In Vitro Comparative Studies of the Calcium-Entry Activators YC-170, CGP 28392, and BAY K 8644

Rogg, H.; Criscione, Leoluca; Truog, A. G.; Meier, M.

doi:10.1097/00005344-198500076-00006

Cited by 29 publications

(13 citation statements)

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“…These values are shown in Table 1. The effects of the calcium channel facilitators Bay K 8644 (Schramm et al, 1983a,b) and CGP 28392 (Erne et al, 1984;Rogg et al, 1985) were examined by evaluating the interaction between antagonists and facilitators. The reversal of nisoldipine-induced inhibition of beating by Bay K 8644 is shown in Figure 3.…”

Section: Resultsmentioning

confidence: 99%

Effects of calcium channel antagonists and facilitators on beating of primary cultures of embryonic chick heart cells

Patmore¹,

Duncan²

1988

British J Pharmacology

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1 Primary aggregate cultures of embryonic chick heart have been used to investigate the effects of calcium channel antagonists and facilitators on myocardial contractility. 2 The number of aggregates showing movement was inhibited in a concentration-dependent manner by calcium antagonists from different subgroups with negative log concentrations inhibiting movement in 50% of aggregates as follows: Class 1-nisoldipine (7.20); Class 2-verapamil (6.36), diltiazem (5.83); Class 3-lidoflazine (5.68), pimozide (6.25). 3 The effects of the dihydropyridine facilitators Bay K 8644 and CGP 28392 on aggregate beating were investigated by evaluating the interaction between calcium channel facilitators and antagonists from the three subgroups of calcium antagonists. Concentrations of antagonists that inhibited beating in 85% of aggregates were used. Both Bay K 8644 and CGP 28392 reversed nisoldipine-, diltiazem-or verapamil-induced inhibition of beating. 4 Bay K 8644 was approximately 10 times more potent than CGP 28392 in reversing nisoldipine-, diltiazem-or verapamil-induced inhibition of beating. 5 For each facilitator the concentrations causing 50% reversal of inhibition of aggregate beating against the three antagonists were similar. There was little evidence for differential modulation by verapamil or diltiazem of the action of the dihydropyridine facilitators. 6 Bay K 8644 did not reverse lidoflazine-or pimozide-induced inhibition of beating, indicating that these drugs may act at a site distinct from the dihydropyridine site on the calcium channel.

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Section: Resultsmentioning

confidence: 99%

Effects of calcium channel antagonists and facilitators on beating of primary cultures of embryonic chick heart cells

Patmore¹,

Duncan²

1988

British J Pharmacology

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“…Bay K 8644 was dissolved in DMSO, the final concentrations of which were 0.01% and 0.1% during the incubations with Bay K 8644 10-6 and 10~mol l', respectively. dihydropyridine calcium channel inhibitors closely related to Bay K 8644, with which they compete for the binding sites (Rogg et al, 1985;Finet et al, 1985), and by other organic Ca2" channel inhibitors (reviews: Fleckenstein, 1985), no consistent effects of Ca2" channel blocking drugs on the release of ACh have been reported. The uptake of…”

Section: Resultsmentioning

confidence: 99%

Failure of the calcium channel activator, Bay K 8644, to increase the release of acetylcholine from nerve terminals in brain and diaphragm

Doležal

Tuček

1987

British J Pharmacology

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1 The calcium channel activator Bay K 8644 did not increase the release of acetylcholine from rat brain cortex prisms incubated in the presence of 3 mmol I 'or 25 mmol V' K4 nor from rat diaphragms incubated in the presence of 5 mmol I' or 25 mmol I' K4. It also did not influence the release of acetylcholine from cortex prisms incubated in the presence of 25 mmol I`'Kand of lowered concentrations of Ca2" ions.2 It is concluded that the voltage-dependent Ca24 channels in the nerve terminals, responsible for the depolarization-induced influx of Ca24 ions into the nerve terminals and thus for the depolarizationevoked release of acetylcholine from the nerve terminals, are different from the voltage-dependent Ca24 channels in the heart and smooth muscle cells.

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“…12 - 15 Such agents (e.g., Bay K-8644, CGP-28392, and YC-170) have been shown to activate voltage-dependent calcium channels, 16 -18 and are called "calcium channel activators" or "calcium agonists". The calcium channel activators are useful pharmacological tools for investigation of the voltage-dependent calcium channels.…”

Section: Soda Et Al Ca Channels Of Shr Aorta and Ace Inhibitionmentioning

confidence: 99%

Long-term inhibition of angiotensin converting enzyme suppresses calcium channel agonist-induced contraction of aorta in hypertensive rats.

1989

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To elucidate functional changes in the vascular smooth muscle of spontaneously hypertensive rats (SHR) after chronic inhibition of angiotensin converting enzyme, we examined the contractile responses to different pharmacological interventions in the isolated aortas from SHR treated with a novel angiotensin converting enzyme inhibitor, CS-622 (10 mg/kg/day) for 20 weeks. In normal K + medium, a marked contraction was elicited by increasing Ca 2+concentration from 0 to 3 mM in aortas from a control group of SHR, but not in aortas from SHR treated with CS-622. In 60 mM K + medium, however, the sensitivity of aorta to Ca 2+ was almost the same in the two groups. A calcium channel activator, CGP-28392 (10~7 to 10"' M), induced a marked contraction in the aortas from control SHR, but not in the aortas from CS-622-treated SHR. When slightly depolarized in 10 or 12 mM K + solution, the aortas from CS-622-treated SHR contracted in response to CGP-28392. The aortic sensitivity to KC1 contraction was much lower in CS-622-treated SHR than in untreated SHR, whereas the sensitivity to phenylephrine contraction was little different in the two groups. These contractile profiles of aortas from CS-622-treated SHR were very similar to those from normotensive Wistar-Kyoto rats but not to those from hydralazine-treated SHR. These data suggest that contractions due to Ca 2+ through voltage-dependent calcium channels are exaggerated in SHR aorta and that long-term treatment with angiotensin converting enzyme inhibitor suppresses the abnormal contractility of SHR vascular smooth muscle, probably through alterations of voltage-related functions of calcium channels. (Hypertension, 1989;14:652-659) A ntihypertensive effects of acute inhibition of angiotensin converting enzyme (ACE) depend on the status of the renin-angiotensin system: acute ACE inhibition produces a marked hypotension in renovascular hypertensive rats and a moderate hypotension in spontaneously hypertensive rats (SHR), whereas it is totally ineffective in reducing blood pressure of deoxycorticosterone acetate-salt hypertensive rats. 1 * 2 However, chronic ACE inhibition has been shown to lower blood pressure of SHR to levels of normotensive Wistar-Kyoto (WKY) rats, which is never accomplished by acute inhibition of ACE.3 These facts suggest that antihypertensive mechanisms underlying chronic ACE inhibition differ from those of acute ACE inhibition. Angiotensin II From the Cardiovascular Division, Biological Research Laboratories, Sankyo Co., Ltd., Tokyo, Japan.Address for reprints: Hiroyuki Koike, PhD, Biological Research Laboratories, Sankyo Co., Ltd., 1-2-58, Hiromachi, Shinagawaku, Tokyo 140, Japan.Received January 31, 1989; accepted in revised form Jury 24, 1989. (Ang II), when infused chronically at a dose below the threshold of the acute pressor effect, does not increase blood pressure initially, but increases blood pressure gradually over several days.4 -6 Thus, Ang II has a slow pressor action that is different from its acute pressor action. A recent report...

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In Vitro Comparative Studies of the Calcium-Entry Activators YC-170, CGP 28392, and BAY K 8644

Cited by 29 publications

References 0 publications

Effects of calcium channel antagonists and facilitators on beating of primary cultures of embryonic chick heart cells

Effects of calcium channel antagonists and facilitators on beating of primary cultures of embryonic chick heart cells

Failure of the calcium channel activator, Bay K 8644, to increase the release of acetylcholine from nerve terminals in brain and diaphragm

Long-term inhibition of angiotensin converting enzyme suppresses calcium channel agonist-induced contraction of aorta in hypertensive rats.

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