Regulation Of Catecholamine Release Research Articles

Regulation of catecholamine release and synthesis in cultured bovine adrenal medullary cells

Adrenal medulla is regarded as a model of neurons containing catecholamine(CA) and is the most suitable tissue for studying the regulation of CA release and synthesis. We used cultured bovine adrenal medullary cells and examined the effects of nicotinic and muscarinic stimulations of these cells on 4 5Ca++ flux and release and synthesis of CA.

S. UV-2) - Isolated bovine adrenal medullary cells : Role of Ca++ in the regulation of catecholamine release

S. UV-2) - Isolated bovine adrenal medullary cells : Role of Ca++ in the regulation of catecholamine release

灌流ウシ副腎でのカテコールアミン遊離とカルシウムイオン動態の調節における細胞内ナトリウムイオンの役割

灌流ウシ副腎でのカテコールアミン遊離とカルシウムイオン動態の調節における細胞内ナトリウムイオンの役割

Sodium in blood vessels. A brief review.

Extracellular Na can be accurately partitioned into free and bound components; the latter component is directly related to the hydration and stiffness of the vascular wall. Cell Na can be similarly partitioned: [Na+]i is about 10mM and the transmembrane gradient about 15:1 in a physiological medium. The transmembrane gradient remains constant over a wide range of change in [Na+]0. Although active Na transport is largely responsible for developing the transmembrane ion distribution pattern, the membrane potential depends mainly on movements of K+ and C1-. No certain direct role can be assigned to Na+ in short-term vasoconstriction, but an indirect role through the regulation of catecholamine release and uptake is now established. There is evidence that the entry of Na+ into cells plays a fundamental role in the protein-synthesizing activity of the vascular smooth muscle cell and is thereby involved in the longer term determination of peripheral vascular resistance.

207) - Serum dopaniine-β-hydroxylase (regulation of catecholamine-release by various agents-IV)

207) - Serum dopaniine-β-hydroxylase (regulation of catecholamine-release by various agents-IV)

Serum dopamine-β-hydroxylase (regulation of catecholamine-release by various agents)

Serum dopamine-β-hydroxylase (regulation of catecholamine-release by various agents)

Regulation of catecholamine release. The muscarinic inhibitory mechanism

Publisher Summary This chapter discusses the muscarinic inhibitory mechanism for regulation of catecholamine release. The elucidation of a muscarinic mechanism which inhibits the release of noradrenaline (NA) from peripheral adrenergic nerve fibers started from the observation, on the perfused rabbit heart, that atropine greatly enhanced the noradrenaline output produced by infusion of acetylcholine. Muscarinic inhibition probably affects a process which in the sequence of events leading to release of transmitter occurs after excitation of nicotinic receptors. Blockade of nicotinic receptors with hexamethonium does not prevent the acetylcholineinduced inhibition of noradrenaline output evoked by sympathetic nerve stimulation. The catecholamine releasing procedures susceptible to muscarinic inhibition are invariably dependent on the presence of extracellular calcium ions. This has been demonstrated for noradrenaline release by sympathetic nerve stimulation, nicotinic drugs and high potassium. On the other hand, tyramine-induced noradrenaline release which does not require calcium is not decreased by methacholine. The correlation between calcium-dependency of transmitter release and presence of muscarinic inhibition was confirmed by studies utilizing a false transmitter amine.

Regulation of catecholamine release: α-Receptor mediated feed-back control in peripheral and central neurones

Publisher Summary This chapter describes a study analyzing the regulation of catecholamine release: α-receptor mediated feedback control in peripheral and central neurons. It tested the influence of phentolamine, after both the neuronal and the extra-neuronal binding of noradrenaline (NA) had been blocked by high concentrations of cocaine and (±)-metanephrine which were added immediately after preperfusion with 3 H-noradrenaline. Phentolamine enhanced the stimulation-induced overflow of tritium even in the presence of these drugs and, thus, by a mechanism other than an inhibition of the neuronal or extraneuronal binding of noradrenaline. The results indicate that α-adrenolytic drugs do not enhance the stimulation-induced overflow of noradrenaline by blocking any of the known pathways of its inactivation within the tissue. Per exclusionem it can be inferred that these drugs increase the amount of transmitter secreted per impulse from the nerve terminals. It is also concluded that α-receptors exist in the vicinity to the cardiac adrenergic nerve endings. When these receptors are activated, the release of noradrenaline declines. A local feedback inhibition curtails the secretory response to stimulation.

Regulation of catecholamine release

Publisher Summary This chapter describes regulation of catecholamine release. The transmitter that is released from the nerve terminals can be affected by several inactivating mechanisms at the nerve terminal–effector cell level. The inactivating mechanisms are: (1) binding to receptors, (2) enzymatic destruction by catechol- O -methyl-transferase (COMT) and monoamine oxidase (MAO) (3) re-uptake into the nerve terminals by the “membrane pump,” (4) extra-neuronal uptake, and (5) diffusion into the perfusate. Variations in the amount of noradrenaline (NA) overflow after a certain number of sympathetic stimuli were often discussed to be because of quantitative variations in the role of these inactivating mechanisms. An example is the effect on the overflow of NA obtained after α-receptor blocking drugs, such as phenoxybenzamine (PBZ). The increase is often found to be 4–10 times the normal NA overflow. This effect has been explained as because of blockade of one or several of the local inactivating mechanisms, thus permitting the non-inactivated NA to reach the perfusate. It has also been proposed that the amount of transmitter released from the nerve terminals per nerve impulse is increased after a α-receptor blocker, such as PBZ.

Effects of cytoplasmic and microsomal fractions on ATP-Mg ++ stimulated catecholamine release from isolated adrenomedullary granules.

There is evidence that Ca++ is required for the release of catecholamine from the adrenal medulla evoked by acetylcholine or a high K+ concentration (1, 2) and that an increased influx of Ca++ into the cell occurs during this process (3). It has therefore been proposed that it is the entry of Ca++ into the cell which somehow triggers the secretory process (4, 5). On the other hand, the release of catecholamine from isolated catecholamine storage granules is shown to be stimulated by ATP and Mg++ (6-8) and this ATP-Mg++ stimulated release of catecholamine also requires a low concentration of Ca++ (<10-5M), present as a contaminant in the reaction mixture (9). The authors suggested that ATP-Mg++ stimulated release of catecholamine from the granules could be a step in the secretory response of the adrenal medulla. To elucidate the exact intracellular mechanism of adrenal medullary secretion, it is necessary to determine whether or not intracellular elements other than catecholamine storage granules are involved in the regulation of catecholamine release from the granules. We have investigated the effects of the cytoplasmic and microsomal fractions on ATP-Mg++ stimulated catecholamine release from the granules. Results suggest that these two fractions are important in regulation of catecholamine release from the adrenal medulla.