A small increment of external K concentration accelerates adrenomedullary catecholamine secretion induced by ouabain and metabolic inhibitors.

Sorimachi, Masaru; Nishimura, Shigeto

doi:10.2170/jjphysiol.33.681

Cited by 3 publications

(2 citation statements)

References 14 publications

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“…neous catecholamine release, but also dramatically potentiated the secretion evoked by small increments of [K]0 (Garcia et al, 1981b). These results have been corroborated by other groups (Sorimachi & Nishimura, 1983;Nakazato et al, 1986). Since the ouabain-mediated potentiation of the K-evoked secretory response observed in normal Krebs was maintained in low-Na Krebs perfused glands, it was concluded that this effect was essentially independent of extracellular Na (Garcia et al, 1981b).…”

Section: Introductionsupporting

confidence: 75%

The key role of sodium in the ouabain‐mediated potentiation of potassium‐evoked catecholamine release in cat adrenal glands

Abajo¹,

Castro²,

Sánchez‐García³

1989

British J Pharmacology

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Ouabain treatment (100 M; 10min) of glands perfused with normal Krebs evoked a long lasting catecholamine release, which reached a plateau at about 36 min and amounted to 0.68 + 0.25 Mg 2 min 1 (n = 9). Such a secretory response was dramatically increased, and its shape modified, when glands were preperfused with K (17.7 mM)-Krebs: a peak of 3.77 + 0.42 Mg 2 min-1 (n = 7) was reached at 18 min. This response was drastically reduced in the presence of nitrendipine (I PM). 6 In summary, our results indicate that both [Na]0 reduction or Na accumulation into the chromaffin cell by inhibition of the Na pump with ouabain, greatly enhance the secretory efficacy of small increments of [K]0, and suggest that sodium may play a role in the regulation of catecholamine release mediated by voltage-dependent Ca channels in adrenal glands.

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Section: Introductionsupporting

confidence: 75%

The key role of sodium in the ouabain‐mediated potentiation of potassium‐evoked catecholamine release in cat adrenal glands

Abajo¹,

Castro²,

Sánchez‐García³

1989

British J Pharmacology

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“…Intra-articular papain has been used to produce fusion of the lapine elbow (Schneider 1965) and the canine tarsocrural joint (Schneider and Schneider 1968). Sodium monoiodoacetate (MIA) is a chemical compound, which when injected intra-articularly, causes a rapid decrease in chondrocyte intra-cellular adenosine triphosphate concentrations resulting in inhibition of glycolysis and chondrocyte death (Sorimachi and Nishimura 1983;Berding and Mikhailov 1983;Saito and Yamaguchi 1985;Treadwell and Mankin 1986). Monoiodoacetate has been used experimentally as a glycol ysis blocking agent to create arthritis in rats, guinea pigs, chickens and horses (Buchmann and Kalbhen 1985;Kalbhen 1981;Williams and Brandt 1982;Stick, Slocumbe and Personnett 1984;Yovich.…”

Section: Introductionmentioning

confidence: 99%

Fusion of the distal intertarsal and tarsometatarsal joints in the horse using intraarticular sodium monoiodoacetate

Bohanon¹,

Schneider

Weisbrode³

1991

Equine Veterinary Journal

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Summary Six normal horses received 3 intra‐articular injections of sodium monoiodoacetate (MIA) in the distal intertarsal (DIT) and tarsometatarsal (TMT) joints of one hindlimb. Injections were at three week intervals, and post injection pain was controlled with routine administration of phenylbutazone for five days following each injection. All horses underwent a gradually increasing exercise programme consisting of walking and trotting beginning one week after the first injection and continuing for 24 weeks. All treated joints showed increasingly severe radiographic evidence of degenerative joint disease with time. Clinical signs were mild or absent during exercise. All treated joints showed radiographic and histological evidence of fusion 24 weeks after the first injection. Amount of radiographic fusion ranged from 54.49 per cent to 88.64 per cent of the joint space. Histologically, the joint space that appeared radiographically fused was filled mainly with woven and lamellar bone. Fibrocartilage and fibrous tissue was seen frequently in the transition between fused and unfused areas. Articular cartilage in unfused areas was thin, fibrillated, hypocellular and histochemically showed diminished proteoglycan content. Existing joint space was filled with fibrin and necrotic, acellular chondroid matrix. We conclude that MIA will produce fusion of the DIT and TMT joints of normal horses in 24 weeks, and may offer a relatively easy, inexpensive and non‐invasive treatment for distal tarsal osteoarthritis in the horse.

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Sodium/Calcium Exchange: Its Physiological Implications

Blaustein

Lederer

1999

Physiological Reviews

1,555

1,549

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The Na+/Ca2+ exchanger, an ion transport protein, is expressed in the plasma membrane (PM) of virtually all animal cells. It extrudes Ca2+ in parallel with the PM ATP-driven Ca2+ pump. As a reversible transporter, it also mediates Ca2+ entry in parallel with various ion channels. The energy for net Ca2+ transport by the Na+/Ca2+ exchanger and its direction depend on the Na+, Ca2+, and K+ gradients across the PM, the membrane potential, and the transport stoichiometry. In most cells, three Na+ are exchanged for one Ca2+. In vertebrate photoreceptors, some neurons, and certain other cells, K+ is transported in the same direction as Ca2+, with a coupling ratio of four Na+ to one Ca2+ plus one K+. The exchanger kinetics are affected by nontransported Ca2+, Na+, protons, ATP, and diverse other modulators. Five genes that code for the exchangers have been identified in mammals: three in the Na+/Ca2+ exchanger family (NCX1, NCX2, and NCX3) and two in the Na+/Ca2+ plus K+ family (NCKX1 and NCKX2). Genes homologous to NCX1 have been identified in frog, squid, lobster, and Drosophila. In mammals, alternatively spliced variants of NCX1 have been identified; dominant expression of these variants is cell type specific, which suggests that the variations are involved in targeting and/or functional differences. In cardiac myocytes, and probably other cell types, the exchanger serves a housekeeping role by maintaining a low intracellular Ca2+ concentration; its possible role in cardiac excitation-contraction coupling is controversial. Cellular increases in Na+ concentration lead to increases in Ca2+ concentration mediated by the Na+/Ca2+ exchanger; this is important in the therapeutic action of cardiotonic steroids like digitalis. Similarly, alterations of Na+ and Ca2+ apparently modulate basolateral K+ conductance in some epithelia, signaling in some special sense organs (e.g., photoreceptors and olfactory receptors) and Ca2+-dependent secretion in neurons and in many secretory cells. The juxtaposition of PM and sarco(endo)plasmic reticulum membranes may permit the PM Na+/Ca2+ exchanger to regulate sarco(endo)plasmic reticulum Ca2+ stores and influence cellular Ca2+ signaling.

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A small increment of external K concentration accelerates adrenomedullary catecholamine secretion induced by ouabain and metabolic inhibitors.

Cited by 3 publications

References 14 publications

The key role of sodium in the ouabain‐mediated potentiation of potassium‐evoked catecholamine release in cat adrenal glands

The key role of sodium in the ouabain‐mediated potentiation of potassium‐evoked catecholamine release in cat adrenal glands

Fusion of the distal intertarsal and tarsometatarsal joints in the horse using intraarticular sodium monoiodoacetate

Sodium/Calcium Exchange: Its Physiological Implications

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