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O Carrier

Publications and source records attributed to O Carrier.

At least 37 records · Page 2Linked to original sources

The influence of reserpine on the responsiveness to norepinephrine and electrolyte contents of rabbit atria.

This study was designed to investigate the relationships between reserpine-induced supersensitivity and electrolyte levels in isolated rabbit atria. Atria from reserpine-treated (1, 3 or 4 mg/kg 24 hr before) and untreated rabbits were placed in an isolated organ bath for determination of dose-response relationships for norepinephrine, or were used for electrolyte assay. Reserpine-treated atria had greater resting and maximum rates of beat than did untreated atria. However, the ED50 concentrations of norepinephrine producing a rate response were similar. Atria pretreated with 1 or 3 mg/kg reserpine were supersensitive to the inotropic effect of norepinephrine. 4 mg/kg reserpine did not induce inotropic supersensitivity. Atrial sodium contents were significantly increased by 3 mg/kg reserpine. Potassium contents were increased by 1 and 4 mg/kg reserpine. Calcium contents were significantly decreased by 4 mg/kg reserpine, while magnesium contents were increased by 1 and 4 mg/kg. Reserpine induced supersensitivity to the inotropic effects of norepinephrine but did not alter the sensitivity to the chronotropic effect of the drug. This supersensitivity may be linked to alterations in the tissue's homeostatic mechanisms for calcium.

Animals↗

Effect of magnesium on isoproterenol-induced alpha and beta receptor responses of vascular smooth muscle.

The presence of 1.2 mM magnesium in normal Ringer's solution decreased the sensitivity (increased ED50) and increased the maximum tension of rabbit aortic strips developed in response to dl-isoproterenol. Magnesium in the medium enhanced the degree of reserpine-induced supersensitivity to isoproterenol in whole aortic strips. On the other hand, in adventitia-free aortae, supersensitivity to isoproterenol was absent in the presence of magnesium. Isoproterenol-induced relaxation responses mediated by beta receptors were not modified by magnesium. However, maximum contractile responses mediated by alpha receptors were increased in the presence of magnesium. The decrease in sensitivity to isoproterenol in the presence of magnesium might be the result of its effect on calcium movements at the membrane and/or at intracellular calcium binding sites. The potentiating effect on the contractile tension responses to isoproterenol by magnesium might be a result of an increase in the amount of available calcium or to conformational changes produced on the membrane leading to a change in the contractility of the cells.

Angiotensin II↗

Role of calcium in postjunctional supersensitivity.

Several hours to days after an animal is given reserpine its cardiovascular system becomes supersensitive to catecholamines. This phenomenon can be demonstrated for vascular tissue by in vitro experiments. This type of supersensitivity has been termed "nonspecific" because the tissue is supersensitive to varied agonists, including acetylcholine, calcium, potassium, and the catecholamines. Animals that have been treated with reserpine have been found to have a transient decrease in the calcium content of their vascular tissue. The responses to norepinephrine of aortic strips from reserpine-treated rabbits, even though of greater magnitude than those of untreated aortic strips, were less dependent on extracellular calcium than responses of strips from untreated rabbits. On the other hand, the responses to potassium were more dependent on extracellular calcium. In addition, when aortic strips from reserpine-pretreated animals are subjected to potassium in a calcium-free medium, they are not supersensitive to the ion. When aortic strips are placed in a calcium-free, depolarizing medium they are still supersensitive to norepinephrine and isoproterenol but not to acetylcholine. Tension decline and 45Ca efflux studies suggest that reserpine-treated tissues retain longer than untreated tissues a calcium fraction involved in contraction. It is concluded that reserpine alters binding or movement of calcium in at least two sites. The lack of supersensitivity to acetylcholine and potassium in a calcium-free medium indicates an effect of reserpine (or the loss of adrenergic transmitter) on the utilization of extracellular calcium, while some other site must be involved in at least part of the supersensitivity to the catecholamines.

Acetylcholine↗