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Differing calcium sensitivities of human cerebral and digital arteries, human metatarsal veins, and rat aorta.
Author(s) -
Iwanov V,
Moulds RF
Publication year - 1991
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/j.1365-2125.1991.tb03856.x
Subject(s) - nifedipine , calcium , aorta , cerebral arteries , vasoconstriction , medicine , blood vessel , voltage dependent calcium channel , anatomy , endocrinology , calcium channel , thoracic aorta , basilar artery , chemistry
1. The effects of the voltage dependent calcium channel blocking agent nifedipine, and of a calcium free bathing medium, on the responses of human blood vessels obtained postmortem to various agonists have been compared with those of the rat aorta. The human vessels studied were digital arteries, basilar arteries and metatarsal veins. 2. Responses to potassium chloride (5‐80 mM), noradrenaline (10(‐9)‐10(‐4) M), 5‐ hydroxytryptamine (10(‐8)‐10(‐4) M) and U46619 (10(‐11)‐10(‐6) M), in the presence and absence of nifedipine (1, 10, and 100 nM) or in a calcium‐free bathing medium, were assessed using an area‐under‐curve analysis. 3. In general, the order of sensitivity of the vessels to inhibition of agonist induced contractures by nifedipine was basilar arteries greater than metatarsal veins = digital arteries = rat aorta. 4. For all the vessels, the order of sensitivity for antagonism of responses to the agonists by nifedipine was potassium chloride greater than 5‐hydroxytryptamine = noradrenaline greater than U46619. 5. A calcium free bath inhibited responses of digital arteries to potassium chloride more than noradrenaline, 5‐hydroxytryptamine or U46619, and responses of rat aorta to a greater extent than responses of the digital arteries. 6. In the rat aorta, a calcium‐free bath inhibited responses to all agonists (except KCl) to a greater degree than did nifedipine. 7. We conclude that inhibition of extracellular calcium entry through voltage dependent calcium channels affects contractile responses of different blood vessels to different extents, and, within the same blood vessel, responses to different contractile agonists to different extents.