DEVELOPMENTAL CHANGES OF THE CATECHOLAMINE-INDUCED CHRONOTROPIC RESPONSES OF CHICKS RELATED TO THE BLOOD PRESSURE RESPONSES
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Reflex bradycardia
Embryonic heart
Abstract The effects of diazepam on cardiovascular function were assessed in conscious rats. Intravenous administration of diazepam (1-30 mg kg−1) produced a dose-dependent decrease in both the mean arterial pressure and the heart rate. Also, reflex bradycardia was produced in rats by intravenous infusion of adrenaline (1ṁ25-2ṁ5 μg kg−1). Intravenous pretreatment of the rats with diazepam, although causing no change in the adrenaline-induced pressor effect, did enhance the adrenaline-induced reflex bradycardia. However, the diazepam enhancement of adrenaline-induced reflex bradycardia was antagonized by pretreatment of rats with an intravenous dose of picrotoxin (an agent blocks chloride channels by binding to sites associated with the benzodiazepine-GABA-chloride channel macromolecular complex). The data indicate that diazepam acts through the benzodiazepine-GABA-chloride channel macromolecular complex within the central nervous system to facilitate reflex bradycardia mediated through baroreceptor reflexes in response to an acute increase in arterial pressure.
Reflex bradycardia
Picrotoxin
Flumazenil
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Abstract The effects of α‐adrenergic (Phenoxybenzamine) and parasympathetic (Atropin) blockade on the cardiovascular response to diving in the duck has been studied. With no significant reduction in the immediate, slight fall in heart rate, a‐adrenergic blockade caused peripheral vasodilatation, and virtually abolished the more delayed phase of profound bradycardia during diving. Atropinization eliminated both elenients of the diving bradycardia., while the arterial and venous pressure greatly increased, suggesting that intense activation of the vasoconstrictor fibres was maintained during submersion. It is concluded that the gradual but profound intensification of the initial, slight bradycardia in the dividing duck is a matter of a secondary reflex adjustment to the pressure level.
Reflex bradycardia
Phenoxybenzamine
Vagovagal reflex
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Reflex bradycardia
Oculocardiac reflex
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1. Digital pressure applied to the eyes evokes reflex bradycardia in human subjects and anaesthetized dogs. The bradycardia is most pronounced when breathing stops. 2. In the dog oculo-cardiac reflex bradycardia is mediated by vegal stimulation and by sympathetic withdrawal. 3. Oculo-cardiac reflex bradycardia in the dog is reduced by central neural inspiratory activity and by the excitation of pulmonary afferents by inflation of the lungs. In human subjects it is reduced when inspiratory efforts are made against a closed glottis. 4. Nasopharyngeal stimulation with water evokes reflex bradycardia in the anaesthetized dog. This bradycardia is reduced by central neural inspiratory activity and by the excitation of pulmonary afferents by inflation of the lungs. 5. Bradycardia occurs in normal human subjects during immersion of the face in water ('diving'). This bradycardia is reduced when inspiratory efforts are made against a closed glottis. 6. Swallowing evokes transient tachycardia in human subjects. During diving or the application of ocular pressure, swallowing reduces the reflex bradycardia which these evoke.
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The effects of the stereochemically pure psychoactive cannabinoid (-)-11-OH-delta 8-tetrahydrocannabinol-dimethylheptyl (HU-210) on blood pressure (BP) and heart rate (HR) were determined in rats. In pentobarbital-anesthetized animals, the compound produced dose-related, long-lasting hypotension and bradycardia at doses between 10 and 1,000 micrograms/kg. BP began to decrease immediately after drug administration, and in no case was an initial pressor response observed. Previous vagotomy (VX) or pretreatment with 6-hydroxydopamine (6-OHDA) did not affect hypotension. Bradycardia was inhibited by VX, but only 60 min after administration of HU-210; it was enhanced by 6-OHDA. The cannabinoid blocked reflex bradycardia induced by phenylephrine (PE). HU-210 also decreased BP and HR in conscious rats. Hypotension lasted 2 h, whereas bradycardia was still present 8 h after drug administration. HU-210 thus shares with delta 9-tetrahydrocannabinol (THC) the ability to decrease BP and HR, but is 5-10 times more potent than the natural compound. Its lack of an initial pressor effect, such as that described for THC, could be related to its specificity for the type-1 cannabinoid (CB1) receptor. Hypotension and bradycardia after HU-210 administration are not due to sympathetic withdrawal. Enhanced parasympathetic tone is involved in bradycardia only at a late stage of the response.
Reflex bradycardia
Delta-9-tetrahydrocannabinol
Phenylephrine
Tetrahydrocannabinol
Cinnarizine
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The degree of reflex bradycardia elicited by a sudden, brief rise in arterial pressure was used as an index of sino-aortic reflex activity in conscious rabbits with early renal hypertension. Change in heart rate was measured every 6 seconds after injected angiotensin which caused a rise in blood pressure of 15 to 60 mm Hg. Ninety-one tests for reflex bradycardia were made in 30 normal rabbits; 14 of them were tested intermittently during the 1 to 40 day period following unilateral nephrectomy and latex encapsulation of the opposite kidney. A total of 62 tests were made after arterial pressure had risen 10 to 80 mm Hg, average 35, above control values. Average decrease in heart rate was significantly less and frequency of negligible reflex bradycardia was much higher in hypertensives than controls. Individual rabbits showed no tendency for reflex bradycardia to return toward normal magnitude. However, the vasomotor component of the sino-aortic reflex mechanism in renal hypertensive rabbits buffered the pre...
Reflex bradycardia
Mean arterial pressure
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In spinal cats whose ventilation is completely controlled the primary cardiac response to hypoxia includes vagal bradycardia. This bradycardia appears at distinct levels of PaO2 which vary as a function of PaCO2. The carotid chemoreceptors are chiefly responsible for eliciting reflex bradycardia while the aortic chemoreceptors make little or no contribution. This divergence of function is mirrored in the reflex control of respiration but not in the pressor response to hypoxia where both sets of receptors are important. A bradycardia which results directly from the action of hypoxia on the central nervous system can be distinguished from both peripheral reflex effects and the direct effects of hypoxia on the heart itself.
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Hypoxia
Peripheral chemoreceptors
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Abstract It has been demonstrated that cardiac receptors, most likely of the left ventricular type, are present also in the duck's heart. These receptors and their reflex responses ( i.e. bradycardia and hypotension) could be blocked by intrapericardial administration of lidocaine. Initially, such receptor blockade did not affect efferent vagal control of heart rate, as revealed by undiminished bradycardia in response to a standardized vagal stimulation. After cardiac receptor blockade, however, the duck's normal bradycardia response to head immersion was greatly reduced. The cardiovascular response to submersion was now instead characterized by a marked rise in arterial pressure, with superimposed bouts of intensified bradycardia and pressure reduction, evidently induced reflexly from the arterial baroreceptors. Meanwhile, the bradycardia response to standardized efferent vagal stimulation was still the same as before intrapericardial lidocaine injection. These results suggest that the marked rise in cardiac filling pressure following the intense chemo‐receptor‐induced constriction of both resistance and capacitance vessels, activates ventricular stretch receptors signalling in vagal afferents. Apparently, the activation of these receptors contributes crucially to the bradycardia and reduction of cardiac output, which balance off the greatly increased peripheral resistance in the diving duck.
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Abstract S jöstrand , T. Circulatory control via vagal afferents. VI. The bleeding bradycardia in the rat, its elicitation and relation to the release of vasopressin. Acta physiol. scand. 1973. 89. 39–50. Bradycardia appears regularly in Sprague‐Dawley rats on arterial hemorrhage. It is usually preceded by an increase of the heart rate of varying duration. On an average the bradycardia starts 21s after the fall in arterial pressure. On reinfusion the bradycardia disappears during 10–20 min following a varying course. Compression of the inferior caval vein provokes bradycardia which appears and disappears similarly but starts earlier in relation to the pressure fall. If blood or saline is intravenously infused simultaneously with the hemorrhage, the bradycardia starts later and is less pronounced in relation to the fall in arterial pressure. The bradycardia is inhibited by hypophysectomy, hydration and infusion of small amounts of ethyl alcohol through the carotid artery. A similar bradycardia may be provoked by intra‐carotid infusion of vasopressin at maintained arterial pressure. It is concluded that the bleeding bradycardia is elicited by receptors on the low pressure side stimulated by a decrease of the venous return or central blood volume and is a part of a reflex control of the blood volume and distribution. The release of vasopressin is stimulated through vagal afferents and, by local transmission, exerts an excitatory effect on the depressor area in the hypothalamus. The significance of the deduced vasopressin releasing reflex under normal and pathological conditions is discussed.
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The vasopressor and bradycardia responses to an intravenous dose of epinephrine were assessed in saline-controlled, 5-hydroxytryptamine-(5-HT) depleted, and 5-HT-potentiated rats. Regardless of the previous treatment epinephrine produced an insignificant change in the basal levels of mean arterial pressure and heart rate. However, brain serotonin alteration did produce some influences on the reflex bradycardia in response to an elevation in arterial pressure. Elevating 5-HT contents in brain with 5-hydroxytryptophan (5-HTP) after peripheral decarboxylase inhibition with Ro 4-4602 produced a significant reduction in reflex bradycardia compared to the controls. In contrast, depleting 5-HT contents in brain with either p-chlorophenylalanine (PCPA) or 5,7-dihydroxytryptamine (5,7-DHT) led to an enhancement of epinephrine-induced bradycardia. Moreover, the enhanced reflex bradycardia induced by PCPA treatment was readily blocked by the replacement of the depleted brain 5-HT with 5-HTP and Ro 4-4602. The results suggest that serotoninergic systems play a role in the elaboration or modulation of reflex bradycardia. Specifically, 5-HT appears to inhibit reflex bradycardia since its depletion facilitated and its elevation inhibited reflex bradycardia.
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