Peripheral Adrenergic Mechanisms Research Articles

Mesto centralnih antihipertenziva u lečenju različitih kategorija arterijske hipertenzije

Primary (essential) hypertension includes about 90% of all cases of hypertension, and the treatment is symptomatic. As the response to the need for suppression of sympathetic activity in the regulation of hypertension, central antihypertensives have been developed, through central and peripheral adrenergic and non-adrenergic mechanisms, to affect the reduction of sympathetic nerve activity, inhibition of norepinephrine release, reduction of systemic vascular resistance, peripheral vasodilatation, reduction of heart rate and lowering of blood pressure. Moxonidine has been proven to be effective and safe, whether used as monotherapy or in combination in the treatment of hypertension in which sympathetic hyperactivity predominates, especially in patients with metabolic syndrome, obese patients, patients with prehypertension and stress induced hypertension with catecholamine hyperactivity

Antiepileptic drugs as analgesics/adjuvants in inflammatory pain: current preclinical evidence.

Inflammatory pain is the most common type of pain that is treated clinically. The use of currently available treatments (classic analgesics - NSAIDs, paracetamol and opioids) is limited by insufficient efficacy and/or side effects/tolerance development. Antiepileptic drugs (AEDs) are widely used in neuropathic pain treatment, but there is substantial preclinical evidence on their efficacy against inflammatory pain, too. In this review we focus on gabapentinoids (gabapentin and pregabalin) and dibenzazepine AEDs (carbamazepine, oxcarbazepine, and recently introduced eslicarbazepine acetate) and their potential for relieving inflammatory pain. In models of somatic, visceral and trigeminal inflammatory pain, that have a translational value for inflammatory conditions in locomotor system, viscera and head/face, AEDs have demonstrated analgesic activity. This activity was mostly consistent, dependent on the dose and largely independent on the site of inflammation and method of its induction, nociceptive stimuli, species, specific drug used, its route of administration and dosing schedule. AEDs exerted comparable efficacy with classic analgesics. Effective doses of AEDs are lower than toxic doses in animals and, when expressed as equivalent human doses, they are largely overlapping with AEDs doses already used in humans for treating epilepsy/neuropathic pain. The main mechanism of antinociceptive/antihyperalgesic action of gabapentinoids in inflammatory pain models seems to be α2δ-dependent suppression of voltage-gated calcium channels in primary sensory neurons that leads to reduced release of neurotransmitters in the spinal/medullar dorsal horn. The suppression of NMDA receptors via co-agonist binding site primarily at spinal sites, activation of various types of K+ channels at spinal and peripheral sites, and activation of noradrenergic and serotonergic descending pain modulatory pathways may also contribute. Inhibition of voltage-gated sodium channels along the pain pathway is probably the main mechanism of antinociceptive/antihyperalgesic effects of dibenzazepines. The recruitment of peripheral adrenergic and purinergic mechanisms and central GABAergic mechanisms may also contribute. When co-administered with classic/other alternative analgesics, AEDs exerted synergistic/additive interactions. Reviewed data could serve as a basis for clinical studies on the efficacy/safety of AEDs as analgesics/adjuvants in patients with inflammatory pain, and contribute to the improvement of the treatment of various inflammatory pain states.

Adrenergic mechanisms of myocardium contractility regulation in genetic model of Alzheimer’s disease

Aim. Study is aimed to investigate contractility impairments and receptor mechanisms of adrenergic regulation of myocardium inotropic function in Alzheimer’s disease model on transgenic mice.Methods. Experiments were performed on isolated preparations of atria and ventricles myocardium of mice. Transgenic mice of B6C3-Tg(APP695)85Dbo Tg(PSENI)85Dbo genotype were used as animal model of Alzheimer’s disease. Contractile responses of myocardium were registered by conventional myographic technique in isometric conditions. To evaluate the expression of adrenergic receptors, immunofluorescence staining of myocardium with specific antibodies was performed.Results. Transgenic mice showed not only a decreased effect of norepinephrine on myocardium inotropic function but also the inversion of the effect of norepinephrine - the use of 10-5-10-4 M of norepinephrine decreased myocardium inotropic function. Immunofluorescent staining showed decrease of expression of β1- and especially β2-adrenergic receptors ventricular myocardium of transgenic mice comparing to wild type mice. Adrenergic deregulation was registered in ventricles, but not in atria. The features of adrenergic regulatory mechanisms of myocardial contractility in transgenic APP/PS1 mice aged 8-10 months are specific, although somewhat similar to wild type mice aged 8-10 months, and are evidently due to Alzheimer’s disease. The inversion of norepinephrine inotropic effect (from positive to negative) may be explained by switching the intracellular cascade pathway of β2-adrenergic receptors effects to another type of G-protein.Conclusion. The results indicate that peripheral adrenergic mechanisms of myocardial contractility regulation are impaired in studied transgenic mice model of Alzheimer’s disease. Obtained data widen our understanding of Alzheimer’s disease pathogenesis, as well as our conception of relations between cardiovascular diseases and neurodegeneration.

Contribution of peripheral α1A-adrenoceptors to pain induced by formalin or by α-methyl-5-hydroxytryptamine plus noradrenaline

We examined the peripheral adrenergic mechanisms involved in pain induced by α-methyl-5-hydroxytryptamine (α-methyl-5-HT) plus (±)-noradrenaline or prostaglandin E 2 and by intraplantar formalin. Agents were injected s.c. into the plantar surface of rats' paws, and the paw lifting and licking response scored. Pain produced by α-methyl-5-HT (10 μg) plus noradrenaline (10 μg) was blocked by pretreatment with the α-adrenoceptor antagonists, phentolamine (10 μg) and prazocin HCl ( α 1; 40 μg), but not by timolo (β; 10 μg) or idazoxan ( α 2; 40 μg). Phenylepherine, but not clonidine, substituted for noradrenaline to induce pain when combined with α-methyl-5-HT. The α 1A-adrenoceptor antagonist, WB-4101 (2-(2,6-dimethoxyphenoxyethyl)aminomethyl-1,4-benzodioxane HCl), but not the α 1B-adrenoceptor antagonist, chloroethylclonidine, also blocked the pain response produced by α-methyl-5-HT plus noradrenaline. Neither of these agents altered pain produced by α-methyl-5-HT plus prostaglandin E 2 (0.1 μg). Formalin-induced pain (1%, 50 μl) was biphasic, and timolol increased the first phase response. The second phase was attenuated by 40% by phentolamine (10 μg) injected 10 min before formalin or at the beginning of the second phase; 30 μg did not produce a larger effect. Prazosin and WP-4101, but not idazoxan or chloroethylclonidine, also attenuated the second phase. Thus, activation of α 1A-adrenoceptors can contribute to pain, but pain induced by α-methyl-5-HT plus prostaglandin E 2 is independent of adrenergic function, indicating that adrenergic function is not necessary for induction of pain by inflammatory mediators. α 1A-Adrenoceptor blockade attenuates pain when administered after development of pain, implying that peripheral adrenergic mechanisms contribute to ongoing maintenance of pain.

Sciatic Cryoneurolysis in Rats

The purpose of this study was to investigate the possibility that sympathetic exacerbation of neuropathic pain activity may be mediated in part by the development of abnormal peripheral adrenergic mechanisms at the site of peripheral nerve injury. We evaluated changes in mechanical stimulation withdrawal thresholds before and after the delivery of selected alpha-adrenergic agonists and antagonists to the immediate area of a prior nerve injury in rats that had developed continuous mechanical allodynia subsequent to sciatic cryoneurolysis (SCN). Allodynia was attenuated (thresholds increased) after administration of the alpha 1 antagonist prazosin, but not the alpha 2 antagonist idazoxan. Similar attenuation occurred with infusions of the alpha 2 agonist dexmedetomidine and at the lowest dose (2.0 micrograms) of the mixed alpha agonist clonidine. In contrast, allodynia was exacerbated (thresholds decreased) by infusion of the highest dose of clonidine (20 micrograms). Infusions of the alpha 2 agonist ST-91, a polar analog of clonidine, did not alter withdrawal thresholds. The findings suggest that a minimal peripheral adrenergic modulation of SCN-induced allodynia occurs via mechanisms that are not localized to the prior injury site. However, overall, the SCN model of neuropathic pain appears to be resistant to adrenergic interventions, providing further evidence that SCN in rats is a model of sympathetically independent pain (SIP).

Sciatic Cryoneurolysis in Rats

The purpose of this study was to investigate the possibility that sympathetic exacerbation of neuropathic pain activity may be mediated in part by the development of abnormal peripheral adrenergic mechanisms at the site of peripheral nerve injury.We evaluated changes in mechanical stimulation withdrawal thresholds before and after the delivery of selected alpha-adrenergic agonists and antagonists to the immediate area of a prior nerve injury in rats that had developed continuous mechanical allodynia subsequent to sciatic cryoneurolysis (SCN). Allodynia was attenuated (thresholds increased) after administration of the alpha1 antagonist prazosin, but not the alpha2 antagonist idazoxan. Similar attenuation occurred with infusions of the alpha2 agonist dexmedetomidine and at the lowest dose (2.0 micro gram) of the mixed alpha agonist clonidine. In contrast, allodynia was exacerbated (thresholds decreased) by infusion of the highest dose of clonidine (20 micro gram). Infusions of the alpha2 agonist ST-91, a polar analog of clonidine, did not alter withdrawal thresholds. The findings suggest that a minimal peripheral adrenergic modulation of SCN-induced allodynia occurs via mechanisms that are not localized to the prior injury site. However, overall, the SCN model of neuropathic pain appears to be resistant to adrenergic interventions, providing further evidence that SCN in rats is a model of sympathetically independent pain (SIP). (Anesth Analg 1995;81:549-54)

A research trail over half a century.

The author describes his major research activities from the time of his PhD thesis work (1937-1940) on properties of erythrocyte membranes to the present. His involvement in research on circulatory shock during World War II led to a continuing interest in the physiology and pharmacology of smooth muscle and cardiac muscle. From 1956 to 1978, his main areas of research were photorelaxation of blood vessels, factors influencing contractility of cardiac muscle, peripheral adrenergic mechanisms, and receptor theory. The major findings of his and his collaborators in these areas are described. He then recounts how an accidental finding in an experiment in 1978 on preparations of rabbit aorta eventually led to the discovery of endothelium dependent relaxation and the endothelium-derived relaxing factor (EDRF); and how additional findings led him to propose in 1986 that EDRF is nitric oxide.

Sympathetic neural contribution to salt-induced hypertension in Dahl rats.

The Dahl strain provides a model for examining mechanisms involved in the genetic sensitivity or resistance to salt-induced hypertension. Dahl salt-sensitive rats develop hypertension when fed a high salt diet; Dahl salt-resistant rats remain normotensive. Based on early experiments, it was thought that hypertension in Dahl salt-sensitive rats epitomized the overriding importance of renal and humoral mechanisms in salt-induced hypertension, but studies in the past 15 years have demonstrated that alterations in sympathetic neural mechanisms also participate critically in the genetic predisposition to salt-induced hypertension in Dahl salt-sensitive rats. This article briefly reviews sympathetic neural mechanisms in Dahl rats, including evidence for a role of afferent baroreceptor as well as central neural and peripheral adrenergic mechanisms in salt-induced hypertension in Dahl salt-sensitive rats.

Mechanisms Mediating the Thermal Response to Morphine Withdrawal in Rats

Studies were undertaken to evaluate the role of peripheral adrenergic mechanisms and the adrenal gland in the thermal responses which accompany morphine withdrawal in the rat. Ovariectomized rats were addicted to morphine and subsequently withdrawn by administration of naloxone. This treatment resulted in a significant rise (5-6 degrees C) in tail skin temperature (TST) and fall in colonic temperature (2-4 degrees C). Systemic administration of clonidine (0.5 mg/kg) completely suppressed this surge in TST and significantly attenuated the fall in core temperature. Similar results were observed following the systemic administration of ST-91, another alpha 2-adrenergic agonist which does not cross the blood-brain barrier. Central administration of ST-91 (50 micrograms/5 microliters, icv) was also successful in attenuating these temperature changes in the morphine-dependent rat. Adrenalectomy and peripheral administration of propranolol (10 mg/kg sc) both resulted in a significant attenuation of the surge in TST and the fall in core temperature in the morphine-dependent rat which suggest some peripherally mediated event is necessary to produce the full skin temperature surge. Collectively, the data suggest a role for the adrenal gland and adrenergic receptors in producing the surge in TST in morphine-dependent rats. It also suggests that the blocking effects of the alpha 2-adrenergic agonist can be mediated both centrally and peripherally.

Neuroeffector mechanisms of the defense reaction in the rat

Electrical stimulation of the dorsal periaqueductal gray matter (DPAG) eliciting flight behavior in awake rats caused an increase in arterial blood pressure (BP), heart rate (HR) and respiration in rats anesthetized with urethane. The hypertension was markedly reduced by 5 mg/kg of intravenously injected hexamethonium or bretylium, virtually abolished by 5 mg/kg of phentolamine and partially antagonized by 0.1 mg/kg of the α 1-adrenoceptor blocker, prazosin. The tachycardia induced by DPAG stimulation was partially antagonized by hexamethonium or bretylium and abolished by propranolol (5 mg/kg, IV) or practolol (5 mg/kg, IV), but not affected by N-butylscopolamine (10 mg/kg, IV). Phentolamine increased basal HR and abolished the tachycardic response caused by either brain stimulation or intravenous noradrenaline. Prazosin moderately decreased the response to noradrenaline, but did not affect basal HR or the tachycardia induced by brain stimulation. The increase in respiratory amplitude occurring during brain stimulation was abolished by phentolamine as well as by prazosin, while the increase in respiratory rate was moderately reduced by phentolamine and propranolol. These results demonstrate that the cardiovascular component of the defense reaction of the rat is almost entirely due to a sharp increase in sympathetic tone. They also suggest that the hyperventilation induced by aversive brain stimulation is modulated by central and peripheral adrenergic mechanisms.

Involvement of central noradrenergic mechanisms in the rebound hypertension following clonidine withdrawal.

The present study was designed to investigate the role of the central nervous system in the rebound hypertension precipitated by abrupt cessation of chronic clonidine (Cl) treatment. Male Wistar rats were treated with Cl (100 micrograms/kg, s.c.) twice daily for 7 days. Systolic blood pressure and heart rate were measured at different time intervals during Cl treatment. Rebound hypertension occurred 16-18 h after the last injection of Cl, but not in control animals given saline (0.1 ml) twice a day for 7 days. Rats were anesthetized with ether during this rebound phase of Cl withdrawal, an electrode inserted into the posterior hypothalamus, and a cannula introduced into the lateral cerebral ventricle. The posterior hypothalamus was electrically stimulated, and voltage-response curves obtained for control and Cl-treated rats revealed that the pressor responsiveness to hypothalamic stimulation was significantly potentiated in the Cl-treated rats. In addition, the depressor response to a single injection of Cl (10 micrograms) into the lateral cerebral ventricle was significantly attenuated in the Cl-treated rats. Additional experiments were performed in pithed rats to determine the involvement of peripheral adrenergic mechanisms in the rebound hypertension. When rats were pithed during the hypertensive phase of withdrawal, the blood pressure of treated rats decreased to a level which was similar to that of control animals. While the pressor responses to total spinal stimulation were similar in both the groups, the effect of exogenous norepinephrine was significantly attenuated in Cl-treated rats., These results suggest that a hyperresponsiveness of central noradrenergic pressor pathways contributes to the rebound hypertension noted following the abrupt cessation of clonidine treatment.

Pharmacological Studies on Possible Contribution of Peripheral Adrenergic Mechanisms to the Function of Rat Adrenocortical Glands (1)

Pharmacological Studies on Possible Contribution of Peripheral Adrenergic Mechanisms to the Function of Rat Adrenocortical Glands (1)

CENTRALLY MEDIATED CARDIOVASCULAR EFFECTS OF INTRACISTERNAL APPLICATION OF CARBACHOL IN ANESTHETIZED RATS

AbstractThe pressor response to the intracisternal (i.e.) injection of carbachol (1 μg) in anesthetized rats was analyzed. This response was significantly reduced by the intravenous (i.v.) injection of guanethidine (5 mg), hexamethonium (10 mg) or phen-tolamine (5 mg), and conversely, potentiated by i.v. desmethylimipramine (0.3 mg), while propranolol (0.5 mg) i.v. selectively inhibited the enlargement of pulse pressure and the tachycardia following i.e. carbachol (1 μg). On the other hand, the pressor response to i.e. carbachol (1 μg) was almost completely blocked by i.e. atropine (3 μg) or hexamethonium (500 μg), and significantly reduced by i.e. chlorpromazine (50 μg) but significantly potentiated by i.e. desmethylimipramine (30 μg). The pressor response to i.e. carbachol (1 μg) remained unchanged after sectioning of the bilateral cervical vagal nerves but disappeared after sectioning of the spinal cord (C7-C8). From the above result it is suggested that the pressor response to i.e. carbachol originates in the central muscarinic mechanism, is exerted through the central and peripheral adrenergic mechanisms, and that the sympathetic trunk is the main pathway.

Possible peripheral adrenergic and central dopaminergic influences in memory consolidation

The posttrial i.p. administration of clonidine (0.1 mg/kg) or haloperidol (0.5 mg/kg) to rats trained on a shuttle avoidance paradigm resulted in lower retention of the task in a retest session carried out 7 days later, compared to animals which received posttrial saline injections. The effect of clonidine was antagonized by either phenoxybenzamine (10 mg/kg) or phentolamine (10 mg/kg) i.p., and that of haloperidol was antagonized by 4, but not by 0.5 mg/kg of apomorphine i.p. Neither apomorphine, nor phentolamine or phenoxybenzamine had any effect on their own. The data suggest that memory consolidation of two-way avoidance may be influenced by presumably peripheral adrenergic mechanisms and by presumably central dopaminergic mechanisms.

Central and peripheral adrenergic mechanisms in the development of deoxycorticosterone-saline hypertension in rats.

The role of the sympathetic nervous system in the development of deoxycorticosterone-sodium chloride (DOCA-saline) hypertension was investigated by measuring plasma levels of norepinephrine, total catecholamines, and dopamine-beta-hydroxylase activity at intervals after the initiation of the DOCA-saline regimen. Plasma norepinephrine was significantly higher in DOCA-saline-treated rats at 4 and 7 weeks and in rats treated with saline alone at 4 weeks compared with that in untreated controls. Total plasma catecholamine levels (epinephrine and norepinephrine) and dopamine-beta-hydroxylase activity were similar in hypertensive rats, untreated controls, and rats that received either DOCA or saline alone. The increases in plasma norepinephrine levels may have resulted from centrally mediated increases in peripheral sympathetic neuronal activity, since the destruction of central catecholaminergic neurons with intracerebroventricularly administered 6-hydroxydopamine (6-OHDA) prevented both the DOCA-saline-induced rise in blood pressure and the increases in plasma norepinephrine. Rats treated with 6-OHDA consistently drank less water or saline than did vehicle-treated controls. The actions of centrally administered 6-OHDA on blood pressure and plasma norepinephrine levels were not secondary to a reduction in salt intake, however, since intact rats given a similar reduced saline intake became hypertensive and demonstrated elevated plasma norepinephrine concentrations. Chronic salt loading may cause a centrally mediated increase in peripheral sympathetic neuronal activity with raised plasma concentrations of norepinephrine. The increased adrenergic activity in the presence of mineralocorticoid-induced sodium retention leads to the development of hypertension.

Role of central and peripheral adrenergic mechanisms in neurogenic hypertension produced by brainstem lesions in rat.

Bilateral lesions of the nucleus tractus solitarius (NTS) in rats result in acute fulminating hypertension (NTS hypertension) as a consequence of central deafferentation of baroreceptors. The hypertension is due to increased peripheral resistance and decreased cardiac output. The hypertension is blocked and cardiac output is increased by phentolamine, trimethaphan (Arfonad), and reserpine but not by propranolol. In the present experiment, systemically administered 6-hydroxydopamine (6-OH-DA) did not alter NTS hypertension if the adrenal glands were intact. Adrenalectomy, however, blocked the lesion-induced rise in blood pressure in 6-OH-DA-treated rats. Intracisternally administered 6-OH-DA (600 µg) lowered the concentration of norepinephrine only in the spinal cord and blocked the development of NTS hypertension. Local injection of 6-OH-DA into the lateral hypothalamus did not affect the hypertension. Injection of 6-OH-DA into the NTS resulted in a mild, transient elevation in blood pressure. The results of these experiments demonstrate that (1) NTS hypertension is due to increased sympathetic neural discharge, (2) during NTS hypertension sufficient adrenomedullary catecholamines are released to produce hypertension when sympathetic terminals are destroyed, (3) central noradrenergic neurons participate in the expression of NTS hypertension, and (4) baroreceptors can inhibit the release of adrenal catecholamines.

Possible peripheral adrenergic and cholinergic mechanisms in pseudoconditioning.

Buzzers and shocks were presented in random sequence and with no temporal association to rats in a shuttle-box, so that they performed pseudoconditioned barrier-crossing responses to the buzzer. Performance of these responses was enhanced by amphetamine and tyramine. The adrenergic blocking agents yohimbine and dibenamine, though ineffective on their own, antagonized the action of amphetamine and tyramine. Hexamethonium and methylatropine, also ineffective by themselves, potentiated the effect of amphetamine but not that of tyramine. Eserine depressed the performance of pseudoconditioned responses when given alone, and it antagonized the stimulant action of both amphetamine and tyramine. The results suggest that amphetamine and tyramine enhance pseudoconditioning through activation of a peripheral adrenergic mechanism and that amphetamine, in addition, triggers an opposing cholinergic mechanism, also peripheral, from which it can be released by the anticholinergic agents hexamethonium and methylatropine. The depressant action of eserine can also be explained by activation of the cholinergic mechanism.

Sympathetic nervous system and hypertension.

The role of the sympathetic nervous system in the pathogenesis of essential human hypertension is not yet established [6, 7, 10, 11, 25, 36]. In spite of this the majority of drugs currently used in the treatment of human hypertension act by modifying peripheral and/or central adrenergic mechanisms [27]. Whereas the site and mode of action is relatively well understood in the peripheral sympathetic nervous system this is much less the case for centrally acting drugs.

Effects of prolonged hydrochlorothiazide administration on neurogenic tone in the hind limb vasculature

Prolonged oral administration of hydrochlorothiazide, (HCT) 10 mg/kg/day, to beagle dogs for a period of 12 months did not produce significant changes in body weight, blood pressure and heart rate. After 10 months of treatment, animals were anesthetized with sodium pentobarbital and pressure-flow relationships were established in the perfused hind limb prior to and following acute denervation and after α-adrenergic blockade. Denervation of the limb resulted in a marked decrease in perfusion pressures in the control animals while there were only slight changes in the HCT-treated dogs. Responses of the hind limb vasculature to lumbar sympathetic stimulation at L-5 level, and to intra-arterial administration of norepinephrine were similar in both groups. Blood pressure responses to bilateral carotid occlusion were also indentical in both treated and control groups. The data obtained suggested that there was a significant reduction in the neurogenic tone to hind limb vasculature of the animals treated with HCT and this inhibition was not due to any alterations in the peripheral adrenergic mechanisms. It is postulated that chronic hydrochlorothiazide treatment attenuated neurogenic tone to vasculature of the hind limb by an action mediated via the central nervous system.

Central integrating mechanism of the Bezold-Jarisch and baroceptor reflexes.

ARTICLESCentral integrating mechanism of the Bezold-Jarisch and baroceptor reflexesTM Lee, JS Kuo, and CY ChaiTM Lee, JS Kuo, and CY ChaiPublished Online:01 Mar 1972https://doi.org/10.1152/ajplegacy.1972.222.3.713MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByEpinephrine stress testing during cardiac catheterization in patients with aortic coarctationAmerican Heart JournalParadoxical reflex bradycardia after epinephrine infusion for arrhythmia induction in the electrophysiology laboratoryHeartRhythm Case Reports, Vol. 4, No. 10Chronic kidney disease impairs renal nerve and haemodynamic reflex responses to vagal afferent input through a central mechanismAutonomic Neuroscience, Vol. 204Major Autonomic Neuroregulatory Pathways Underlying Short- and Long-Term Control of Cardiovascular Function2 February 2016 | Current Hypertension Reports, Vol. 18, No. 3The sympathoinhibitory effects of systemic cholecystokinin are dependent on neurons in the caudal ventrolateral medulla in the ratD. M. Sartor, and A. J. M. Verberne1 November 2006 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 291, No. 5Effect of 5-HT depletion on cardiovascular vagal reflex sensitivity in awake and anesthetized ratsBrain Research, Vol. 1054, No. 1Clinical Relevance of the Bezold–Jarisch ReflexAnesthesiology, Vol. 98, No. 5Antinociceptive effect of cardiopulmonary chemoreceptor and baroreceptor reflex activation in the ratPain, Vol. 99, No. 1Neural responses to intravenous serotonin revealed by functional magnetic resonance imagingLuke A. Henderson, Pearl L. Yu, Robert C. Frysinger, Jean-Philippe Galons, Richard Bandler, and Ronald M. Harper1 January 2002 | Journal of Applied Physiology, Vol. 92, No. 1Responses of adrenal sympathetic preganglionic neurons to stimulation of cardiopulmonary receptorsBrain Research, Vol. 887, No. 1Central integration of the Bezold-Jarish reflex in the catBrain Research, Vol. 744, No. 2Cardiovascular effects induced by the stimulation of neuropeptide FF receptors in the dorsal vagal complex: an autoradiographic and pharmacological study in the ratBrain Research, Vol. 711, No. 1-2Fos-determined distribution of neurons activated during the Bezold-Jarisch reflex in the medulla oblongata in conscious rabbits and ratsBrain Research, Vol. 683, No. 1Involvement of muscarinic M1 receptor in the central pathway of the serotonin-induced Bezold-Jarisch reflex in ratsJournal of the Autonomic Nervous System, Vol. 49, No. 1Bezold-Jarisch reflex in postoperative pediatric cardiac surgical patientsThe Annals of Thoracic Surgery, Vol. 52, No. 3Interactions between circulating peptides and the central nervous system in hemodynamic regulationThe American Journal of Cardiology, Vol. 64, No. 6Functional mapping of the brainstem during centrally evoked bradycardia: A 2-deoxyglucose studyBehavioural Brain Research, Vol. 28, No. 3Existence of a powerful inhibitory mechanism in the medial region of caudal medulla—with special reference to the paramedian reticular nucleusBrain Research Bulletin, Vol. 20, No. 4Production by Systemic Enkephalin of Hemodynamic Effects by Afferent Modulation of Autonomic Nervous System ToneThe N-methyl-D-aspartate (NMDA) receptor antagonist MK-801, attenuates the Bezold-Jarisch reflex in the anaesthetized ratNeuropharmacology, Vol. 26, No. 8Interactions Between Respiration and Circulation1 January 2011COMPARATIVE CARDIOVASCULAR RESPONSES TO INTRAVENOUS CAPSAICIN, PHENYLDIGUANIDE, VERATRUM ALKALOIDS AND ENKEPHALINS IN THE CONSCIOUS DOG15 May 2014 | Journal of Autonomic Pharmacology, Vol. 6, No. 1Reflexes unique to myocardial ischemia and infarctionJournal of the American College of Cardiology, Vol. 5, No. 6Facilitation of the Bezold-Jarisch reflex by central stimulation of alpha2 adrenoceptors in dogsNaunyn-Schmiedeberg's Archives of Pharmacology, Vol. 325, No. 3Cardiac Mechanoreceptors1 January 2011Interaction of Cardiovascular Reflexes in Circulatory Control1 January 2011GlykosideMedullary origin of vagal preganglionic axons to the heart of the catJournal of the Autonomic Nervous System, Vol. 5, No. 1The influence of vagal afferents on the left ventricular contractile response to intracoronary administration of catecholamines in the conscious dog.Circulation Research, Vol. 49, No. 1Harmaline-induced tremorExperimental Brain Research, Vol. 42-42, No. 3-4Neural organisation and control of the baroreceptor reflex21 June 2005Cardio-inhibitory mechanism in the gigantocellular reticular nucleus of the medulla oblongataBrain Research, Vol. 178, No. 2-3Role of cardiac vagal c-fibers in cardiovascular control21 June 2005Effect of visceral afferent activation on leg extension induced by sciatic afferent stimulationBrain Research Bulletin, Vol. 3, No. 2Interaction between the Hypothalamic Defence Reaction and Cardiac Ventricular Receptor ReflexesActa Physiologica Scandinavica, Vol. 96, No. 4Aspects of the Central Integration of Arterial Baroreceptor and Cardiac Ventricular Receptor Reflexes in the CatActa Physiologica Scandinavica, Vol. 93, No. 1The central neural regulation by baroreceptors of peripheral catecholaminergic mechanismsBiochemical Pharmacology, Vol. 23Role of Central and Peripheral Adrenergic Mechanisms in Neurogenic Hypertension Produced by Brainstem Lesions in RatCirculation Research, Vol. 34, No. 3Acute Fulminating Neurogenic Hypertension Produced by Brainstem Lesions in the RatCirculation Research, Vol. 32, No. 5THE CENTRAL NEURAL REGULATION BY BARORECEPTORS OF PERIPHERAL CATECHOLAMINERGIC MECHANISMS More from this issue > Volume 222Issue 3March 1972Pages 713-720 Copyright & PermissionsCopyright © 1972 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1972.222.3.713PubMed5022685History Published online 1 March 1972 Published in print 1 March 1972 Metrics