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At least 883 records · Page 49Linked to original sources
PubMed1983

Reflex cardiovascular responses to chemoreceptor stimulation in conscious dogs with cardiac hypertrophy.

Carotid chemoreceptor reflex activation (CCRA) has been previously shown to result in intense alpha-adrenergic peripheral vasoconstriction, a biphasic coronary vascular response characterized by an early vasodilation and a late alpha-adrenergic vasoconstriction, and a cholinergic increase in cardiac cycle length in normal conscious dogs. In the present study, we investigated the extent to which these reflex cardiovascular responses to CCRA are modified after the development of pressure-overload right ventricular (RV) hypertrophy induced by chronic (9-12 mo) pulmonary arterial stenosis. With heart rate constant and respiration allowed to vary spontaneously, the magnitude of the late CCRA-induced (intracarotid nicotine) increase (P less than 0.01) in right coronary resistance was markedly attenuated (P less than 0.01) in conscious dogs with RV hypertrophy [0.29 +/- 0.07 (SE) mmHg X ml-1 X min] compared with normal dogs (1.87 +/- 0.36). When respiration was controlled to eliminate pulmonary inflation reflex activation, the late CCRA-induced increase (P less than 0.01) in right coronary resistance was still found to be depressed (P less than 0.01) in the RV hypertrophy group (1.11 +/- 0.20 mmHg X ml-1 X min) compared with normal dogs (3.65 +/- 0.75). This late CCRA-induced right coronary vasoconstriction was not potentiated by beta-adrenergic receptor blockade but was abolished (P less than 0.01) by alpha-adrenergic receptor blockade. In contrast to the depressed right coronary vasoconstriction, the CCRA-induced alpha-adrenergic constriction (P less than 0.01) of the iliac arterial vascular bed was similar in both groups, and the cholinergic increase (P less than 0.01) in cardiac cycle length was enhanced (P less than 0.01) in the RV hypertrophy group compared with normal dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Cardiorespiratory response to cyanide of arterial chemoreceptors in fetal lambs.

Cardiorespiratory response to the stimulation of the carotid and aortic receptors by sodium cyanide was examined in fetal lambs in utero at 0.8 (120 days) gestation. Injections of 50-400 micrograms cyanide into the inferior vena cava or the carotid artery of intact fetuses elicited bradycardia and respiratory responses that varied from a single gasp to rhythmic respiratory movements but no significant change in arterial blood pressure. Carotid sinus denervation eliminated the cardiorespiratory response to intracarotid injection of cyanide and sinoaortic denervation abolished the response to inferior vena caval injection. It is concluded that in fetal lamb in utero the aortic and carotid bodies are active, and hypoxic stimulation of these chemoreceptors results in cardiorespiratory response characterized by slowing of fetal heart rate, respiratory effort, and no consistent change in arterial blood pressure.

Animals↗
PubMed1990

Cellular basis of transduction in carotid chemoreceptors.

Understanding transduction mechanisms is central to much of sensory physiology. The carotid chemoreceptors monitor the PO2 of arterial blood en route to the brain and are powerfully excited when the arterial PO2 falls to less than 60 mmHg. The type I cell is generally believed to be the transducer. These cells release catecholamines in response to agents that excite the receptor (hypoxia, cyanide, K(+)-induced depolarization, etc.). Adherent to the cells are the saucer-shaped nerve endings of the axons of the sinus nerve. We and others have used patch-clamp techniques to study the electrophysiological properties of the type I cells. We have also investigated type I cell chemistry with microfluorometric techniques, to measure intracellular Ca2+ concentration ([Ca2+]i), mitochondrial NADH, and mitochondrial membrane potential (delta psi m). During hypoxia there are graded increases in NADH, [Ca2+]i (which presumably will promote transmitter release), and graded depolarization of delta psi m. These results suggest that the Ca2+ is largely derived from an intracellular store, probably from mitochondria, and that release is entrained to delta psi m. Comparative studies with other cells indicate an increased sensitivity of the mitochondria of type I cells to changes in PO2. The data suggest that the electrophysiological responses of type I cells to hypoxia are not central to the response, although the excitability of the cells may provide a mechanism for the modulation of the response by varying voltage-gated Ca2+ influx.

Animals↗
PubMed2003

CO2 transduction in avian intrapulmonary chemoreceptors is critically dependent on transmembrane Na+/H+ exchange.

Avian intrapulmonary chemoreceptors (IPC) are vagal respiratory afferents that are inhibited by high lung Pco(2) and excited by low lung Pco(2). Previous work suggests that increased CO(2) inhibits IPC by acidifying intracellular pH (pH(i)) and that pH(i) is determined by a kinetic balance between the rate of intracellular carbonic anhydrase-catalyzed CO(2) hydration/dehydration and transmembrane extrusion of acids and/or bases by various exchangers. Here, the role of amiloride-sensitive Na(+)/H(+) exchange (NHE) in the IPC CO(2) response was tested by recording single-unit action potentials from IPC in anesthetized ducks, Anas platyrhynchos. For each of the IPC tested, blockade of the NHE using dimethyl amiloride (DMA) elicited a marked (>50%) dose-dependent decrease in mean IPC discharge (P < 0.05), suggesting that NHE is important for pH(i) regulation and CO(2) transduction in IPC. In addition, activation of the NHE using 12-O-tetradecanoylphorbol 13-acetate stimulated six of the seven IPC tested, although the overall effect was not statistically significantly (P = 0.07). Taken together, these findings suggest that CO(2) transduction in IPC is dependent on transmembrane NHE although it is likely to be much slower than carbonic anhydrase-catalyzed hydration-dehydration of CO(2).

Amiloride↗
PubMed1977

Dynamic responses of CO2-sensitive avian intrapulmonary chemoreceptors.

Single-unit extracellular potentials from CO2-sensitive intrapulmonary chemoreceptors (IPC) were recorded with tungsten microelectrodes from the nodose ganglia of unidirectionally, artificially ventilated White Leghorn cockerels. The responses of IPC to step and sinusoidal forcing functions of fractional concentration of carbon dioxide (FCo2) indicate that 1) about two-thirds of IPC are bidirectionally rate sensitive, 2) delay to forcing varies from essentially zero to several times larger than the time of nitrogen gas passage through the lung and, on the average, is significantly shorter to step decrease than step increase in fco2, and 3) IPC with irregular discharge intervals are more rate sensitive and respond to higher frequencies than IPC with regular interspike intervals. The physical and chemical properties of the "receptor-lung" complex are probably important in determining the dynamic responses of IPC by partitioning of CO2 from other gases within the lumen of the parabronchus. IPC are located along the length of the bronchial gas exchange areas of the avian lung and transmit information to the CNS concerning the mean level, rate, and direction of change in the partial pressure of carbon dioxide (PCo2).

Action Potentials↗
PubMed1985

Influence of central chemoreceptor afferent inputs on respiratory muscle activity.

Respiratory activity can be substantially affected by perturbations confined to the superficial areas of the ventrolateral surface of the medulla, the putative site of central chemoreceptors. In this study we compared the effect of thermal and pharmacological interventions that are known to alter respiration on the electrical activity of the rib cage muscles, diaphragm, and abdominal muscles. With cooling of the intermediate areas to 20 degrees C, tidal volume decreased 50%. The electrical activity of the diaphragm decreased less than the other muscles (diaphragm less than inspiratory intercostal less than expiratory intercostal). Abdominal muscle activity was depressed as much as expiratory intercostal activity but reappeared with further cooling to 10 degrees C if cooling was prolonged and the vagi were intact. gamma-Aminobutyric acid (GABA) and its agonist muscimol, like cooling, reduced expiratory and inspiratory intercostal activity more than diaphragm activity. Nicotine, a respiratory stimulant, applied to the intermediate areas increased inspiratory intercostal activity more than the diaphragm. The results suggest that under the conditions of the experiments the rib cage musculature, and probably the abdominal muscles as well, are more responsive than the diaphragm to depression or excitation of chemosensitive elements in the superficial regions of the medulla.

Animals↗
PubMed1993

Excitatory amino acid receptors in commissural nucleus of the NTS mediate carotid chemoreceptor responses.

Stimulation of carotid body chemoreceptors by saline saturated with 100% CO2 elicited an increase in mean arterial pressure, respiratory rate, tidal volume, and minute ventilation (VE). Microinjections of L-glutamate into a midline area 0.5-0.75 mm caudal and 0.3-0.5 mm deep with respect to the calamus scriptorius increased VE. Histological examination showed that the site was located in the commissural nucleus of the nucleus tractus solitarii (NTS). The presence of excitatory amino acid receptors [N-methyl-D-aspartic acid (NMDA); kainate, quisqualate/alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) and trans 1-amino-cyclopentane-trans-1,3-dicarboxylic acid (ACPD)] in this area was demonstrated by microinjections of appropriate agonists. Simultaneous blockade of NMDA and non-NMDA receptors by combined injections of DL-2-aminophosphonoheptanoate (AP-7; 1 nmol) and 6,7-dinitro-quinoxaline-2,3-dione (DNQX; 1 nmol) abolished the responses to stimulation of carotid body on either side. Combined injections of AP-7 and DNQX did not produce a nonspecific depression of neurons because the responses to another agonist, carbachol, remained unaltered. Inhibition of the neurons in the aforementioned area with microinjections of muscimol (which hyperpolarizes neuronal cell bodies but not fibers of passage) also abolished the responses to subsequent carotid body stimulation on either side.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Increased venous PCO2 enhances dynamic responses of avian intrapulmonary chemoreceptors.

We quantified the neural discharge of intrapulmonary chemoreceptors (IPC) innervating the left lungs of anesthetized Pekin ducks. Right and left lungs were separately unidirectionally ventilated. Alternating steps in CO2 concentration (0-6%, 11-s period) were delivered to the left lung under control conditions [mixed venous PCO2, (PVCO2) 43 +/- 4 Torr] and under venous CO2 load conditions (PVCO2 79 +/- 6 Torr). During venous CO2 loading the right lung was ventilated with 10-20% CO2, while the left lung was ventilated with a sufficient flow of gas containing 0% CO2 to maintain normal expired PCO2 (indicated by constant IPC discharge rate). Venous loading increased the peak-to-peak amplitude of the oscillation in IPC discharge by 4.3 +/- 1.8 s-1 (n = 11, P < 0.05), left lung ventilation was increased 2.6-fold, and the IPC step response became more prompt. The mean IPC discharge rate during the CO2 stepping cycle was not significantly affected (11.8 +/- 1.4 during control vs. 10.3 +/- 1.3 s-1 during venous loading). Increased IPC discharge oscillations were due to enhancement of the dynamic overshoot in receptor discharge after the 6-0% downstep in inspired CO2 and to a depression of discharge during 6% inspired CO2. We propose that the phasic enhancement of IPC discharge oscillations during venous CO2 loading may cause feedback inhibition of ventilatory drive.

Administration, Inhalation↗
PubMed1994

Interaction between chemoreceptor and stretch receptor inputs at medullary respiratory neurons.

The interaction between afferent inputs from carotid body chemoreceptors (CCRs) and from slowly adapting pulmonary stretch receptors (PSRs) on the discharge patterns of medullary inspiratory (I) and expiratory (E) neurons was characterized in thiopental sodium-anesthetized, paralyzed, ventilated dogs. A cycle-triggered ventilator was used to produce control and test pulmonary afferent input patterns. The CCRs were stimulated by phase-synchronized bolus injections of CO2-saturated saline into the common carotid arteries. Only those neurons whose discharge time course was altered by both inflation and CCR activation were studied. The dorsal respiratory group (DRG) I inflation-insensitive neurons were also included. Cycle-triggered histograms of unit activity were obtained for the neuronal responses to inflation, CO2 bolus, and their combination, as well as for the spontaneous control condition. Linearity of the interaction was tested by comparing the sum of the net individual responses to the net response of the combined afferent inputs. The results suggest that a linear (additive) interaction between CCR and PSR inputs exists for the DRG I inflation-sensitive neurons, the ventral respiratory group (VRG) I decrementing, and caudal VRG E augmenting neurons, while a nonadditive interaction exists for caudal VRG E decrementing bulbospinal neurons. The implications of these findings are discussed.

Afferent Pathways↗
PubMed1999

Chronic hypercapnia resets CO2 sensitivity of avian intrapulmonary chemoreceptors.

Avian intrapulmonary chemoreceptors (IPC) are vagal sensory neurons that participate in the control of breathing. IPC action potential frequency is inversely proportional to PCO2, but it is unclear whether low PCO2 or high pH is the immediate stimulus for signal transduction in IPC. To address this question, comparisons were made between single cell neural responses of 34 IPC recorded in 6 anesthetized ducks (Anas platyrhynchos) acclimatized 12 days to 7.5% inspired CO2 and 22 IPC recorded in 9 normal anesthetized ducks. We hypothesized that if respiratory-linked pH changes determine IPC activity, action potential frequency as a function of inspiratory PCO2 (PICO2) should be greater after acclimatization due to metabolic acid-base compensation and higher pH. Conversely, if PCO2 alone determines IPC discharge, action potential frequency vs. PCO2 should be unchanged by acclimatization. Results indicate that after acclimatization ventilation was depressed at 28 and 42 Torr PICO2 (P < 0.05) and mean plasma pH at 40 Torr PCO2 increased from 7.38 +/- 0. 03 to 7.56 +/- 0.02 (P < 0.05), indicating significant metabolic acid-base compensation and HCO-3 retention. Mean IPC discharge rate was elevated by CO2 acclimatization at all PCO2 studied. In acclimatized vs. normal animals, regression analysis of IPC discharge as a function of lnPCO2 showed increased mean intercepts of 81.1 +/- 4.0 vs. 48.4 +/- 3.6 impulses/s (P < 0.05) and increased mean slopes of -19.0 +/- 1.0 vs. -12.0 +/- 1.1 impulses. s-1. lnPCO2-1 (P < 0.05). Results indicate that IPC response to CO2 is mediated by H+ from CO2 hydration and not by CO2 directly.

Adaptation, Physiological↗
PubMed2000

Benzolamide, acetazolamide, and signal transduction in avian intrapulmonary chemoreceptors.

Intrapulmonary chemoreceptors (IPC) are CO(2)-sensitive sensory neurons that innervate the lungs of birds, help control the rate and depth of breathing, and require carbonic anhydrase (CA) for normal function. We tested whether the CA enzyme is located intracellularly or extracellularly in IPC by comparing the effect of a CA inhibitor that is membrane permeable (iv acetazolamide) with one that is relatively membrane impermeable (iv benzolamide). Single cell extracellular recordings were made from vagal filaments in 16 anesthetized, unidirectionally ventilated mallards (Anas platyrhynchos). Without CA inhibition, action potential discharge rate was inversely proportional to inspired PCO(2) (-9.0 +/- 0.8 s(-1). lnTorr(-1); means +/- SE, n = 16) and exhibited phasic responses to rapid PCO(2) changes. Benzolamide (25 mg/kg iv) raised the discharge rate but did not alter tonic IPC PCO(2) response (-9.8 +/- 1.6 s(-1). lnTorr(-1), n = 8), and it modestly attenuated phasic responses. Acetazolamide (10 mg/kg iv) raised IPC discharge, significantly reduced tonic IPC PCO(2) response to -3.5 +/- 3.6 s(-1). lnTorr(-1) (n = 6), and severely attenuated phasic responses. Results were consistent with an intracellular site for CA that is less accessible to benzolamide. A model of IPC CO(2) transduction is proposed.

Acetazolamide↗
PubMed2001

ANP, BNP, and CNP enhance bradycardic responses to cardiopulmonary chemoreceptor activation in conscious sheep.

We demonstrated previously that atrial natriuretic peptide (ANP) enhances reflex bradycardia to intravenous serotonin [5-hydroxytryptamine (5-HT)] (von Bezold-Jarisch reflex) in rats. To determine whether 1) ANP affects this cardiopulmonary vagal reflex in another species and 2) B-type (BNP) and C-type (CNP) natriuretic peptides share with ANP the ability to modulate this reflex, we used intravenous phenylbiguanide (PBG), a 5-HT(3) agonist, as the stimulus to evoke a von Bezold-Jarisch reflex (dose-related, reproducible bradycardia) in conscious adult sheep (n = 5). Three doses of PBG (13 +/- 3, 20 +/- 3, and 31 +/- 4 microg/kg) injected into the jugular vein caused reflex cardiac slowing of -7 +/- 1, -15 +/- 2, and -36 +/- 3 beats/min, respectively, under control conditions. These doses of PBG were repeated during infusions of ANP, BNP, or CNP (10 pmol. kg(-1). min(-1) iv), or vehicle (normal saline). Each of the natriuretic peptides significantly (P < 0.05) enhanced the sensitivity of bradycardic responses to PBG by 94 +/- 8% (ANP), 142 +/- 55% (BNP), and 61 +/- 16% (CNP). Thus not only did ANP sensitize cardiopulmonary chemoreceptor activation in a species with resting heart rate close to that in humans, but BNP and CNP also enhanced von Bezold-Jarisch reflex activity in conscious sheep.

Animals↗
PubMed2001

Location of central respiratory chemoreceptors in the developing tadpole.

The location of central respiratory chemoreceptors in amphibian larvae may change as the central chemoreceptive function shifts from driving gill to driving lung ventilation during metamorphosis. We examined this possibility in the in vitro brain stem of the pre- and postmetamorphic Rana catesbeiana tadpole by microinjecting hypercapnic artificial cerebrospinal fluid (aCSF) while recording fictive lung ventilation. The rostral and caudal brain stem were separately explored systematically using injections of 11 nl of aCSF equilibrated with 100% CO2 that transiently acidified a 500-microm region, producing a maximum reduction in pH of 0.23 +/- 0.06 at the site of injection. In postmetamorphic tadpoles, chemoreceptive sites were concentrated in the rostral compared with the caudal brain stem. No such segregation was observed in the premetamorphic tadpole. We conclude that, as in lung rhythmogenic function, respiratory chemosensitivity emerges rostrally in the amphibian brain stem during development.

Animals↗
PubMed1984

Renorenal reflex responses to mechano- and chemoreceptor stimulation in the dog and rat.

The renal functional effects of renal mechano- (MR) and chemoreceptor (CR) stimulation were examined in dogs and rats. In dogs increasing ureteral pressure (increases UP) increased ipsilateral (ipsi) renal blood flow and renin secretion rate, decreased contralateral (contra) renal blood flow, but did not affect contra renal excretion or renin secretion rate. Increasing renal venous pressure (increases RVP) increased ipsi renin secretion rate but did not affect contra renal function. Retrograde ureteropelvic perfusion with 0.9 M NaCl at unchanged UP did not affect either ipsi or contra renal function. In rats,increases UP and retrograde ureteropelvic perfusion with 0.9 M NaCl at unchanged UP did not affect mean arterial pressure, heart rate, contra renal blood flow, or glomerular filtration rate but increased contra urine flow rate and urinary sodium excretion. Increasing ureteral pressure with 0.1 M NaCl increased contra urine flow rate and urinary sodium excretion, whereas retrograde ureteropelvic perfusion with 0.1 M NaCl was without effect. Thus increases UP and retrograde ureteropelvic perfusion with 0.9 M NaCl stimulated renal MR and CR, respectively. The contra diuretic and natriuretic responses to renal MR and CR stimulation were abolished by either ipsi or contra renal denervation. Renal MR and CR stimulation increased ipsi afferent renal nerve activity (RNA) and decreased contra efferent RNA. These results indicate that in dogs renal MR stimulation results in a modest contralateral excitatory renorenal reflex, whereas in rats renal MR and CR stimulation produce a contralateral inhibitory renorenal reflex.

Animals↗
PubMed1975

A respiratory venous chemoreceptor in the young puppy.

An extracorporeal venovenous shunt system utilizing a membrane oxygenator to alter venous blood gases was used to study the regulation of ventilation in 28 newborn and 4 adult dogs. There was no effect of the extracorporeal circuit per se (without the oxygenator in the system) on essential cardiovascular or respiratory function. When the puppies were placed on the extracorporeal circuit with the oxygenator in the system to effect changes in mixed venous blood gas composition there was a significant increase in venous P02 (Pv02), a decrease in venous Pco2 (Pvco2), a rise in venous pH (PHv), and a marked fall in minute ventilation (VE). There were no significant changes in cardiovascular function or arterial blood gases to account for the depression of ventilation. Acute changes in Pvo2 produced appropriate directional changes of VE under conditions where other arterial and venous blood gases were held constant. At a low Pvco2/Paco2 ratio, ventilation was depressed compared to those conditions with a high ratio. At any Pvc02/Paco2 ratio, ventilation could be depressed by raising the Pvo2. In adult animals ventilation could not be altered by changing venous blood gases. These experiments support the existence of a respiratory chemoreceptor sensitive to both PO2 and PCO2 in the prepulmonary or venous circulation of the newborn animal.

Animals↗
PubMed1975

Integration of chemoreceptor stimuli by rostral brainstem respiratory areas.

Ventilatory regulation by brainstem sites rostral to the midpontile level was assessed in decerebrate cats by comparing the effects of punctate pneumotaxic center lesions with those of midpontile transection. After either procedure, PACO2 was significantly elevated. Moreover an equal suppression of hypercapnia-induced minute volumes and maintenance, at some PACO2 levels, of minute volume responses to hypoxia was observed. Tidal volume elevations accounted for the maintenance of hypoxia-induced minute volumes. Following pneumotaxic center lesions, hypercapnia-induced tidal volumes were higher than those exhibited subsequent to midpontile transection. After carotid sinus nerve section, PACO2 was elevated and hypoxia-induced alterations were abolished. Bilateral vagotomy resulted in apneusis. These data demonstrate that, in the brainstem area examined, only the pneumotaxic center influences the PACO2 level or set point for respiratory activity. A locus of tidal volume generation is ascribed to rostral brainstem sites outside this pneumotaxic center. Data obtained support the hypothesis of a differential brainstem integration of peripheral and central chemoreceptor afferent stimuli.

Animals↗
PubMed1976

Integration of chemoreceptor stimuli by caudal pontile and rostral medullary sites.

Ventilatory regulation by pontile pneumotaxic and apneustic centers and by rostral medullary sites was evaluated in intercollicular decerebrate cats. Following pneumotaxic center ablation, PAco2 was significantly elevated. Moreover, in response to hypercapina or hypoxia, frequency responses were significantly diminished whereas tidal volume responses were unchanged or elevated. Interruption of apneustic center function by caudal pontile transection or radiofrequency lesions in the caudal pons and/or rostral medulla resulted in significant decreases of tidal volume responses and significant elevations of frequency responses to both hypercapnia and hypoxia. Neither minute volume responses nor the PAco2 level was altered. It is concluded that the apneustic center exercises a primary role in the brainstem definition of tidal volume responses for both peripheral and central chemoreceptor afferent stimuli. The apneustic center is also considered to exert an impoetant function in the definition of respiratory frequency. A medially placed pathway in the rostral medulla is proposed to interconnect the apneustic center with the medullary respiratory nuclei.

Animals↗
PubMed1981

Neural response of carotid chemoreceptors following dopamine blockade.

The role of endogenous carotid body dopamine in the afferent chemoreceptor circuit was studied by means of haloperidol-induced dopamine antagonism. In 19 cats that were anesthetized with pentobarbital sodium and paralyzed, single carotid body nerve fibers were dissected free and placed on unipolar platinum wire electrodes. In 10 of these cats, the neural response to room air and the last 2 min of 6-min inhalations of 3, 6, and 9% CO2 were recorded, and blood samples were drawn for gas tension measurements. Haloperidol was administered at a dose (250 micrograms/kg) shown to block the inhibitory effect of injected dopamine. Following a 15-min equilibration, the CO2 response was again tested. In four other cats the CO2 response was tested with a hyperoxic background. In the remaining five cats the response to isocapnic hypoxia was recorded during administration of 15, 12, and 8% O2 before and following haloperidol. There was a significant increase in room air discharge activity and in hypoxic sensitivity following haloperidol. However, there was no significant change in hypercapnic sensitivity. These results suggest that there is a modulatory role for endogenous dopamine only in the hypoxic response.

Animals↗