Baroreflex inhibition during coronary occlusion is mediated by prostaglandins

1989 ◽  
Vol 257 (1) ◽  
pp. R216-R223 ◽  
Author(s):  
I. H. Zucker ◽  
M. J. Panzenbeck ◽  
J. F. Hackley ◽  
K. Haiderzad
Keyword(s):  
Coronary Artery ◽  
Arterial Pressure ◽  
Coronary Occlusion ◽  
Strong Support ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Coronary Ischemia ◽  
Renal Sympathetic

The present study was undertaken to determine whether the baroreflex control of renal sympathetic nerve activity (RSNA) was attenuated by an acute coronary artery occlusion and if so, what was the role played by cardiac prostaglandins in this attenuation. Arterial pressure was lowered with an infusion of sodium nitroprusside before and during a 5- to 10-min occlusion of the left circumflex coronary artery. The protocol was repeated 30 min after indomethacin (5 mg/kg) had been given. In addition, this study was carried out in a group of vagotomized dogs and in a group of thoracic-sympathectomized dogs. In intact dogs, coronary occlusion reduced the slope of the mean arterial pressure-RSNA relationship by 75% from -7.7 +/- 1.8% change in RSNA per millimeter Hg before indomethacin treatment. After indomethacin, there was no inhibition of the baroreflex slope during coronary occlusion. The reduction in the slope during coronary occlusion was abolished in dogs that were vagotomized but preserved in thoracic-sympathectomized dogs. In this latter group, indomethacin inhibited the attenuation of the slope during coronary occlusion. These data provide strong support for the notion that some cyclooxygenase product (most likely a prostaglandin) is released during coronary ischemia and stimulates or sensitizes cardiac vagal afferent endings, which, in turn, attenuate the baroreflex-mediated increase in RSNA during lowered arterial pressure.

Angiotensin II modulates arterial baroreflex function via a central alpha 1-adrenoceptor mechanism in rabbits

1995 ◽  
Vol 269 (5) ◽  
pp. R1009-R1016 ◽  
Author(s):  
Y. Nishida ◽  
K. L. Ryan ◽  
V. S. Bishop
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Ang Ii ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Baroreflex Function ◽  
Before And After ◽  
Dose Dependent ◽  
Renal Sympathetic

To test the hypothesis that angiotensin II (ANG II) modulates arterial baroreflex function via a central alpha 1-adrenoceptor mechanism, we examined the effects of intravertebral infusion of ANG II on baroreflex function curves before and after intravertebral administration of the alpha 1-adrenoreceptor antagonist prazosin. Rabbits were chronically instrumented with subclavian and vertebral arterial catheters, venous catheters, and aortic and vena caval occludes. Baroreflex curves were obtained by relating heart rate (HR) to mean arterial pressure during increases and decreases in arterial pressure. Intravertebral infusions of ANG II (5, 10, and 20 ng.kg-1.min-1) produced a dose-dependent shift of the midrange of the curve toward higher pressures (64 +/- 1 to 68 +/- 1, 76 +/- 1, and 85 +/- 2 mmHg, respectively). Pretreatment with prazosin (10 micrograms/kg) via the vertebral artery markedly reduced the shift in the baroreflex curve induced by the highest dose of ANG II (64 +/- 2 to 70 +/- 2 mmHg). These data suggest that ANG II resets the operating point of the HR baroreflex curve to a higher blood pressure and that this effect is mediated via a central alpha 1 mechanism. When the effects of vertebral ANG II on the baroreflex control of renal sympathetic nerve activity (RSNA) were examined, intravertebral administration of ANG II, while reducing the gain and the maximum RSNA, did not reset the RSNA baroreflex curve. These data suggest that ANG II acutely resets the HR baroreflex but not the RSNA baroreflex and that the resetting involves an alpha 1-adrenergic mechanism.

α2-Adrenergic receptors in NTS facilitate baroreflex function in adult spontaneously hypertensive rats

2002 ◽  
Vol 282 (6) ◽  
pp. H2336-H2345 ◽  
Author(s):  
Linda F. Hayward ◽  
Alecia P. Riley ◽  
Robert B. Felder
Keyword(s):  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Spontaneously Hypertensive ◽  
Aortic Depressor Nerve ◽  
Baroreflex Function ◽  
Wistar Kyoto ◽  
Renal Sympathetic

We examined the effect of α2-adrenoreceptor blockade in the nucleus of the solitary tract (NTS) on baroreflex responses elicited by electrical stimulation of the left aortic depressor nerve (ADN) in urethane-anesthetized spontaneously hypertensive rats (SHR, n = 11) and normotensive Wistar-Kyoto rats (WKY, n = 11). ADN stimulation produced a frequency-dependent decrease in mean arterial pressure (MAP), renal sympathetic nerve activity (RSNA), and heart rate (HR). In SHR, unilateral microinjection of idazoxan into the NTS markedly reduced baroreflex control of MAP, RSNA, and HR and had a disproportionately greater influence on baroreflex control of MAP than of RSNA. In WKY, idazoxan microinjections did not significantly alter baroreflex function relative to control vehicle injections. These results suggest that baroreflex regulation of arterial pressure in SHR is highly dependent on NTS adrenergic mechanisms. The reflex regulation of sympathetic outflow to the kidney is less influenced by the altered α2-adrenoreceptor mechanisms in SHR.

Loss of regional ventricular postextrasystolic potentiation after coronary occlusion in dogs

1977 ◽  
Vol 233 (3) ◽  
pp. H392-H348
Author(s):  
B. Crozatier ◽  
D. Franklin ◽  
P. Theroux ◽  
H. Tomoike ◽  
S. Sasayama ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Coronary Occlusion ◽  
Myocardial Function ◽  
Premature Ventricular Contraction ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Ventricular Contraction ◽  
Regional Myocardial Function ◽  
Irreversible Damage ◽  
Postextrasystolic Potentiation

Postextrasystolic potentiation following coronary artery occlusion was studied serially using pairs of ultrasonic crystals to measure regional myocardial function in control, marginally ischemic, and ischemic segments of the left ventricle in dogs. Prior to coronary occlusion (CO), percent shortening in control (normal) segments increased by an average of 51.4 +/- 4.6% in the beat after a premature ventricular contraction (post-PVC beat), and this response changed little after coronary occlusion. During the 1st min after CO, in ischemic segments, systolic expansion developed but was replaced by active shortening in post-PVC beats; however, after 3 min of CO (average) and thereafter, there was no net positive shortening in post-PVC beats. In marginally ischemic segments early after CO, hypokinesia developed, but there was marked augmentation of percent shortening (208.6 +/- 32.6%) which persisted in post-PVC beats even after 2 h. It is concluded that loss of postextrasystolic potentiation occurs rapidly in ischemic regions after CO and is not indicative of irreversible damage; partially ischemic regions retain this mechanism for prolonged periods.

Baroreflex control of sympathetic nerve activity after elevations of pressure in conscious rabbits

1985 ◽  
Vol 248 (6) ◽  
pp. H827-H834 ◽  
Author(s):  
K. P. Undesser ◽  
J. Y. Pan ◽  
M. P. Lynn ◽  
V. S. Bishop
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Afferent Activity ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Pressure Stimulus ◽  
Renal Sympathetic

The purpose of this study was to assess the effect of rapid baroreceptor resetting on the baroreflex control of renal sympathetic nerve activity in conscious rabbits. Renal sympathetic nerve activity was recorded and used as an index of the efferent limb of the baroreflex. Heart rate and arterial pressure were also recorded. Arterial pressure was raised with either phenylephrine or angiotensin II to a level that eliminated renal sympathetic nerve activity and was maintained at this level for periods of time ranging from 1 to 60 min. On returning pressure to control levels, renal sympathetic nerve activity remained suppressed for up to 90 min, with the duration of the suppression dependent on the magnitude and duration of the pressure stimulus. During this period of suppressed nerve activity, baroreflex curves were generated. The curves produced at this time were also suppressed as compared with control baroreflex curves. With time, the suppressed baroreflex curves returned to control. Further studies were performed to show that the suppression of renal sympathetic nerve activity was mediated via the prolonged increase in baroreceptor afferent activity during the pressure stimulus and was not due to a central effect of phenylephrine. This study indicates that although baroreceptor afferent activity may reset rapidly, there does not appear to be an augmentation of renal sympathetic nerve activity as would be expected.

Antifibrillatory effects of α1-adrenoceptor blocking drugs in experimental coronary artery occlusion and reperfusion

1993 ◽  
Vol 71 (2) ◽  
pp. 103-111 ◽  
Author(s):  
B. G. Benfey
Keyword(s):  
Coronary Artery ◽  
Ventricular Fibrillation ◽  
Guinea Pig ◽  
Ventricular Arrhythmias ◽  
Coronary Occlusion ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Coronary Reperfusion ◽  
Isolated Hearts ◽  
Anesthetized Dogs

The myocardium of animals and man possesses α1-adrenoceptors in addition to β-adrenoceptors. Ischemia increases sympathetic tone, and ventricular arrhythmias can occur by β- and α1-adrenoceptor stimulation. I believe that α1-adrenoceptor blocking drugs have antifibrillatory effects and will review the data that support this condition. The effect of α1,-adrenoceptor blocking drugs on the incidence of ventricular fibrillation in acute coronary artery occlusion and (or) reperfusion has been determined in 24 studies in conscious and anesthetized dogs and rats, anesthetized cats and pigs, and rat and guinea-pig isolated hearts. The drugs reduced the incidence of fibrillation from 35 to 24% in coronary occlusion and from 61 to 29% in reperfusion.Key words: heart, coronary occlusion, coronary reperfusion, ventricular fibrillation, α1-adrenoceptor blocking drugs.

Effect of exercise training on RSNA, baroreflex control, and blood pressure responsiveness

1993 ◽  
Vol 265 (2) ◽  
pp. R365-R370 ◽  
Author(s):  
C. E. Negrao ◽  
M. C. Irigoyen ◽  
E. D. Moreira ◽  
P. C. Brum ◽  
P. M. Freire ◽  
...  
Keyword(s):  
Exercise Training ◽  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Ang Ii ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Analog To Digital ◽  
Male Wistar Rats ◽  
Reflex Control ◽  
Renal Sympathetic

The effect of exercise training (ET) on renal sympathetic nerve activity (RSNA), baroreflex control of RSNA and heart rate (HR), and arterial pressure (AP) responsiveness to phenylephrine and angiotensin II (ANG II) was studied in six trained (T) and six sedentary (S) male Wistar rats. ET was performed on a motor treadmill for 13 wk. The RSNA signals of unanesthetized rats were processed by an analog-to-digital converter to quantify the nerve discharges associated with changes in AP and HR. The reflex control of RSNA and HR were evaluated during progressive injections of phenylephrine and sodium nitroprusside. Mean arterial pressure (MAP) was similar in both groups. RSNA was significantly lower in T rats (28 +/- 2 vs. 36 +/- 3%). T rats had an impairment of baroreflex control of RSNA in response to nitroprusside (4.9 +/- 0.89 vs. 12.3 +/- 1.2 bars.cycle-1.mmHg-1). ET decreased AP responsiveness for phenylephrine and ANG II. Therefore ET produces 1) no change in resting MAP but a significant decrease in RSNA and AP responsiveness and 2) partial impairment of baroreflexes, i.e., bradycardic responses and RSNA during MAP decrease.

VENTRICULAR FIBRILLATION INDUCED BY CORONARY OCCLUSION DURING HYPOTHERMIA IN DOGS AND THE EFFECTS OF QUINIDINE, QUINACRINE, AND OXYTOCIN

1963 ◽  
Vol 41 (1) ◽  
pp. 511-517 ◽  
Author(s):  
D. R. Varma ◽  
K. I. Melville
Keyword(s):  
Coronary Artery ◽  
Ventricular Fibrillation ◽  
Left Coronary Artery ◽  
Coronary Occlusion ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Surface Cooling ◽  
Normal Body Temperature ◽  
Oesophageal Temperature ◽  
Consistent Method

In dogs under pentobarbitone anesthesia, acute occlusion of the anterior descending branch of the left coronary artery at normal body temperature induced ventricular fibrillation in 30% of the animals, while hypothermia by surface cooling led to fibrillation in 40% of the animals. On the other hand, temporary coronary occlusion with hypothermia at 23 °C oesophageal temperature invariably induced ventricular fibrillation (15 experiments) within an average of 5.4 minutes of occlusion. Prior injections of quinidine and quinacrine protected 40 and 70%, respectively, of the dogs against this type of ventricular fibrillation (10 experiments each). Oxytocin (1–2 i.u./kg) offered no protection (six experiments) nor did it reverse established fibrillation under these conditions. It is concluded that temporary coronary artery occlusion at 23 °C oesophageal temperature in dogs is an effective and consistent method of producing ventricular fibrillation. It is also postulated that reduction of the coronary blood supply to the heart might be a precipitating factor in hypothermic ventricular fibrillation in surgery.

Sympathetic activity is not increased in l-NAME hypertensive rats

2010 ◽  
Vol 298 (1) ◽  
pp. R89-R95 ◽  
Author(s):  
Fernanda Machado dos Santos ◽  
Daniel Penteado Martins Dias ◽  
Carlos Alberto Aguiar da Silva ◽  
Rubens Fazan ◽  
Helio Cesar Salgado
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Femoral Vein ◽  
Plasma Norepinephrine ◽  
Hypertensive Rats ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Conscious Rats ◽  
Norepinephrine Content ◽  
Renal Sympathetic

The role played by the sympathetic drive in the development of N G-nitro-l-arginine methyl ester (l-NAME)-induced hypertension is not firmly established. Therefore, the present study was undertaken in conscious rats in which hypertension was induced by treatment with l-NAME over the course of either 2 or 14 days. Mean arterial pressure (MAP) was measured via a catheter placed in the femoral artery, drugs were administered via a cannula placed in the femoral vein, and renal sympathetic nerve activity (RSNA) was monitored using an implanted electrode. Despite the remarkable increase in arterial pressure, heart rate did not change after treatment with l-NAME. RSNA was similar in l-NAME-induced hypertensive rats treated over the course of 2 or 14 days, as well as in normotensive rats. It was also demonstrated that l-NAME-induced hypertensive rats displayed a resetting of the baroreflex control of RSNA to hypertensive levels, with decreased sensitivity over the course of 2 or 14 days. Furthermore, the sympathetic-vagal balance examined in the time and frequency domain and the renal and plasma norepinephrine content did not differ between groups. In conclusion, the evaluation of the sympathetic drive in conscious rats demonstrated that the arterial hypertension induced by l-NAME treatment over the course of 2 and 14 days does not show sympathetic overactivity.

Catecholamines in cerebrospinal fluid are increased by behavioral arousal and myocardial ischemia

1992 ◽  
Vol 263 (1) ◽  
pp. H83-H87
Author(s):  
D. A. Johnson ◽  
J. M. Pinto ◽  
D. A. Kirby ◽  
B. Lown
Keyword(s):  
Cerebrospinal Fluid ◽  
Coronary Artery ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Catecholamines ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Separate Experiment ◽  
Behavioral Arousal ◽  
Malignant Ventricular Arrhythmia

To study the central neural mechanisms involved in malignant ventricular arrhythmia, concentrations of norepinephrine in the cerebrospinal fluid were measured during behavioral stimulation and during coronary artery occlusion. Pigs were instrumented via thoracotomy with catheters to measure mean arterial pressure and plasma catecholamines and with silk snares around the left anterior descending coronary artery for occlusion after recovery from surgery. Cannulas were placed in the lateral ventricle of the brain to sample cerebrospinal fluid. Behavioral arousal was induced by lifting the pig in a canvas sling for 5 min. Mean arterial pressure, heart rate, and both plasma and cerebrospinal fluid norepinephrine concentrations increased significantly after lifting stimulation. In a separate experiment, 5 min after coronary artery occlusion, both plasma catecholamines and norepinephrine in cerebrospinal fluid were significantly elevated. Furthermore, pigs in which ventricular fibrillation occurred after occlusion had significantly higher concentrations of norepinephrine in cerebrospinal fluid before coronary artery occlusion.

Interregional Differences in the Systolic and Diastolic Response of Nonischemic Myocardium to Remote Coronary Occlusion 

1999 ◽  
Vol 91 (3) ◽  
pp. 815-815 ◽  
Author(s):  
Stephan C. U. Marsch ◽  
Hernan R. Muñoz ◽  
Serge Dalmas ◽  
Pierre Foëx
Keyword(s):  
Coronary Artery ◽  
Coronary Occlusion ◽  
Coronary Artery Occlusion ◽  
Posterior Wall ◽  
Anterior Wall ◽  
Artery Occlusion ◽  
Regional Function ◽  
Circumflex Coronary Artery ◽  
Twofold Increase ◽  
Left Circumflex Coronary Artery

Background Previous work showed a twofold increase in stiffness of nonischemic myocardium at the base during ischemia of the left anterior wall. Whether the diastolic response of nonischemic myocardium to remote ischemia depends on the localization of the ischemic or the nonischemic area is unknown. Methods In dogs with open chests, regional function in ischemic and nonischemic myocardium was assessed (sonomicrometry) before and 5 min after occlusion of the left anterior descending coronary artery (LAD; n = 7) or the left circumflex coronary artery (LCX; n = 7). Results In nonischemic myocardium at the base, left anterior descending and left circumflex coronary artery occlusion both resulted in a twofold increase in chamber stiffness, whereas contractility and peak lengthening rate remained unchanged. In nonischemic myocardium of the posterior wall, left anterior descending coronary artery occlusion resulted in a significant (P<0.05 vs. control, P<0.05 vs. base) increase (mean+/-SD) in chamber stiffness (25+/-6%), contractility (17+/-5%), and peak lengthening rate (28+/-6%). In nonischemic myocardium at the apex, left circumflex coronary artery occlusion resulted in a significant (P<0.05 vs. control, P<0.05 vs. base) increase in chamber stiffness (15+/-5%), contractility (16+/-4%), and peak lengthening rate (19+/-6%). Conclusions Stiffening of remote nonischemic myocardium occurs regardless of the localization of the ischemic and nonischemic area. The systolic and diastolic responses of nonischemic myocardium are not necessarily homogenous but may vary among different regions.

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