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Biomedical subjects

A J Pappano

Publications and source records attributed to A J Pappano.

85 records · Page 5Linked to original sources
PubMed1969

Increase in PNa and PK of cultured heart cells produced by veratridine.

Noninnervated cultured chick embryonic heart cells are depolarized by veratridine (10(-5) 10(-6) g/ml) within a few minutes to membrane potentials of -12 +/- 2 mv. Action potentials and beating cease. Before depolarization begins, the repolarizing phase of the action potential is prolonged and leads to a long-lasting depolarizing afterpotential, probably due to a holding open of Na(+) channels. There is no direct effect on automaticity. Maximum rate of rise of the action potential decreases as a function of the depolarization. The inexcitability is transiently reversed by repolarizing current pulses and by 5 mM Ba(++) (but not Sr(++)) which increases membrane resistance (R(m)) and produces a small transient repolarization. Cocaine does not reverse the depolarization. The depolarization also occurs in Cl(-)-free Ringer and in Na(+)-free Li(+)-Ringer, but not in Na(+)-free sucrose-Ringer. In most cases, R(m), measured in the presence and absence of Cl(-), initially decreases but sometimes increases. Some of the decrease or increase in g(K) may be indirectly produced by anomalous or delayed rectification, respectively. Tetrodotoxin, although having no effect on the action potential magnitude or rate of rise, prevents the depolarizing action of veratridine but not its effect on decreasing R(m). It is concluded that veratridine depolarizes by increasing the resting Na(+) permeability (P(Na)); it also tends to increase P(K), but this action may be obscured by anomalous rectification when E(m) is allowed to change. The equilibrium potential for veratridine action is about halfway between E(Na) and E(K), similar to that of acetylcholine at the vertebrate neuromuscular junction.

Action Potentials↗
PubMed1966

Lithium's failure to replace sodium in mammalian sympathetic ganglia.

Ganglionic responses to electrical stimulation, acetylcholine, and potassium ions were studied in superior cervical ganglia of. cats perfused with media containing lithium chloride instead of sodium chloride. In lithium-Locke, ganglionic transmission and depolarization evoked by acetylcholine were blocked completely but reversibly, while the depolarization produced by potassium ions was unaltered.

Acetylcholine↗
PubMedDate not supplied

Release of 3H-norepinephrine from adrenergic nerves in chick heart.

The metabolic disposition of 3H-norepinephrine (3H-NE) was studied in adrenergic nerves of the chick heart. Spontaneous overflow of 3H was associated with considerable metabolism of NE; about 90% of the 3H-NE appeared as acid and neutral metabolites. Overflow of 3H increased markedly during depolarization by K+ and over 70% of the 3H was unmetabolized 3H-NE. This 3H-NE seems to have been protected from intraneuronal metabolism (probably by vesicles) and to have been released by exocytosis. By contrast, tyramine-induced overflow included a large proportion of metabolites (approximately 70%) perhaps because of a nonexocytotic release mechanism similar to that in adult tissues.

Adrenergic Fibers↗
PubMedDate not supplied

N-ethylmaleimide increases the L-type calcium current in guinea-pig ventricular myocytes.

The effects of the alkylating agent N-ethylmalemide (NEM) on the L-type Ca current (ICa) of guinea-pig ventricular myocytes were studied with the whole-cell voltage-clamp technique at 21-23 degrees C. NEM (50-100 microM) produced an increase in ICa comparable to that produced by cAMP-increasing agents (isoprenaline, forskolin, phosphodiesterase inhibitors). The effects of NEM on ICa were not additive with those of the phosphodiesterase blockers papaverine and isobutylmethylxanthine. They were neither suppressed nor prevented by carbachol (100 microM) and could also not be prevented by pertussis toxin treatment or by cell dialysis with GDP beta S (300 microM) or GTP gamma S (300 microM). NEM, at low concentration (50 microM), increased twitch contraction measured in right ventricular strips. At a higher concentration (> or = 100 microM), this effect was followed by a decrease of the twitch and an increase in basal tension. It is proposed that NEM acts by transiently increasing cAMP levels to increase ICa and the twitch. Our experiments are not consistent with a mechanism involving Gi inhibition for NEM effect.

Animals↗