A calcium-stimulated, ouabain-inhibited ATPase in a myocardial fraction enriched with sarcolemma

An active intracellular to extracellular Ca²⁺ efflux has been proposed in heart muscle. A myocardial sarcolemmal ATPase stimulated by an intracellular pCa and serving as a Ca²⁺ pump has been postulated. A recently developed myocardial sarcolemmal preparation has not permitter a search for such an enzymatic activity. In these studies, an ATPase has been demonstrated in the sarcolemma which is activated by Mg²⁺, stimulated as the Ca²⁺ is raised to a pCa of 6, and is inhibited by ouabain. These findings suggest a mechanism by which Ca²⁺ within the myocardium may be modulated and thus how the force of contraction may be altered by cardiac glycosides.     

Noradrenaline as a putative neurotransmitter mediating hypotension—induced FOs—like immunoreactivity in the supraoptic nucleus of the rat

Hemorrhage or hypotension induces extensive Fos-like immunoreactivity in the magnocellular neurosecretory cells in the supraoptic nucleus of the hypothalamus in rat,especially in the vasopressin neurons.The present study was to explore the neurotransmitter mediating this effect,Microinfusion of the alpha-adrenergic blocker into the supraoptic nucleus reduced the hypotension-induced FOs.whereas beta-antagonist did not affect it significantly.Alaha1-and alpha2-antagonist,prazosin and yohimbine,both reduced the Fos-Positive cell counts.However,the effective dosage of yohimbine was much larger,Alpha1-agonist,methoxamine,induced abundant Fos-like immunoreactivity in the vasopressin cells in this nucleus,while beta-and alpha2-agonist did not elicit such effect.Administration of the noradrenergic re-uptake inhibitor desipramine,to this nucleus to locally accumulate the spontaneously released noradrenaline from the nerve terminals also induced Fos expression,mostly in the vasopressin cells.