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V M Miller

Publications and source records attributed to V M Miller.

At least 145 records · Page 8Linked to original sources
PubMed1986

Endothelium-dependent responses in isolated blood vessels of lower vertebrates.

Endothelium-dependent relaxations to acetylcholine have been identified in mammalian arteries and veins. To determine the occurrence of such relaxations in other classes of vertebrates, rings of descending aortas of turtles, cayman and bullfrogs and ventral aortas of trout were suspended for isometric force measurements. Acetylcholine and the calcium ionophore A23187 initiated concentration-dependent relaxations in aortas from cayman and bullfrogs contracted with norepinephrine. These relaxations were not affected by meclofenamate, were reversed by methylene blue and abolished by endothelium removal. Acetylcholine caused concentration-dependent contractions in aortas (with and without endothelium) from trout and turtles; these tissues contracted minimally to norepinephrine. In the aortas of the trout contracted with acetylcholine, the calcium ionophore A23187 initiated endothelium-dependent relaxations which were reversed by methylene blue and abolished by meclofenamate. A23187 contracted turtle aortas; an effect reduced by endothelium removal. These data demonstrate endothelium-dependent relaxations and contractions in blood vessels of reptiles, amphibians and teleosts. Thus, endothelium-dependent modulation of the responses of the vascular smooth muscle represents a cardiovascular regulatory mechanism which appears early in vertebrate phylogeny.

Acetylcholine↗
PubMed1985

Endothelial alpha 2-adrenoceptors in canine pulmonary and systemic blood vessels.

The present study was designed to determine whether alpha 2-adrenoceptors mediate endothelium-dependent relaxations in veins and arteries of the pulmonary and systemic vasculature of the dog. Rings of either pulmonary or femoral artery and vein with and without endothelium were suspended for isometric force measurements in a buffered salt solution (37 degrees C; gassed with 95% O2 and 5% CO2). Removal of the endothelium caused a shift to the left of the concentration-response curves to epinephrine, norepinephrine and the selective alpha 2-adrenoceptor agonist UK 14,304, but not of that to the selective alpha 1-adrenoceptor agonist phenylephrine. In the presence of alpha 1- and beta-adrenoceptor blockers, norepinephrine and UK 14,304 initiated relaxations of previously contracted rings. These relaxations were inhibited by the alpha 2-adrenoceptor antagonist, rauwolscine, and were absent in rings without endothelium. In the pulmonary artery and femoral vein, the endothelium-dependent responses to UK 14,304 were masked in part by direct alpha 2-adrenergic activation of the vascular smooth muscle.

Animals↗
PubMed1985

Heterogeneity of endothelium-dependent responses in mammalian blood vessels.

A number of naturally occurring substances can evoke endothelium-dependent responses in isolated blood vessels. In most arteries studied, acetylcholine, adenosine diphosphate (ADP), adenosine triphosphate (ATP), arachidonic acid, bradykinin, and thrombin cause endothelium-dependent relaxations. In veins, however, the endothelium-dependent inhibitory effect of acetylcholine, ATP, and thrombin often is transient and/or modest, as it is masked by the direct stimulating action of these substances on the venous smooth muscle; arachidonic acid evokes endothelium-dependent augmentation of the contractile response to norepinephrine. Aggregating platelets cause an endothelium-dependent relaxation of certain but not all arteries and veins that is probably mediated by released serotonin and ADP. The endothelium of the coronary artery may enhance the relaxations caused by catecholamines. Vasopressin causes endothelium-dependent relaxations in cerebral and coronary arteries but not in systemic blood vessels. Hypoxia causes endothelium-dependent increases in tension in systemic arteries and in pulmonary arteries and veins but not in limb veins. The heterogeneity in endothelium-dependent responsiveness may reflect variations in sensitivity of either endothelial or vascular smooth-muscle cells of different anatomical origin.

Acetylcholine↗
PubMed1985

Endothelium-dependent contractions to arachidonic acid are mediated by products of cyclooxygenase.

Arachidonic acid produces endothelium-dependent relaxation in canine arteries and endothelium-dependent contraction in veins. In canine femoral arteries, the relaxation is prevented by inhibitors of cyclooxygenase. To determine the role of cyclooxygenase in the contraction evoked by arachidonic acid in the veins, rings of canine femoral and intrapulmonary veins, with and without endothelium, were suspended in organ chambers and set at their optimum length for isometric tension measurements. In rings of femoral and pulmonary vein contracted with norepinephrine, arachidonic acid produced a concentration-dependent increase in tension that was eliminated by removal of the endothelium or by treatment with the inhibitors of cyclooxygenase (indomethacin, meclofenamate, or acetylsalicyclic acid). The contractions were not prevented by inhibitors of thromboxane synthetase or prostacyclin synthetase or lipoxygenase. Pulmonary and femoral veins with or without endothelium relaxed to low, but contracted to high concentrations of prostacyclin and prostaglandin E2. Prostaglandin F2 alpha caused endothelium-independent contractions in both blood vessels. The present study suggests that the endothelium-dependent contractions to arachidonic acid observed in canine veins are mediated by prostanoids other than thromboxane and prostacyclin.

Animals↗
PubMed1980

Spatial correlates of hippocampal unit activity are altered by lesions of the fornix and endorhinal cortex.

Behavioral and electrophysiological evidence supports the role of the hippocampus in the processing of spatial information. In the present study, neuronal activity recorded from chronically implanted hippocampal microelectrodes was correlated with a rat's spatial orientation while traversing a radial maze for food reward. Place units were found in all fields of the dorsal hippocampus and dentate gyrus. Rotation of the maze relative to extramaze cues failed to disrupt the intact animal's spatial task performance of the spatial correlates of the unit activity. Lesions of the fornix or entorhinal cortex disrupted performance of the task. Unit activity correlated to the animal's spatial orientation was also disrupted by either lesion. There was no correlation between the disruption of the unit activity and location of the unit within hippocampal fields. Unit activity from lesioned animals showed correlation to the physical properties of the maze rather than to the orientation of the maze in space. These results further support the role of the hippocampus in the processing of spatial information.

Animals↗
PubMed1979

Spinal cord, hypothalamic, and air temperature: interaction with arousal states in the marmot.

Yellow-bellied marmots, Marmota flaviventris, prepared with U-shaped thermodes in the epidural space of the thoracic vertebral canal, a thermode in the preoptic hypothalamus, and cortical surface and hippocampal electrodes, were used to investigate the interaction of arousal states with temperature regulation. It was found that arousal state of the animal influences the thermoregulatory responses initiated in either the spinal cord or hypothalamus. Further, changes in ambient temperature affected both the gain and the threshold of these responses. The interaction of the hypothalamus and spinal cord was not an additive function, however the threshold for shivering of each could be altered by temperature manipulation of the other. Future studies in modeling of temperature regulation should consider the contributions of temperature receptors of the spinal cord and the arousal state of the animal during the stimulation period.

Animals↗