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Biomedical subjects

P Zapata

Publications and source records attributed to P Zapata.

At least 73 records · Page 4Linked to original sources
PubMed1977

Axonal transport of labeled material into sensory nerve ending of cat carotid body.

The origin of nerve endings on glomus cells in the carotid body has been the subject of much controversy in recent years. Specifically, the problem is whether these nerve endings, which contain clear-core ("synaptic") vesicles and mitochondria arise from sensory neurons in the petrosal ganglion or from efferent neurons located in the brain stem or elsewhere. To study this problem, [3H]proline was applied to cat petrosal ganglia, the animals were allowed to survive for 3 h-7 days, and the peripheral distribution of the label was analyzed by sample oxidation/scintillation counting and by EM autoradiography. The time courses of distribution of label along the nerves and the accumulation of label in the carotid body indicated the presence of fast, intermediate and slow components of axonal flow. EM autoradiographs of carotid bodies showed the label localized almost exclusively to nerve fibers and to nerve terminals on glomus cells. As much as 60--90% of the nerve terminals were labeled in a given ultrathin-section autoradiograph. Passive movement of label from the injection site, or fibers of passage (efferent) through the ganglion, did not contribute to the labeled material since administration of [3H]proline onto the desheathed nerve away from the ganglion was ineffective in labeling the carotid body. The results suggest that most, if not all, nerve terminals on glomus cells in cat carotid body arise from neurons in the petrosal ganglion.

Animals↗
PubMed1976

Axon regeneration following a lesion of the carotid nerve: electrophysiological and ultrastructural observations.

Carotid nerves of the cat were crushed and allowed to regenerate in order to study the properties of regerating fibers and the role of carotid body parenchymal cells (glomus or type I, and sustentacular or type II) in the transduction of chemosensory activity. Such activity is reinitiated 6 days after the nerves are crushed close (1-2 mm) to the carotid body. The process of recovery is delayed when a crush is made at successively greater distances (5-6 and 10-12 mm) from the carotid body. Ultrastructural studies show that the reappearance of nerve endings on the glomus-sustentacular cell complex coincides in time with the onset of chemosensory activity. The regenerated nerve endings increase in size and number and appear normal by 48 days. Some barosensory activity can be elicited 6 days after a nerve crush close to the carotid sinus, but rhythmic barosensory discharges only occur after the 21st day when myelinated axons reappear in the carotid sinus adventitia. Results suggest that recovery of chemosensory function depends on the reestablishment of apposition between regenerating carotid nerve fibers and parenchymal cells of the carotid body.

Animals↗
PubMed1976

Effects of deneravation and decentralization upon taste buds.

Denervation of vallate papillae results in failure of tactile and gustatory reception at a time when impulse conduction in the distal stump of the glossopharyngeal nerve is still unimpaired; delay of receptor deficit depends on axon length between receptor and axotomy sites; taste buds disappear by 10 days. Decentralization, through intracranial rhizotomy, does not modify lingual receptors structure or function.

Animals↗
PubMed1976

Acute changes in ventilation and blood pressure induced by inhalation of tobacco smoke.

Inhalation of cigarette smoke through a tracheal cannula was induced in cats anesthetized with pentobarbital. Smoking of tobacco cigarettes produced increased ventilation and systemic hypertension, which were found to be due to their nicotine content. Respiratory stimulation and the increase in diastolic pressure were abolished by acute section of 'buffer nerves', but the mediation of carotid nerves was more important than that of the vagi for evoking reflex hyperventilation. Tobacco smoking induced a marked increase in the frequency of chemosensory impulses recorded from the carotid nerves, an effect due to its nicotine content.

Animals↗
PubMed1976

Respiratory and circulatory reflexes induced by nicotine injections: role of carotid body chemoreceptors.

Intravenous and intracarotid injections of nicotine were delivered to cats anesthetized with pentobarbital. Low doses of nicotine were found to induce reflex hyperventilation and hypertension, mainly due to excitation of carotid body chemoreceptors. The frequency of discharge of carotid nerve chemosensory fibres was increased by nicotine in doses as low as 1 mug/kg when injected intravenously and 50 ng when injected into the carotid artery. Nicotine also activates vagal afferent fibres; some of them produce reflex excitation of the respiratory and vasomotor centres, but others provoke reflex inhibition. High doses of nicotine can act directly upon the medulla provoking acceleration or arrest of ventilation. Nicotine can also induce 'late' changes of b.p. (delay 5 sec or more) which are not mediated by the carotid or vagus nerves.

Acetylcholine↗
PubMed1975

Effects of dopamine on carotid chemo- and baroreceptors in vitro.

1. The effects of dopamine on the sensory discharges originating from arterial chemo- and baroreceptors were studied in vitro using carotid bodies or sinuses excised from anaesthetized cats and superfused with Locke's solution. 2. Intrastream injections of dopamine 10-200 mug produced a transient depression of the frequency of chemoreceptor discharges. This effect was observed in response to the first injection in eighteen out of twenty preparations. 3. The inhibitory effect of dopamine can counteract partially or totally the excitation of chemoreceptors evoked by simultaneous application of acetylcholine or cyanide. 4. This inhibitory effect of dopamine is reduced or abolished by pretreatment with dopaminergic (Spiroperidol) or alpha-adrenergic (Dibenamine) blockers. 5. In response to repeated injections of dopamine applied at short intervals, the inhibitory effect is replaced by a biphasic effect (early inhibition followed by late excitation), a late and long-lasting excitation or no changes in chemoreceptor activity. The late excitatory effects of dopamine are not blocked by dopaminergic or alpha-adrenergic blockers. 6. Noradrenaline does not affect the chemoreceptor activity of the superfused carotid body. DL-DOPA induces only a late and long-lasting excitatory effect. 7. In carotid sinus preparations, dopamine induces a weak but long-lasting increase in the frequency of baroreceptor discharges. 8. It is concluded that dopamine may play a modulatory role in the generation of chemoreceptor activity through local regulatory processes.

Acetylcholine↗
PubMed1972

Membrane potentials recorded from the mucosa of the toad's tongue during chemical stimulation.

An isolated stretch of tongue mucosa was obtained from the Chilean toad (Callyptocephalella gayi). The preparation was observed under transmitted illumination through a binocular microscope. The surface cells were impaled with micro-electrodes and different chemical agents were applied to the area. The following results were obtained.1. The surface cells had resting potentials of -6 to -40 mV (mean of -17.6 mV) with the preparation bathed in Ringer solution.2. The cells underwent depolarization by application of different salts (NaCl, NaF, KCl, Na(2)SO(4), CaCl(2) and MgCl(2)) in concentrations of 0.25-1.0 M. The potentials evoked by the salt solutions often overshot the zero membrane potential level by several millivolts. The positive-going potential change produced by application of salts was increased during hyperpolarization of the membrane by inward current and was decreased by current of the opposite sign. Application of salts during depolarization of the membrane to a certain positive level produced a negative-going potential change. The potentials evoked by different salts were about the same, qualitatively, when recordings were made from different areas of the tongue, i.e. top of the fungiform and filiform papillae, doughnut-shaped folds at the base of the fungiform papillae, areas between papillae and from the side of the tongue totally devoid of papillary structures.3. Quinine applied in concentrations of 2 x 10(-2)M did not change the resting polarization of the surface epithelial cells. However, quinine applied to cells already depolarized by outward currents induced further depolarization. When it was delivered to cells hyperpolarized by inward current the substance induced further hyperpolarization.4. Sucrose (0.5-1.0 M) did not change the membrane potential of lingual cells regardless of the level of cell polarization induced by injected currents.5. Hydrochloric, sulphuric, nitric and acetic acids produced minimal biphasic effects: a brief hyperpolarization followed by a slower secondary depolarization.6. Water increased the membrane potential of the surface cells. Salts applied at the peak of the water-evoked hyperpolarization induced cell depolarization which was much larger than that evoked during application of salts to cells bathed in Ringer solution.

Acetates↗
PubMed1968

Pharmacology of pH effects on carotid body chemoreceptors in vitro.

1. The carotid body and the carotid nerve were removed from anaesthetized cats and placed in a small Perspex channel through which Locke solution (at various pH values and usually equilibrated with 50% O(2) in N(2)) was allowed to flow. The glomus was immersed in the flowing solution while the nerve was lifted into oil covering the saline. Sensory discharges were recorded from the nerve and their frequency was used as an index of receptor activity. At times, a small segment of carotid artery, containing pressoreceptor endings, was removed together with the glomus. In this case, pressoreceptor discharges were recorded from the nerve.2. The amplitude of either chemo- or pressoreceptor discharges was not changed by strong acid solutions. Acid decreased the frequency of the baroreceptor discharges only when pH fell to less than 4.0. Solutions at low pH increased the chemosensory discharge, but acid depressed the increased chemoreceptor discharge elicited by KCl. These experiments indicated that H(+) ions probably acted as membrane ;stabilizers' without depolarizing either the nerve fibres or endings.3. Acid solutions increased the action of acetylcholine chloride (AChCl) (100-200 mug) on chemoreceptors. This effect probably was due either to inactivation of tissue cholinesterase or to enhanced sensitivity of the sensory endings to ACh.4. Choline chloride (10(-3)M), which favours ACh synthesis, protected the preparation against decay during prolonged experimentation. Hemicholinium-3 (HC-3), which blocks ACh synthesis in low concentrations (10(-5)M), depressed the chemosensory response to acid and to hypoxia when such stimuli were applied repeatedly. This concentration of HC-3 did not change effects of applied ACh.5. Substances which affect ACh release markedly changed the chemoreceptor discharge increase induced by acidity and other forms of stimulation. In the absence of Ca(2+), acid, anoxia, and interruption of flow provoked receptor depression while receptor excitation induced by ACh and KCl persisted. All stimuli excited and showed increased effectiveness as the Ca(2+) concentration was raised, but their effects declined as Ca(2+) was increased above normal values. Mg(2+) ions depressed the chemoreceptor effects induced by all these stimuli. The action of Mg(2+) was not due entirely to nerve ending block. Morphine sulphate (which decreases ACh release in other structures) also depressed the receptor response to acid and flow interruption.6. Cholinergic blocking agents such as mecamylamine, hexamethonium, atropine, dihydro-beta-erithroidine (DHE), HC-3 (10(-4)M), choline and acetylcholine (in combination with choline) depressed the effects of acid and ACh on the chemoreceptors. The effect induced by interruption of flow was depressed only by mecamylamine and DHE.7. Agents which affect the fate of released ACh, such as acetylcholinesterase and eserine salicylate, did not affect clearly the response of chemoreceptors to acid.8. The results suggest that acid stimulates chemoreceptor fibres through an indirect mechanism, viz. through increased release and/or decreased destruction of a presynaptic transmitter from the glomus cell. This transmitter is probably ACh (see following paper, Eyzaguirre & Zapata, 1968).

Acetylcholine↗
PubMed1968

The release of acetylcholine from carotid body tissues. Further study on the effects of acetylcholine and cholinergic blocking agents on the chemosensory discharge.

1. Both carotid bodies were removed from cats and placed in a small Perspex channel through which Locke solution was allowed to flow under a layer of paraffin oil. Stimulation of the upstream (;donor') organ elicited an increased sensory discharge in the downstream (;detector') preparation (Loewi effect).2. This effect was enhanced by eserine, depressed by hexamethonium and blocked by either mecamylamine or acetylcholinesterase. The Loewi effect did not disappear when chronically denervated (4 days) ;donor' carotid bodies were stimulated.3. These experiments led to the conclusion that ACh is released by the carotid body tissues (probably from the glomus cells) during stimulation and that this substance is responsible for the initiation of the chemosensory discharges.4. In single preparations the chemosensory endings proved to be very sensitive to ACh especially in the presence of eserine which, in all probability, inactivated the tissue cholinesterase. Curarizing agents such as mecamylamine, hexamethonium, (+)-tubocurarine and atropine blocked the response of the sensory endings to applied ACh in what appeared to be ;surmountable' antagonism.

Acetylcholine↗