Effects of Bay K 8644 on cat adrenal catecholamine secretory responses to A23187 or ouabain

Artalejo, Cristina R.; Garcı́a, Antonio G.

doi:10.1111/j.1476-5381.1986.tb16248.x

Cited by 18 publications

(10 citation statements)

References 17 publications

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“…Garcia and his colleagues have suggested that Bay-K-8644 required the pre-activated state of Ca channels to gain access to its site of action (MONTIEL et al, 1984;ARTALEJO and GARCIA, 1986). Consistent with this view, our previous findings indicated that Bay-K-8644 showed a marked stimulatory effect on CA secretion from cat adrenal under conditions in which the transmembrane potential gradient was diminished by increasing the surface potential (negativity) with a lowered concentration of Ca or by substituting Sr for Ca (SoRIMACHI et al, 1985b(SoRIMACHI et al, , 1986.…”

Section: Discussionsupporting

confidence: 66%

“…The above-described view is also consistent with the findings that Bay-K-8644 exerted its stimulatory effect substantially after experimental manipulations leading to a rise in internal Na (that is, treatment with K deprivation, ouabain, or KCN). However, it should be also kept in mind that a certain portion of this potentiation by Bay-K-8644 could take place at the site of voltage-dependent Ca channels (ARTALEJO and GARCIA, 1986). On the basis of the following two observations, Garcia and his colleagues considered that Bay-K-8644 did not activate Ca influx linked with Na efflux.…”

Section: Discussionmentioning

confidence: 99%

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Potentiation by Bay-K-8644 of the adrenal catecholamine secretory response to Ca re-introduction and ouabain: Possible activation of Ca influx linked with Na efflux.

Yano

Sorimachi

1989

Jpn.J.Physiol

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Catecholamine (CA) secretion induced by Ca re-introduction or ouabain in the presence of Ca is markedly potentiated by Bay-K-8644 in the perfused cat adrenal. The mechanism of potentiation by this Ca agonist was investigated using perfused cat adrenal and isolated bovine chromaffin cells. The stimulatory effect of Bay-K-8644 on the response to Ca was very slight when cat adrenal was perfused with a Ca-deficient medium, in which 1 mM Mg was added or the concentration of Na was lowered. The inhibitory effect of Mg was reversed by inhibition of the Na pump with K deprivation, ouabain, or KCN. The secretion induced by ouabain during maintained depolarization at a lowered concentration (0.25 mM) of Ca, which is supposed to be due to Ca influx in exchange for Na efflux, was larger in the Bay-K-8644 treated adrenal than that in the untreated adrenal. The increase in secretion by the delayed addition of Bay-K-8644 during perfusion with a high K medium containing ouabain was larger when the concentration of Na in a high K medium was higher. When isolated chromafpn cells were stimulated with a Na-free (Tris) medium containing 0.5 mM Ca, CA secretion from and 45Ca uptake into the cells preincubated with a divalent cation-free medium were potentiated by Bay-K-8644. The stimulatory effect of Bay-K-8644 was not seen when a Ca-free treatment medium contained Mg or lacked Na, but the inhibitory effect of Mg was reversed by the addition of ouabain or KCN to the pretreatment medium. When isolated cells preloaded with 45Ca were superfused with a Ca-free medium, Ca re-introduction increased the rate of Ca efflux only under conditions in which significant increases in CA secretion and 45Ca uptake were previously observed under the static incubation system. Bay-K-8644 further increased this Ca efflux rate under these conditions. These results support the view that Ca influx linked with Na efflux is through a pathway with properties similar to those of voltagedependent Ca channels, and suggest that this Ca pathway is activated by Bay-K-8644, which is an activator of voltage-dependent Ca channels.

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Section: Discussionsupporting

confidence: 66%

Section: Discussionmentioning

confidence: 99%

Potentiation by Bay-K-8644 of the adrenal catecholamine secretory response to Ca re-introduction and ouabain: Possible activation of Ca influx linked with Na efflux.

Yano

Sorimachi

1989

Jpn.J.Physiol

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“…This consideration is based partly on in vitro studies demonstrating that calcium entry blockers, including dihydropyridine derivatives, inhibit the release of adrenal catecholamines induced by various stimuli (Cohen & Gutman 1979;Cena et al 1983;Lopez et al 1989;Owen et al 1989). It is also available indicating that the calcium channel activator Bay-K-8644 enhances adrenal catecholamine release in response to moderate depolarization, nicotine, ouabain and calcium reintroduction Montiel et al 1984;Sala et al 1985;Artalejo & Garcia 1986;Ladona et al 1987). These pharmacological findings led to the suggestion that voltagedependent calcium channels are involved in adrenal catecholamine release.…”

Section: Introductionmentioning

confidence: 94%

Short Communication: Effects of Nifedipine and Bay‐k‐8644 on the Release of Catecholamines From the Dog Adrenal Gland in Response to Splanchnic Nerve Stimulation

Takeuchi

Kimura

Satob

1993

Clin Exp Pharma Physio

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1. The effects of nifedipine and Bay-K-8644 on the release of adrenal catecholamines were examined in anaesthetized dogs. 2. Splanchnic nerve stimulation (SNS) at 1 and 3 Hz produced frequency-dependent increases in adrenaline (ADR) and noradrenaline (NA) output determined from adrenal venous blood. 3. Neither nifedipine (10 and 30 micrograms/kg, i.v.) nor Bay-K-8644 (10 and 30 micrograms/kg, i.v.) modified the SNS-induced increases in catecholamine output. Basal catecholamine output tended to be increased and decreased by nifedipine and Bay-K-8644, respectively. 4. Nifedipine produced significant decreases in arterial pressure and renal blood flow rate. Bay-K-8644 produced a significant increase in arterial pressure associated with a decrease in renal blood flow rate. 5. These results suggest that dihydropyridine-sensitive calcium channels do not play a major role in adrenal catecholamine release evoked by SNS.

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“…Results are from a typical paired experiment out of 3. the secretory response regardless of the order they are applied to the gland, suggests that membrane potential may modulate the secretory efficacy of cardiac glycosides. Artalejo & Garcia (1986) have proposed that ouabain enhances the spontaneous rates of catecholamine release by a dual mechanism: (1) chromaffin cell depolarization which subsequently would open voltage-dependent calcium channels and (2) activation of a Na-Ca exchange system in reverse mode. Both mechanisms showed a strong dependence on [Na]0, which indicates that they must be related to the ionic redistribution secondary to the inhibition of Na pump caused by the cardiac glycoside.…”

Section: Perfusion Of Isolated Adrenal Glands Of the Catmentioning

confidence: 99%

“…Effect ofnitrendipine on the catecholamine release induced by ouabain in predepolarized glands It has recently been suggested that the catecholamine secretory response evoked by ouabain in cat adrenal glands results from a dual mechanism: (a) chromaffin cell depolarization with secondary opening of voltage-dependent calcium channels, and (b) activation of a membrane Na/Ca exchange system in reverse mode (Artalejo & Garcia, 1986 (Lastowecka & Trifaro, 1974;Abajo et al, 1987).…”

Section: Perfusion Of Isolated Adrenal Glands Of the Catmentioning

confidence: 99%

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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Effects of Bay K 8644 on cat adrenal catecholamine secretory responses to A23187 or ouabain

Cited by 18 publications

References 17 publications

Potentiation by Bay-K-8644 of the adrenal catecholamine secretory response to Ca re-introduction and ouabain: Possible activation of Ca influx linked with Na efflux.

Potentiation by Bay-K-8644 of the adrenal catecholamine secretory response to Ca re-introduction and ouabain: Possible activation of Ca influx linked with Na efflux.

Short Communication: Effects of Nifedipine and Bay‐k‐8644 on the Release of Catecholamines From the Dog Adrenal Gland in Response to Splanchnic Nerve Stimulation

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

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