocardiography and hemodynamic recording of heart rate, LV pressure (LVP), +LV dP/d t, −LV dP/d t, and LV end-diastolic pressure (LVEDP) in vivo and in vitro 41 days after the onset of hyperglycemia. Whole ventricle basal PKC activity was increased by 44.4 and 18.4% in the particulate and soluble fractions, respectively, from D rats compared with that from DR rats using r-32P phosphorylation of appropriate peptide substrates. When measured by Western blot gel densitometry, particulate PKC-α and PKC-δ content increased by 89 and 24%, respectively, but soluble PKC-β and soluble and particulate PKC-ε were unchanged compared with that of DR rats. Similarly, gracilis muscle PKC activity and PKC-α and PKC-δ were elevated in the gracilis muscle, whereas that of the circulating neutrophil did not differ between the D and DR rats. Thus, in vivo, the early diabetic cardiomyopathy of the D rat is characterized by a restrictive LV with increased septal thickness and is associated with elevated PKC activity and increased amounts of myocardial particulate PKC-α and PKC-δ, which are also seen in the skeletal muscle. We conclude that increased PKC isozymes may play a pivotal role during IDM in the development of diabetic cardiomyopathy and skeletal muscle myopathy.

Impairment of cardiopulmonary baroreflexes in Dahl salt-sensitive rats fed low salt

1984 ◽  
Vol 247 (1) ◽  
pp. H119-H123 ◽  
Author(s):  
A. Ferrari ◽  
F. J. Gordon ◽  
A. L. Mark
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Activity ◽  
Volume Expansion ◽  
Diastolic Pressure ◽  
Splanchnic Nerve ◽  
Left Ventricular ◽  
Low Salt ◽  
Circulatory Control ◽  
Cardiopulmonary Baroreflex

Abnormalities in neural circulatory control contribute to salt-induced hypertension in Dahl sensitive (DS) rats. This study tested the hypothesis that there is impairment in cardiopulmonary baroreflex function in prehypertensive DS rats. The study was performed in DS and Dahl resistant (DR) rats fed low-salt diet. Arterial baroreceptors were denervated. Sympathetic activity was recorded from the splanchnic nerve during stimulation of cardiopulmonary baroreceptors with volume expansion (iv dextran). Resting mean arterial pressure averaged 93 +/- 6 (SE) in DS vs. 98 +/- 5 mmHg in DR rats. Resting left ventricular end-diastolic pressure (LVEDP) was 13.5 +/- 1.0 in/DS vs. 11.4 +/- 0.9 mmHg in DR rats. Volume expansion with the same amount of dextran caused greater increases in LVEDP in DS (+13 +/- 1 mmHg) than DR (+10 +/- 1 mmHg) but less inhibition of sympathetic activity (-40 +/- 4 vs. -50 +/- 2%) in DS compared with DR rats, respectively. Cardiopulmonary baroreflex gain calculated as percent inhibition of sympathetic activity divided by increases in LVEDP was -3.2 +/- 0.2 in DS vs. -4.9 +/- 0.6%/mmHg in DR rats. Reflex responses to dextran were abolished by vagotomy. Volume expansion also induced increases in mean arterial pressure. These were/greater in DS than DR rats (+43 +/- 4 vs. +28 +/- 5 mmHg, respectively) before vagotomy but were similar in the two groups after vagotomy. The distensibility (delta volume/delta pressure) of the left atrium was similar in DS and DR rats. We conclude that prehypertensive DS rats have impairment of the cardiopulmonary baroreflex.(ABSTRACT TRUNCATED AT 250 WORDS)

Creep of the canine pericardium in vivo

1986 ◽  
Vol 64 (7) ◽  
pp. 892-896 ◽  
Author(s):  
Iris Kingma ◽  
Gerald H. Groves ◽  
Eldon R. Smith ◽  
John V. Tyberg
Keyword(s):  
Surface Area ◽  
Diastolic Pressure ◽  
In Vitro Study ◽  
Left Ventricular ◽  
Small Time ◽  
Time Dependent ◽  
Initial Increase ◽  
Pericardial Pressure

In eight open chest dogs we assessed the creep of the pericardium by measuring the increase in surface area of the pericardium, occurring after pericardial surface pressure (Ppe) was rapidly increased by inflating an air-containing balloon positioned between the pericardium and the left ventricular (LV) epicardium. We observed an increase in LV end diastolic pressure (EDP) of 3.6 ± 3.4 mmHg (1 mmHg = 133.3 Pa) (p < 0.05) (mean ± SD) and a reduction in LV anteroposterior (AP) diameter of 8.8 ± 6.1 mm (p < 0.01), both of which were stable after 10 s. Mean Ppe increased 11.6 ± 3.3 mmHg (p < 0.001). Pericardial surface lengths at 45 and 135° to the long axis of the LV were measured with two pairs of ultrasonic crystals attached to the outer surface of the pericardium. The beam of ultrasound travelling between each pair was directed parallel to the pericardial surface through a film of conducting medium. Initial increase in surface area (calculated as the product of two pericardial lengths) occurring during the first 15 s after balloon inflation was 5.8 ± 2.5% (p < 0.001). During the next 30 min, while mean pericardial pressure did not change, pericardial surface area increased another 2.8% (p < 0.005). This time-dependent 2.8% increase in pericardial surface area (equivalent to an increase in volume of approximately 5%) is due to creep. Our results are consistent with results of a previous in vitro study and could account for a small, time-dependent, rightward shift of the pericardial pressure–volume relation to be seen when pericardial pressure increases as in volume loading, pericardial effusion, or congestive heart failure.

Hyperinflation-induced cardiorespiratory failure in rats

2009 ◽  
Vol 107 (1) ◽  
pp. 275-282 ◽  
Author(s):  
Jeremy A. Simpson ◽  
Keith R. Brunt ◽  
Christine P. Collier ◽  
Steve Iscoe
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Lung Volume ◽  
Troponin T ◽  
Respiratory Acidosis ◽  
Left Ventricular ◽  
Cardiovascular Failure ◽  
Cardiorespiratory Failure ◽  
Arterial Hypoxemia ◽  
Ventricular Afterload

We previously showed that severe inspiratory resistive loads cause acute (<1 h) cardiorespiratory failure characterized by arterial hypotension, multifocal myocardial infarcts, and diaphragmatic fatigue. The mechanisms responsible for cardiovascular failure are unknown, but one factor may be the increased ventricular afterload caused by the large negative intrathoracic pressures generated when breathing against an inspiratory load. Because expiratory threshold loads increase intrathoracic pressure and decrease left ventricular afterload, we hypothesized that anesthetized rats forced to breathe against such a load would experience only diaphragmatic failure. Loading approximately doubled end-expiratory lung volume, halved respiratory frequency, and caused arterial hypoxemia and hypercapnia, respiratory acidosis, and increased inspiratory drive. Although hyperinflation immediately reduced the diaphragm's mechanical advantage, fatigue did not occur until near load termination. Mean arterial pressure progressively fell, becoming significant (cardiovascular failure) midway through loading despite tachycardia. Loading was terminated (endurance 125 ± 43 min; range 82–206 min) when mean arterial pressure dropped below 50 mmHg. Blood samples taken immediately after load termination revealed hypoglycemia, hyperkalemia, and cardiac troponin T, the last indicating myocardial injury that was, according to histology, mainly in the right ventricle. This damage probably reflects a combination of decreased O2 delivery (decreased venous return and arterial hypoxemia) and greater afterload due to hyperinflation-induced increase in pulmonary vascular resistance. Thus, in rats breathing at an increased end-expiratory lung volume, cardiorespiratory, not just respiratory, failure still occurred. Right heart injury and dysfunction may contribute to the increased morbidity and mortality associated with acute exacerbations of obstructive airway disease.

Sign in / Sign up

Export Citation Format

Share Document