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Biomedical subjects

S F Perry

Publications and source records attributed to S F Perry.

At least 73 records · Page 4Linked to original sources
PubMed1998

Pulsatile urea excretion in gulf toadfish (Opsanus beta): evidence for activation of a specific facilitated diffusion transport system.

When toadfish are made ureotelic by a crowding/confinement protocol, they excrete approximately 90 % of their urea nitrogen (urea-N) production in large, irregular pulses (1-2 pulses per day) from the gill region. We investigated three hypotheses as to the mechanism of pulsatile excretion: (i) the presence of an active reabsorptive 'back-transport' mechanism that is periodically inhibited to allow urea-N excretion to occur; (ii) the periodic occurrence of a generalized, non-specific increase in gill permeability; and (iii) the presence of a specific facilitated diffusion transport system that is periodically activated. Exposure of toadfish during non-pulse periods to treatments designed to block a 'back-transport' mechanism (Na+-free sea water or the urea analogues 30 mmol l-1 thiourea or 30 mmol l-1 acetamide in the external water) did not stimulate a leakage of urea-N, thereby opposing the first hypothesis. The second hypothesis was opposed by several results. Neither injection of the potent branchial vasodilator L-isoprenaline (10(-5) mol l-1) nor infusion of NH4Cl, the latter at levels known to stimulate urea-N efflux in perfused gills, had any effect on urea-N excretion. Furthermore, during natural pulse events, when the normally very low gill permeability to urea (3x10(-7) cm s-1) increased at least 35-fold, there was no accompanying increase in permeability to either 3H2O (1.5x10(-5) cm s-1) or the paracellular marker [14C]PEG-4000 (10(-8) cm s-1). However [14C]thiourea permeability (1.5x10(-7) cm s-1) increased approximately fivefold, in support of the third hypothesis. Furthermore, when 30 mmol l-1 urea was placed in the external water, a concentration (60 000 micromol-N l-1) approximately three times that of blood (20 000 micromol-N l-1), each efflux pulse event (measured with [14C]urea) was accompanied by a net uptake, such that blood urea-N levels rose rather than fell. A proportional 1:1 relationship between influx per unit external concentration and efflux per unit internal (i.e. plasma) concentration indicated a fully bidirectional transport system. The simultaneous presence of 60 mmol l-1 thiourea in the external water inhibited the influx component by 73 %, further supporting this conclusion. These data, together with recent molecular, morphological and endocrinological evidence, strongly suggest that pulsatile urea-N excretion is caused by the periodic activation of a facilitated urea transporter in the gills, similar to the vasopressin-regulated urea transporter in the mammalian kidney.

Animals↗
PubMed1997

Strychnine eliminates reciprocation and augmentation of respiratory bursts of the in vitro frog brainstem.

We have recorded rhythmic bursts of efferent action potentials from nerves of respiratory muscles in the frog (Rana pipiens), using a modified in vitro preparation, in which the brainstem lies in situ in the ventral half of the skull. The burst in the sternohyoid branch of the hypoglossal nerve (Hsh) was augmenting, and alternated with a relatively brief augmenting burst in the main branch of the hypoglossal nerve (Hm). The laryngeal branch of the vagus nerve (XI) displayed a biphasic burst, beginning before peak activity of Hsh and spanning the Hm burst. The spatio-temporal patterns of these bursts closely resemble those recorded from the same nerves in intact and in decerebrate frogs, indicating that the bursting rhythm of this in situ preparation constitutes fictive breathing. The nature of neurotransmission responsible for burst reciprocity and augmentation was investigated by applying the glycine receptor blocker, strychnine. Low levels of strychnine (1 and 5 M) increased the frequency of fictive breathing without changing the shape or timing of Hsh, Hm and XI bursts; at higher doses (10 and 20 M) the bursts in all nerves abruptly changed shape and timing to become synchronous and decrementing. The strychnine-induced changes were associated with the appearance of a prominent peak (10-20 Hz) on the spectral analysis of the nerve discharge, possibly indicating a fundamental change in neurogenesis of the respiratory pattern. We conclude that the burst augmentation and reciprocation discharge characteristics of fictive breathing in the frog require strychnine-sensitive inhibitory networks.

Animals↗
PubMed1997

Laryngeal motor control in frogs: role of vagal and laryngeal feedback.

Using decerebrate frogs (Rana catesbeiana), we investigated the role of vagal and laryngeal sensory feedback in controlling motor activation of the larynx. Vagal and laryngeal nerve afferents were activated by electrical stimulation of the intact vagal and laryngeal nerves. Pulmonary afferents were activated by lung inflation. Reflex responses were recorded by measuring efferent activity in the laryngeal branch of the vagus (Xl) and changes in glottal aperture. Two glottic closure reflexes were identified, one evoked by lung inflation or electrical stimulation of the main branch of the vagus (Xm), and the other by electrical stimulation of Xl. Lung inflation evoked a decrementing burst of Xl efferent activity and electrical stimulation of Xm resulted in a brief burst of Xl action potentials. Electrical stimulation of Xl evoked a triphasic mechanical response, an abrupt glottal constriction followed by glottal dilatation followed by a long-lasting glottal constriction. The first phase was inferred to be a direct (nonreflex) response to the stimulus, whereas the second and third represent reflex responses to the activation of laryngeal afferents. Intracellular recordings of membrane potential of vagal motoneurons of lung and nonlung types revealed EPSPs in both types of neurons evoked by stimulation of Xm or Xl, indicating activation of glottal dilator and constrictor motoneurons. In summary, we have identified two novel reflexes producing glottic closure, one stimulated by activation of pulmonary receptors and the other by laryngeal receptors. The former may be part of an inspiratory terminating reflex and the latter may represent an airway protective reflex.

Action Potentials↗
PubMed1997

The chloride cell: structure and function in the gills of freshwater fishes.

This review focuses on the structure and function of the branchial chloride cell in freshwater fishes. The mitochondria-rich chloride cell is believed to be the principal site of trans-epithelial Ca2+ and Cl- influxes. Though currently debated, there is accruing evidence that the pavement cell is the site of Na+ uptake via channels linked electrically to an apical membrane vacuolar H(+)-ATPase (proton pump). Chloride cells perform an integral role in acid-base regulation. During conditions of alkalosis, the surface area of exposed chloride cells is increased, which serves to enhance base equivalent excretion as the rate of Cl-/HCO3- exchange is increased. Conversely, during acidosis, the chloride cell surface area is diminished by an expansion of the adjacent pavement cells. This response reduces the number of functional Cl-/HCO3- exchangers. Under certain conditions that challenge ion regulation, chloride cells proliferate on the lamellae. This response, while optimizing the Ca2+ and Cl- transport capacity of the gill, causes a thickening of the blood-to-water diffusion barrier and thus impedes respiratory gas transfer.

Acid-Base Equilibrium↗
PubMed1997

Angiotensins stimulate catecholamine release from the chromaffin tissue of the rainbow trout.

Immunohistochemical and pharmacological techniques were utilized to investigate the relationships between angiotensins and catecholamine release from the chromaffin tissue of rainbow trout (Oncorhynchus mykiss). Double labeling with [Asp1, Ile5]angiotensin II-fluorescein isothiocyanate (ANG II-FITC) and anti-dopamine beta-hydroxylase revealed specific ANG II binding sites on chromaffin cells. Injection (1 nmol/kg body wt) of either ANG II-FITC, [Asn1, Val5, Asn9]ANG I, [Asp1, Ile5, His9]ANG I, [Asn1, Val5]ANG II, [Asp1, Val5]ANG II, or [Asp1, Ile5]ANG II elicited catecholamine release from in situ perfusion preparations of the head kidney. Catecholamine release elicited by [Asn1, Val5]ANG II (10(-13) to 10(-7) mol/kg body wt) was dose dependent, and the secretion of epinephrine (Epi) was greater than that of norepinephrine (NE). Relative to the results obtained with the [Asn1, Val5]ANG II treatment (1 nmol/kg body wt), Epi release was 72 and 82% lower in response to injections (1 nmol/kg body wt) of [Asn1, Val5]ANG I [amino acid (AA) positions 1-7] and [Asn1, Val5]ANG I (AA 1-6), respectively. Pretreatment with either losartan (10(-5) M), PD-123319 (10(-5) M), or hexamethonium (10(-3) M) had no effect on [Asn1, Val5]ANG II-elicited catecholamine release. Pretreatment with captopril (10(-4) M) significantly reduced [Asn1, Val5, Asn9]ANG I-elicited Epi and NE release and decreased basal catecholamine release. These results provide direct evidence that angiotensins can elicit catecholamine release from the chromaffin tissue via specific ANG II binding sites and indicate that the synthesis of ANG II may be either local or systemic.

Angiotensin I↗
PubMed1996

Bicarbonate permeability and immunological evidence for an anion exchanger-like protein in the red blood cells of the sea lamprey, Petromyzon marinus.

Physiological and immuno-blotting experiments were used to determine whether the red blood cell membrane of a primitive vertebrate, the sea lamprey Petromyzon marinus, contained a counterpart similar to the vertebrate anion exchange protein known as AE1 or band 3. Results of the physiological experiments which measured CO2 production after adding H14CO3- to the extracellular saline, indicated significant transmembrane bicarbonate movement in lamprey blood which unlike that in most vertebrates, was insensitive to inhibition by 4,4' diisothiocyanatostilbene-2,2' disulfonic acid. The present study also showed that lamprey red blood cells possess acetazolamide-sensitive carbonic anhydrase which is an important component of CO2 production by vertebrate red blood cells. Polyclonal immunoglobulins against a 12 amino acid domain in the C-terminus of the mouse AE1 recognized a trout red blood cell membrane protein with a relative molecular mass of 97 kDa, but failed to immunoreact with any membrane proteins from the red blood cells of lamprey. Antibodies against trout AE1 immunoreacted with trout red blood cell membrane proteins of approximately 97 kDa, 200 kDa and > 200 kDa. Interestingly, only a 200-kDa membrane protein from the red blood cells of the primitive lamprey immunoreacted with the trout anti-AE1 immunoglobulin proteins. Therefore, lamprey red blood cells appear to possess an AE1-like protein that may be physiologically different than that in most other vertebrates.

Animals↗
PubMed1996

Modulation of catecholamine storage and release by the pituitary-interrenal axis in the rainbow trout, Oncorhynchus mykiss.

This study examined the effects of pituitary-interrenal hormones on catecholamine storage and release in the rainbow trout Oncorhynchus mykiss. An extract of trout pituitary elicited the release of adrenaline, but not noradrenaline, using an in situ perfusion preparation. A variety of doses of adrenocorticotropic hormone (2-2000 mU) caused the release of both catecholamines in situ which was unaffected by pre-treatment with the ganglion blocker, hexamethonium, or the serotonergic receptor antagonist, methysergide, but was abolished in calcium-free media. Intra-arterial injections of adrenocorticotrophic hormone in vivo caused an elevation of plasma adrenaline but not noradrenaline levels. Injections of cortisol in situ did not elicit catecholamine release. Trout given an intraperitoneal implant of cortisol (50 mg.kg-1 body weight) had significantly higher plasma cortisol concentrations when compared to controls after 7 days of implantation. Increases in the levels of stored catecholamines were observed in various regions of the kidney and posterior cardinal vein following 3 and 7 days of cortisol treatment. The ability of the chromaffin cells to release catecholamines in response to cholinergic stimulation was assessed in situ after 7 days of treatment. Basal (non-stimulated) adrenaline outflowing perfusate levels were greater in the cortisol-treated fish. Cortisol treatment increased the responsiveness of the catecholamine release process to low doses of the cholinoceptor agonist carbachol. Three or 7 days of cortisol treatment did not alter the in vitro activity of the enzyme phenylethanolamine-N-methyl transferase. The results of this study demonstrate that interactions within the pituitary-adrenal axis can influence both catecholamine storage and release in the rainbow trout.

Adrenocorticotropic Hormone↗
PubMed1996

The effects of soft-water acclimation on gill structure in the rainbow trout Oncorhynchus mykiss.

Rainbow trout (Oncorhynchus mykiss) were exposed to ion-poor (soft) water to test the hypothesis that naturally induced proliferation of branchial chloride cells causes a thickening of the blood-to-water diffusion barrier. This was achieved by using a combination of scanning and transmission electron-microscopic techniques. Fish were exposed to soft-water conditions ([Na+]= 0.055 mmol l-1, [Cl-] approximately 0.029 mmol 1(-1), [Ca2+] approximately 0.059 mmol 1(-1), and [K+] approximately 0.007 mmol 1(-1)) for 1, 2, and 4 weeks. Marked chloride cell proliferation was evident at all sampling times with an approximate doubling of the gill epithelial surface area covered by chloride cells exposed to the water ("chloride cell fractional area"). The increases in chloride cell fractional area resulted from both increased numbers of cells and expanded apical surfaces of exposed individual cells. As a result of chloride cell proliferation, soft-water exposure was associated with a doubling of the lamellar blood-to-water diffusion distance from 3.26+/-0.08 microM to 6.58+/-0.43 microM as determined from transmission electron micrographs. These data demonstrated a positive correlation between chloride cell fractional area and blood-to-water diffusion distance. We conclude that, in trout, chloride cell proliferation during soft-water exposure, while presumably benefiting ionic regulation, may impair gas transfer owing to the associated thickening of the blood-to-water diffusion barrier.

Acclimatization↗
PubMed1996

Effect of haemoglobin oxygenation on Bohr proton release and CO2 excretion in the rainbow trout.

CO2 excretion in trout is dependent upon the Haldane effect and the release of protons (Bohr protons) from haemoglobin during oxygenation of the blood. Oxygenation of whole blood from trout in vitro, resulted in a non-linear release of Bohr protons over the haemoglobin-oxygen (Hb-O2) equilibrium curve, where the majority of Bohr protons were released between 60 and 100% of Hb oxygen saturation (SO2). Oxygenation of the blood over this region of the Hb-O2 equilibrium curve elevated the HCO3- flux rate across the HCO3-/CI- exchanger on the red cell membrane by about 30% during CO2 excretion in vitro. Oxygenation of the Hb between 0 and 60% SO2 did not elevate CO2 excretion rate in vitro. These data indicate that utilization of different regions of the Hb-O2 dissociation curve in trout in vivo will influence CO2 excretion by altering the rate of HCO3- entry into the red cell during gill blood transit.

Animals↗
PubMed1995

Fictive respiratory rhythm in the isolated brainstem of frogs.

Spontaneous rhythmically bursting activity was recorded from the trigeminal, vagal and hypoglossal nerve roots of the isolated brainstem from the frogs Rana catesbeiana and Rana pipiens superfused with a bicarbonate-free HEPES-buffer solution. Burst frequency, burst duration and the activity profile of the spontaneous neural discharges in vitro resembled those of a less radical preparation, the decerebrate, fictively breathing frog. After complete midsagittal section, each half of the isolated brainstem generated its own rhythmic neural activity which resembled that of the intact isolated brainstem. The spontaneous activity generated within each half of the brainstem is probably coordinated by decussating axons or by groups of neurons located along the midline of the brainstem Our results suggest that these coordinating entities extend the length of the brainstem (in a rostro-caudal dimension) and the degree of contact rather than the location of the contact between the two halves of the brainstem determines the synchronization of the right and left halves. Burst frequency of both the intact and hemisected brainstem preparation was decreased by alkaline challenge and increased by acid challenge. We conclude that this endogenous rhythmic activity represents the efferent motor output underlying lung ventilation in these animals.

Animals↗
PubMed1995

Two regions in the isolated brainstem of the frog that modulate respiratory-related activity.

Using microinjection techniques, we have explored the isolated, complete midline sectioned brainstem of the frog (Rana catesbeiana) to identify regions that influence the endogenous respiratory-related motor activity. Ten-nanoliter injections of lidocaine (1%), GABA (100mM) and glutamate (10 and 100 mM) into discrete regions of the rostral and the caudal brainstem produced different effects on the phasic neural discharge. In the rostral site lidocaine, GABA and glutamate injections altered neural burst frequency with little or no effect on burst amplitude. In the caudal site, responses to lidocaine and GABA injections consisted primarily of decreases in neural burst amplitude, often, but not always associated with minor decreases in burst frequency. In the same region, the response to glutamate was characterized by a temporary interruption of the rhythmic neural burst activity. The largest responses to substance injection in both regions were obtained at sites ranging between 200 and 500 microns from the ventral surface, in the ventral medullary reticular formation. The results reveal the existence of two areas in the frog brainstem that influence respiratory motor output, one related to the respiratory burst frequency and the other related to the amplitude of the motor output.

Animals↗
PubMed1995

Cholinoceptor-mediated control of catecholamine release from chromaffin cells in the American eel, Anguilla rostrata.

The cholinergic agonist-induced secretion of catecholamines from chromaffin cells in the American eel, Anguilla rostrata, was assessed using a saline-perfused posterior cardinal vein preparation. Direct membrane depolarization with 60 mmol.l-1 K+ caused a significant release of catecholamines (adrenaline+noradrenaline) into the perfusate which was unaffected by pre-treatment with the ganglion blocker, hexamethonium (final concentration = 10(-3) mol.l-1). The nicotinic receptor agonist, 1,1-dimethyl-4-phenyl-piperazinium iodide, evoked catecholamine release in response to several doses exceeding 10(-7) mol; at 10(-5) mol the response was abolished by pre-treatment with the ganglion blocker, hexamethonium (final concentration = 10(-3) mol.l-1). The muscarinic receptor agonist, pilocarpine, did not elicit catecholamine release in response to any of the doses administered (10(-8)-10(-4) mol). A single injection of the mixed nicotinic/muscarinic cholinoceptor agonist, carbachol (10(-5) mol), caused the release of catecholamines which was abolished by pre-treatment with hexamethonium but which was unaffected by pre-treatment with the muscarinic receptor antagonist atropine (final concentration = 10(-5) mol.l-1). The results of this study indicate that the process of cholinergic agonist-induced catecholamine secretion from the chromaffin cells in the American eel is mediated exclusively by activation of nicotinic receptors with no involvement of the muscarinic receptor.

Animals↗
PubMed1994

Neural organization of the ventilatory activity in the frog, Rana catesbeiana. I.

In order to elucidate the neural basis for lung ventilation in the frog, we have investigated the efferent neural activity to oropharyngeal muscles in the decerebrate, paralyzed, unanesthetized bullfrog, Rana catesbeiana. Efferent motor output was recorded from the mandibular branch of the trigeminal (Vmd), the laryngeal branch of the vagus (Xl), and the main and sternohyoid branches of the hypoglossal nerve (Hm and Hsh, respectively). Two types of rhythmic bursting outputs were observed: (1) a high-frequency, low-amplitude, reciprocal oscillation between Vmd, a buccal levator nerve, and Hsh, a buccal depressor nerve; and (2) a low-frequency, high-amplitude, synchronous bursting of Vmd, Hm, Hsh, and Xl. The first type is inferred to represent fictive oropharyngeal ventilation. The second type of burst was divided into four intervals: (a) augmenting activity of Hsh; (b) activation of Xl with continued activation of Hsh; (c) activation of Vmd and Hm (a buccal levator nerve), continued activation of Xl, and termination of Hsh activity; and (d) warning activity in Vmd and Hm associated with a prominent second wave in Xl. This coordinated activity is inferred to represent fictive pulmonary ventilation because the neurograms in these four intervals correspond closely to EMGs and neurograms recorded in the intact frog during the four phases of pulmonary ventilation, namely, buccal depression, pulmonary expiration, pulmonary inspiration, and glottal closure. Hypercapnia, vagotomy, and cutaneous pinching enhanced the high-amplitude, low-frequency rhythm, but not the low-amplitude, high-frequency oscillation. Lung inflation generally inhibited the former and not the latter, but in some cases lung inflation stimulated pulmonary ventilation. We conclude that oropharyngeal and pulmonary ventilation of the frog are produced by one or, possibly, two intrinsically active generators.

Animals↗
PubMed1994

Cholinergic control of stanniocalcin release in the rainbow trout, Oncorhynchus mykiss, and the American eel, Anguilla rostrata.

An in vivo whole animal 45Ca influx bioassay was used to study the cholinergic control of the release of stanniocalcin (STC) in the rainbow trout (Oncorhynchus mykiss) and the American eel (Anguilla rostrata). In both species calcium influx (JinCa2+) was lowered in response to hypercalcemia induced by intravascular (trout) or intraperitoneal (eel) injections of CaCl2. In trout, this response was blocked by the cholinergic antagonist atropine (0.25 mumol kg-1) and mimicked by the cholinoceptor agonist carbachol (0.25 mumol kg-1). These observations are consistent with a cholinergic stimulation of STC release in response to hypercalcemia in trout. In eels, pretreatment with atropine did not block the lowering of JinCa2+ in response to hypercalcemia. This suggests that cholinergic stimulation is not obligatory for stanniocalcin release in eels. However, carbachol treatment did elicit STC release as revealed by the lowering of JinCa2+. This response to carbachol was not observed in stanniectomized eels. Thus, in the American eel it appears that there is a potential for cholinergic control of STC release but that other factors such as the local plasma calcium concentration may also be involved, at least in response to severe acute hypercalcemia.

Anguilla↗
PubMed1994

Acid-base disequilibrium in the arterial blood of rainbow trout.

An extracorporeal blood circulation and a stopflow technique were used to examine the acid-base status of arterial blood in the rainbow trout, Oncorhynchus mykiss. Arterial blood was routed from the coeliac artery through an external circuit in which pH (pHa), partial pressure of oxygen (PaO2) and partial pressure of carbon dioxide (PaCO2) were monitored continuously. The stopflow condition was imposed by turning off the pump which drove the external loop. A radioisotopic CO2 excretion assay was performed on blood samples collected periodically to evaluate plasma carbonic anhydrase (CA) activity and hence red blood cell (rbc) lysis. An acid-base disequilibrium was found in the post-branchial blood; pHa increased by 0.04-0.06 units, and PaCO2 by 0.03-0.10 Torr, during the stopflow period. The disequilibrium appeared to arise primarily from the slow (uncatalyzed) rate of plasma H2CO3 dehydration. This was confirmed by the intra-arterial injection of bovine CA (22 mg kg-1) prior to the stopflow; the disequilibrium was abolished. When the CA inhibitor acetazolamide (30 mg kg-1) was injected, a negative pH disequilibrium of 0.04 units, accompanied by a rise in PaCO2 of 0.57 Torr, was observed during the stopflow. These results can be explained by the acetazolamide-induced inhibition of rbc CA, which leads to continuing rbc CO2 "excretion" in the post-branchial blood.

Acetazolamide↗
PubMed1994

Fetal lung growth. Influence of pulmonary arterial flow and surgery in sheep.

Aberrant pulmonary arterial flow has been associated with pulmonary hypoplasia, which is a common cause of death in newborns. The current experiments were designed to confirm whether interruption of postductal main pulmonary artery (MPA) flow causes pulmonary hypoplasia. In addition, the effect of fetal surgery on lung growth was investigated. Fetal sheep, instrumented at 107 to 115 d gestation (MPA ligated [n = 5], sham operated [n = 3], and monitored [no thoracotomy, n = 5]), and unoperated twin fetuses (140-d controls, n = 5) were used for analysis of lung growth at 136 to 140 d gestation. Morphometric measurement of lung tissue volumes and assays of DNA, protein, and saturated phosphatidylcholine (SPC) were used to assess lung growth. MPA ligation significantly decreased lung growth and maturation as indicated by decreased surface area and volumes of fine nonparenchyma, future airspace, and parenchymal tissue, and by decreased lung weights, total DNA, protein, and SPC content. There was a significant increase in the volume percentage of coarse nonparenchyma and a decrease in the volume percentage of future airspace. The pattern of lung growth after MPA ligation suggests that growth of peripheral airspace and parenchymal tissue components does not occur, resulting in a significant decrease in the amount of new tissue formed and delayed tissue maturation. Fetal surgery significantly changed only DNA, protein, and SPC content. Studies of the regulation of lung growth must consider the role of pulmonary arterial flow and the smaller, but significant effects of fetal surgery.

Analysis of Variance↗