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At least 1,243 records · Page 69Linked to original sources
PubMed1984

Differentiation of algal chemoreceptors. A comparative receptor study with two seaweed pairs: Cutleria multifida/Syringoderma phinneyi and Desmarestia aculeata/Ectocarpus siliculosus (Phacophyceae).

Gamete encounter in the reproduction of brown algae is supported by lures produced by the female cells. These signals are low-molecular-mass, volatile, olefinic hydrocarbons. Specific receptors on the motile male gametes recognize the pheromones at threshold concentrations as low as 6.5 pmol/l. The pheromones are possibly bound by dispersion and dipolar interactions. Tight fitting has to compensate for these weak contact forces. This causes strong chiral discrimination (relative affinities to enantiomeric lures 1:100). Structurally related messengers with identical substitution patterns and overall space filling are mutually distinguished in several species by means of altered topologies in their receptor mould. Responses to systematically varied synthetic bis-alkenyl-cyclopentene pheromones showed that the sensors of Syringoderma and Cutleria androgametes consist of a mosaic of attachment sites individually adapted to specific structural elements in the messenger molecule. They may be permutated to afford optimal binding. An alternative strategy: distinct reading of electron density combined with variation of sensitivity, brings about 'fidelity' in signal transmission by the alkylated cycloheptadiene pheromones in two species of Desmarestia and Ectocarpus. Inhibition of chemotaxis by ectocarpene is observed in Ectocarpus males in the presence of desmarestene, the lure of Desmarestia, and related parapheromones. This indicates complex interactions between different species of algae sharing a common habitat, in their defense of living space.

Animals↗
PubMed1991

Cardiac chemoreceptors: pharmacological curiosities or physiological tools?

1. We have tested in unanaesthetized rabbits two hypotheses regarding a physiological role for cardiogenic chemoreflexes in acute central hypovolaemia. 2. In rabbits, the sympathoinhibitory phase of acute central hypovolaemia depends on the activation of a brain-stem delta-opioid receptor mechanism by a signal from the heart. Blockade of this by fourth ventricular injection of the delta-receptor antagonist ICI 174864 had no effect on the reflex haemodynamic responses to left atrial phenylbiguanide or intrapericardial nicotine. 3. Intravenous administration of the 5-HT3 receptor antagonist MDL 72222, or intrapericardial administration of the nicotinic ganglionic cholinoceptor antagonist mecamylamine HCl, had no effect on the haemodynamic response to acute central hypovolaemia. 4. We conclude that phenylbiguanide-sensitive myocardial afferents and nicotine-sensitive epicardial afferents play no part in the response to acute hypovolaemia in rabbits, and that the reflex effects evoked by chemically exciting these afferents do not depend on a brain-stem delta-opioid mechanism.

Afferent Pathways↗
PubMed2000

An oxygen-, acid- and anaesthetic-sensitive TASK-like background potassium channel in rat arterial chemoreceptor cells.

The biophysical and pharmacological properties of an oxygen-sensitive background K+ current in rat carotid body type-I cells were investigated and compared with those of recently cloned two pore domain K+ channels. Under symmetrical K+ conditions the oxygen-sensitive whole cell K+ current had a linear dependence on voltage indicating a lack of intrinsic voltage sensitivity. Single channel recordings identified a K+ channel, open at resting membrane potentials, that was inhibited by hypoxia. This channel had a single channel conductance of 14 pS, flickery kinetics and showed little voltage sensitivity except at extreme positive potentials. Oxygen-sensitive current was inhibited by 10 mM barium (57% inhibition), 200 microM zinc (53% inhibition), 200 microM bupivacaine (55% inhibition) and 1 mM quinidine (105 % inhibition). The general anaesthetic halothane (1.5%) increased the oxygen-sensitive K+ current (by 176%). Halothane (3 mM) also stimulated single channel activity in inside-out patches (by 240%). Chloroform had no effect on background K+ channel activity. Acidosis (pH 6.4) inhibited the oxygen-sensitive background K+ current (by 56%) and depolarised type-I cells. The pharmacological and biophysical properties of the background K+ channel are, therefore, analogous to those of the cloned channel TASK-1. Using in situ hybridisation TASK-1 mRNA was found to be expressed in type-I cells. We conclude that the oxygen- and acid-sensitive background K+ channel of carotid body type-I cells is likely to be an endogenous TASK-1-like channel.

Acidosis↗
PubMed2001

Low-dose acetazolamide reduces CO(2)-O(2) stimulus interaction within the peripheral chemoreceptors in the anaesthetised cat.

1. Using the technique of end-tidal CO(2) forcing, we measured the effect of the carbonic anhydrase inhibitor acetazolamide (4 mg kg(-1), I.V.) on the CO(2) sensitivities of the peripheral and central chemoreflex loops both during hyperoxia and hypoxia in 10 cats anaesthetised with alpha-chloralose-urethane. 2. In the control situation, going from hyperoxia (arterial P(O2) (P(a,O2)) 47.40 +/- 3.62 kPa, mean +/- S.D.) into moderate hypoxia (P(a,O2) 8.02 +/- 0.30 kPa) led to an almost doubling of the peripheral CO(2) sensitivity (S(P)): a rise from 0.09 +/- 0.07 to 0.16 +/- 0.06 l min(-1) kPa(-1). After acetazolamide, however, lowering the P(a,O2) from 46.95 +/- 5.19 to 8.02 +/- 0.66 kPa did not result in a rise in S(P), indicating the absence of a CO(2)-O(2) stimulus interaction. 3. In hypoxia, acetazolamide reduced S(P) from 0.16 +/- 0.06 to 0.07 +/- 0.05 l min(-1) kPa(-1). In hyperoxia, however, the effect on S(P) was much smaller (an insignificant reduction from 0.09 +/- 0.07 to 0.06 +/- 0.05 l min(-1) kPa(-1)). 4. Acetazolamide reduced both the hyperoxic and hypoxic sensitivities (S(C)) of the central chemoreflex loop: from 0.45 +/- 0.16 to 0.27 +/- 0.13 l min(-1) kPa(-1) and from 0.40 +/- 0.16 to 0.26 +/- 0.13 l min(-1) kPa(-1), respectively. In hyperoxia, the apnoeic threshold B (X-intercept of the ventilatory CO(2) response curve) decreased from 2.91 +/- 0.57 to 0.78 +/- 1.9 kPa (P = 0.005). In hypoxia, B decreased from 1.59 +/- 1.22 to -0.70 +/- 2.99 kPa (P = 0.03). 5. Because acetazolamide abolished the CO(2)-O(2) interaction, i.e. the expected increase in S(P) when going from hyperoxia into hypoxia, we conclude that the agent has a direct inhibitory effect on the carotid bodies. The exact mechanism by which the agent exerts this effect will remain unclear until more detailed information becomes available on the identity of the carbonic anhydrase iso-enzymes within the carotid bodies and their precise subcellular distribution.

Acetazolamide↗
PubMed1981

Enkephalin receptors in the emetic chemoreceptor trigger zone of the dog.

1 The emetic action of Met-enkephalin, morphine and naloxone was studied following their administration into the cerebral ventricles of dogs through chronically implanted cannulae and the effect on the responses of ablating the chemorceptor trigger zone (CTZ) was investigated. The opiate antagonist, naloxone, was used to determine the role of enkephalin receptors in emetic responses.2 Administration of Met-enkephalin (1.0 mug/kg) into the IVth ventricle regularly evoked emesis with an average latency of 35 s. A dose of morphine (2.5 mug/kg) which was five times larger was required for a consistent emetic response when introduced into the lateral cerebral ventricle (i.c.v.) as compared to the dose required by the IVth ventricular route. The latency of emetic responses by the latter route of injection of morphine was shorter. This is in accord with an action of morphine on the emetic CTZ.3 After bilateral ablation of the CTZ, intraventricular injections of Met-enkephalin and morphine failed to produce emesis even when given in doses that were 5 to 10 times the dose which regularly elicited emesis in animals with intact CTZ. The emesis produced in dogs by intraventricular Met-enkephalin and morphine is thus fully accounted for by an action on the CTZ.4 Naloxone (i.c.v.) in doses up to 10.0 mug/kg did not cause emesis. However, higher doses of naloxone elicited dose-dependent emesis in dogs. The 100% emetic dose of naloxone was found to be 160 mug/kg and the latency of emesis was 180 s. Unlike Met-enkephalin and morphine, naloxone continued to elicit emesis in CTZ-ablated animals.5 Pretreatment with intraventricular naloxone (1 to 8 mug/kg) blocked the emetic responses induced by intraventricular Met-enkephalin and morphine but not that to apomorphine. The selective protective action of the opiate antagonist against Met-enkephalin and morphine supports the presence of enkephalin receptors in the emetic CTZ.

Animals↗
PubMed1997

The role of carotid chemoreceptors in the effects of hypoxia on renal blood flow in the late gestation sheep fetus.

Previous studies of the effect of hypoxia on fetal renal haemodynamics have demonstrated a fall, a rise or no change in renal blood flow (RBF). The underlying mechanisms are not understood but involve a balance between neural vasoconstrictor and opposing vasodilator mechanisms. Since carotid chemoreflex mechanisms contribute to vasoconstriction in other fetal vascular beds and in the adult renal vasculature, we examined their effects on RBF during 1 h of acute hypoxia in late gestation fetal sheep (n = 12). Renal blood flow was measured continuously and urine collected at 15 min intervals. Seven fetuses underwent bilateral section of the carotid sinus nerves (CSD fetuses). During hypoxia CSD fetuses showed a transient initial rise in RBF (P < 0.05) and then a subsequent fall (P < 0.05) to levels comparable with that recorded in intact fetuses. There was no change in urine output in either intact or CSD fetuses during hypoxia. Thus the initial fall in RBF during hypoxia is a carotid chemoreflex but other mechanisms, e.g. vasoconstrictor hormones, contribute to the sustained response.

Animals↗