Biomedical subjects

Lena Sundin

Publications and source records attributed to Lena Sundin.

6 recordsLinked to original sources

PubMed2005

Endothelin receptors in teleost fishes: cardiovascular effects and branchial distribution.

By observing gill blood flow using epi-illuminating microscopy, in parallel with cardiovascular recordings and immunohistochemistry, we have tried to identify the receptor mediating endothelin (ET) type 1 (ET1)-induced pillar cell contraction in the lamellae of the Atlantic cod (Gadus morhua). Intra-arterial injection of the specific ET(B) receptor agonist BQ-3020 induced dose-dependent increases in ventral aortic blood pressure, gill vascular resistance, and pillar cell area (indicating contraction). The specific ET(A) receptor antagonist BQ-610 did not prevent either pillar cell contraction or increased gill vascular resistance induced by ET-1 injection. The cardiovascular responses were corroborated by the detection of ET(B) receptor-like immunoreactivity (IR) associated with pillar cells in the lamellar region and in neuroendocrine cells. ET(B) receptor-like IR was also found lining the muscle layer of lamellar arterioles and filament arteries. In contrast, strong ET(A) receptor-like IR was found on branchial nerves throughout the filaments. In addition, ET-like IR was concentrated in neuroendocrine cells in the filament and lamellae. We also present data suggesting that ET-mediated pillar cell contraction is widespread among teleost fish, including Atlantic cod, rainbow trout (Oncorhynchus mykiss), sculpin (Myoxocephalus scorpius), and mackerel (Scomber scombrus). Taken together, our results suggest that an ET(B)-like receptor mediates pillar cell contraction in fishes, whereas ET(A)-like receptors may serve another function in the gill, inasmuch as ET(A) receptor-like IR is found on branchial nerves.

Animals↗

PubMed2004

Adenosinergic and cholinergic control mechanisms during hypoxia in the epaulette shark (Hemiscyllium ocellatum), with emphasis on branchial circulation.

Coral reef platforms may become hypoxic at night during low tide. One animal in that habitat, the epaulette shark (Hemiscyllium ocellatum), survives hours of severe hypoxia and at least one hour of anoxia. Here, we examine the branchial effects of severe hypoxia (<0.3 mg oxygen l(-1) for 20 min in anaesthetized epaulette shark), by measuring ventral and dorsal aortic blood pressure (P(VA) and P(DA)), heart rate (fh), and observing gill microcirculation using epi-illumination microscopy. Hypoxia induced a flow of blood in two parallel blood vessels, termed longitudinal vessels, in the outer borders of the free tip of the gill filament. Hypoxia also induced significant falls in fh, P(VA) and P(DA), and a biphasic change in ventilation frequency (increase followed by decrease). Adenosine injection (1 micromol kg(-1)) also initiated blood flow in the longitudinal vessels, in addition to significant drops in P(VA), P(DA) and fh, and a biphasic response in ventilation frequency (decrease followed by increase) indicating that adenosine influences ventilation. Aminophylline (10 mg kg(-1)), an A(1) and A(2) adenosine receptor antagonist, blocked the effects of adenosine injection, and also significantly reduced blood flow in the longitudinal vessels during hypoxia. In the second part of the study, we examined the cholinergic influence on the cardiovascular circulation during severe hypoxia (<0.3 mg l(-1)) using antagonists against muscarinic (atropine 2 mg kg(-1)) and nicotinic (tubocurarine 5 mg kg(-1)) receptors. Injection of acetylcholine (ACh; 1 micromol kg(-1)) into the ventral aorta caused a marked fall in fh, a large increase in P(VA), but small changes in P(DA) (suggesting increased R(gill)). Atropine was able to inhibit the branchial vascular responses to ACh but not the hypoxic bradycardia, suggesting the presence of muscarinic receptors on the heart and gill vasculature, and that the hypoxia induced bradycardia is of non-cholinergic origin. The results suggest that adenosine mediates increases in the arterio-venous circulation in the gill during hypoxia. This may serve to increase blood supply to heart and gill tissue.

Acetylcholine↗

PubMed2003

Effects of afferent input on the breathing pattern continuum in the tambaqui (Colossoma macropomum).

This study used a decerebrate and artificially-ventilated preparation to examine the roles of various afferent inputs in breathing pattern formation in the tambaqui (Colossoma macropomum). Three general breathing patterns were observed: (1) regular breathing; (2) frequency cycling and (3) episodic breathing. Under normoxic, normocapnic conditions, 50% of control fish exhibited regular continuous breathing and 50% exhibited frequency cycling. Denervation of the gills and oro-branchial cavity promoted frequency cycling. Central denervation of the glossopharyngeal and vagus nerves produced episodic breathing. Regardless of the denervation state, hyperoxia produced either frequency cycling or episodic breathing while hypoxia and hypercarbia shifted the pattern to frequency cycling and continuous breathing. We suggest that these breathing patterns represent a continuum from continuous to episodic breathing with waxing and waning occupying an intermediate stage. The data further suggest that breathing pattern is influenced by both specific afferent input from chemoreceptors and generalised afferent input while chemoreceptors specific for producing changes in breathing pattern may exist in fish.

Afferent Pathways↗

PubMed2003

Pulsatile urea excretion in the gulf toadfish: mechanisms and controls.

Opsanus beta expresses a full complement of ornithine-urea cycle (OUC) enzymes and is facultatively ureotelic, reducing ammonia-N excretion and maintaining urea-N excretion under conditions of crowding/confinement. The switch to ureotelism is keyed by a modest rise in cortisol associated with a substantial increase in cytosolic glutamine synthetase for trapping of ammonia-N and an upregulation of the capacity of the mitochondrial OUC to use glutamine-N. The entire day's urea-N production is excreted in 1 or 2 short-lasting pulses, which occur exclusively through the gills. The pulse event is not triggered by an internal urea-N threshold, is not due to pulsatile urea-N production, but reflects pulsatile activation of a specific branchial excretion mechanism that rapidly clears urea-N from the body fluids. A bidirectional facilitated diffusion transporter, with pharmacological similarity to the UT-A type transporters of the mammalian kidney, is activated in the gills, associated with an increased trafficking of dense-cored vesicles in the pavement cells. An 1814 kB cDNA ('tUT') coding for a 475-amino acid protein with approximately 62% homology to mammalian UT-A's has been cloned and facilitates phloretin-sensitive urea transport when expressed in Xenopus oocytes. tUT occurs only in gill tissue, but tUT mRNA levels do not change over the pulse cycle, suggesting that tUT regulation occurs at a level beyond mRNA. Circulating cortisol levels consistently decline prior to a pulse event and rise thereafter. When cortisol is experimentally clamped at high levels, natural pulse events are suppressed in size but not in frequency, an effect mediated through glucocorticoid receptors. The cortisol decline appears to be permissive, rather than the actual trigger of the pulse event. Fluctuations in circulating AVT levels do not correlate with pulses; and injections of AVT (at supraphysiological levels) elicit only minute urea-N pulses. However, circulating 5-hydroxytryptamine (5-HT) levels fluctuate considerably and physiological doses of 5-HT cause large urea-N pulse events. When the efferent cranial nerves to the gills are sectioned, natural urea pulse events persist, suggesting that direct motor output from the CNS to the gill is not the proximate control.

Adaptation, Physiological↗

PubMed2002

Branchial innervation.

Inspection of the dorsal end of fish gills reveals an impressive set of nerve trunks, connecting the gills to the brain. These trunks are branches of cranial nerves VII (the facial) and especially IX (the glossopharyngeal) and X (the vagus). The nerve trunks carry a variety of nervous pathways to and from the gills. A substantial fraction of the nerves running in the branchial trunks carry afferent (sensory) information from receptors within the gills. There are also efferent (motor) pathways, which control muscles within the gills, blood flow patterns and possibly secretory functions. Undertaking a more careful survey of the gills, it becomes evident that the arrangement of the microanatomy (particularly the blood vessels) and its innervation are strikingly complex. The complexity not only reflects the many functions of the gills but also illustrates that the control of blood flow patterns in the gills is of crucial importance in modifying the efficiency of its chief functions: gas transfer and salt balance. The "respiratory-osmoregulatory compromise" is maintained by minimizing the blood/water exchange (functional surface area of the gills) to a level where excessive water loss (marine teleosts) or gain (freshwater teleosts) is kept low while ensuring sufficient gas exchange. This review describes the arrangement and mechanisms of known nervous pathways, both afferent and efferent, of fish (notably teleosts) gills. Emphasis is placed primarily on the autonomic nervous system and mechanisms of blood flow control, together with an outline of the afferent (sensory) pathways of the gill arches.

Animals↗

PubMed2002

Extrabranchial chemoreceptors involved in respiratory reflexes in the neotropical fish Colossoma macropomum (the tambaqui).

In a previous study, complete denervation of the gills in the tambaqui Colossoma macropomum did not eliminate the increase in breathing amplitude seen during exposure of this species to hypoxia. The present study was designed to examine other sites of putative O(2)-sensitive receptors that could be involved in this reflex action. Superfusion of the exposed brain of decerebrate, spinalectomized fish did not reveal the presence of central chemoreceptors responsive to hyperoxic, hypoxic, hypercarbic, acidic or alkaline solutions. Subsequent central transection of cranial nerve IX and X, removing not only all innervation of the gills but also sensory input from the lateral-line, cardiac and visceral branches of the vagus nerve, did not eliminate the increase in breathing amplitude that remained following peripheral gill denervation alone. Administration of exogenous catecholamines (10 and 100 nmol kg(-1) adrenaline) to fish with intact brains and minimal surgical preparation reduced both respiratory frequency and amplitude, suggesting that humoral release of adrenaline also could not be responsible for the increase in breathing amplitude that remained following gill denervation. Denervation of the mandibular branches of cranial nerve V and the opercular and palatine branches of cranial nerve VII in gill-denervated fish (either peripheral gill denervation or central section of cranial nerves IX and X), however, did eliminate the response. Thus, our data suggest that hypoxic and hyperoxic ventilatory responses as well as ventilatory responses to internal and external injections of NaCN in the tambaqui arise from O(2)-sensitive receptors in the orobranchial cavity innervated by cranial nerves V and VII and O(2)-sensitive receptors on the gills innervated by cranial nerves IX and X. Our results also revealed the presence of receptors in the gills that account for all of the increase in ventilation amplitude and part of the increase in ventilation frequency during hyperoxic hypercarbia, a group or groups of receptors, which may be external to the orobranchial cavity (but not in the central nervous system), that contribute to the increase in ventilation frequency seen in response to hyperoxic hypercarbia and the possible presence of CO(2)-sensitive receptors that inhibit ventilation frequency, possibly in the olfactory epithelium.

Animals↗