Calcium antagonists

Zsoter, T

doi:10.1016/0002-8703(80)90633-x

Cited by 46 publications

(17 citation statements)

References 30 publications

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“…In addition, it has been suggested that Ca antagonists increase blood flow in a number of organ regions, including the mesenteric, femoral, renal and coronary vasculatures, by a direct action on vascular tone by inhibiting Ca2 + influx across the vascular smooth muscle cell membranes (Yamagushi, Ikezewa, Takada & Kiyomoto, 1974;Fleckenstein, 1977;Zsot&r, 1980). Some workers believe that these Ca antagonists, surprisingly, do not exert any venodilator actions (Zsoter, 1980). Such information has prompted clinical studies with the use of Ca antagonists in the treatment of a variety of cardiovascular disorders, including angina pectoris, arrhythmias, hypertension, and ischaemic heart disease (Sandler, Clayton & Thronicroft, 1968;Schamroth, Krikler & Garrett, 1972;Livesley, Catley, Campbell & Oram, 1973;Hosada & Kimura, 1976;Heupler & Proudfit, 1979;Zsoter, 1980 (Altura, 1971;Altura & Altura, 1974).…”

mentioning

confidence: 99%

Differential Effects of the Calcium Antagonist, Verapamil, on Lumen Sizes of Terminal Arterioles and Muscular Venules in the Rat Mesenteric, Pial and Skeletal Muscle Microvasculatures

Altura

Gebrewold

1980

British J Pharmacology

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The actions of the local perivascular application of verapamil to rat mesenteric, pial and cremaster muscle arterioles and muscular venules (15 to 35 pm i.d.), was examined in situ, at the microcirculatory level, by use of a high-resolution closed circuit television microscope recording system. Local application of verapamil (I to 100 pg) to cremaster muscle arterioles and venules of the rat induces dose-dependent vasodilatation and increased perfusion of capillaries. However, neither arteriolar nor muscular venular lumen sizes and capillary blood flow of the rat mesenteric or pial vasculatures were altered by even high doses of verapamil. Although these direct in sitti microvascular findings do indicate that verapamil can induced dilatation of microscopic resistance and capacitance vessels in skeletal muscle, our data do not support the concept that verapamil induces non-specific peripheral vasodilatation.

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confidence: 99%

Differential Effects of the Calcium Antagonist, Verapamil, on Lumen Sizes of Terminal Arterioles and Muscular Venules in the Rat Mesenteric, Pial and Skeletal Muscle Microvasculatures

Altura

Gebrewold

1980

British J Pharmacology

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“…1978;Ople. 1980;Zsoter, 1980) and since even cardio-selective beta-receptor antagonists can cause significant airways obstrtiction in susceptible subjects (Gauld. Pain and Rubinfeld.…”

Section: Discussionmentioning

confidence: 99%

“…in those patients with cardiovascular disease in whom a beta-receptor antagoni.st might nortnaliy be considered but who hitve associated respiratory disease (Hills, 1970;'jaiprakash et al, 1980;Rabkin et a!.. 1980;Zsoter. 1980).…”

Section: Discussionmentioning

confidence: 99%

“…Finally, verapamil is but one of an increasingly large group of agents exhibiting the property of calcium antagonism (Opie, 1980;Zsoter, 1980). Since this group is heterogeneous (Zsoter, 1980), it is possible that other members of this class of drugs may be shown to have more specific and more potent effects on bronchial smooth muscle than the prototype, verapamil.…”

Section: Discussionmentioning

confidence: 99%

“…Since this group is heterogeneous (Zsoter, 1980), it is possible that other members of this class of drugs may be shown to have more specific and more potent effects on bronchial smooth muscle than the prototype, verapamil.…”

Section: Discussionmentioning

confidence: 99%

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The Potential Bronchodilator Action of Verapamil

et al. 1984

Aust J Exp Biol Med

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Summary Although calcium antagonists such verapamil are used primarily in cardiovascular disease, they appear to relax smooth muscle generally. Therefore, the possibility that verapamil might have bronchodilator properties was explored using the guinea‐pig tracheal ring technique. Verapamil was found to produce considerable tracheal smooth muscle relaxation from a threshold concentration of 2 × 10−7M and with maximum effect at 10−3M. The responses to the contractile agonists histamine and prostaglandin F2α and especially methacholine and serotonin were substantially reduced by prior administration of verapamil. Verapamil 2 × 10−4M was equally effective as isoprenaline 10−8M in producing 50% maximum direct relaxation but was more effective than isoprenaline as an antagonist of the contractile agonists, methacholine, histamine and serotonin, but not prostaglandin F2α. Verapamil abolished the contractile responses to barium chloride. It is concluded that, although verapamil was not very potent as a direct bronchodilator, it could potentially be of prophylactic benefit in asthma because of its efficacy as an antagonist of common contractile agonists.

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Nifedipine therapy for recurrent ischemic pain following myocardial infarction

Stone

Muller

1982

Clinical Cardiology

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Summary: The efficacy of nifedipine in relieving recurrent ischemic episodes following acute myocardial infarction was studied in 11 patients a mean of 9.2 days post infarction (range 2-42 days). Prior to infarction, all of the patients had a history of exertional angina only, yet following the infarction, episodes of recurrent ischemia occurred at rest in spite of maximal medical management with beta-blockers and/or nitrate preparations, which lowered the heart rate to a mean of 65 beats/min, and the blood pressure to a mean of 109/70 mmHg. Ischemic episodes were associated with ST -segment elevation in 7 patients and ST-segment depression or Twave inversion in 4 patients. Coronary angiography was performed in 8 patients, and demonstrated multivessel coronary disease in 7. The episodes of rest ischemia were prevented in all but one patient by the addition of nifedipine (mean daily dose 60 mg, range 40-120 mg) without causing a change in heart rate or blood pressure. Two patients continued to have myocardial ischemia with minimal exertion, although rest pains were abolished, and they underwent coronary bypass surgery for relief of exertional pain. Only one patient continued to have episodes of ischemia at rest, although the frequency of ischemic episodes was decreased, and bypass surgery was necessary for pain relief. The other 8 patients have been managed medically for a mean of 5.4 months (range 1-12 months) and have remained pain free on 223 combined regimens of nifedipine, beta blockers, and/or nitrate preparations. We conclude that nifedipine may be efficacious for the relief of recurrent myocardial ischemia at rest following acute infarction. In some patients nifedipine may eliminate the need for coronary artery bypass surgery and in others it may provide clinical stability prior to operation.

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Calcium antagonists

Cited by 46 publications

References 30 publications

Differential Effects of the Calcium Antagonist, Verapamil, on Lumen Sizes of Terminal Arterioles and Muscular Venules in the Rat Mesenteric, Pial and Skeletal Muscle Microvasculatures

Differential Effects of the Calcium Antagonist, Verapamil, on Lumen Sizes of Terminal Arterioles and Muscular Venules in the Rat Mesenteric, Pial and Skeletal Muscle Microvasculatures

The Potential Bronchodilator Action of Verapamil

Nifedipine therapy for recurrent ischemic pain following myocardial infarction

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