Differing calcium sensitivities of human cerebral and digital arteries, human metatarsal veins, and rat aorta.

Abstract

Keywords digital artery metatarsal vein basilar artery calcium nifedipine rat aorta potassium noradrenaline U46619 5-hydroxytryptamine

Overlap in the Pharmacology of L-type Ca2+-channel Blockers and 5-HT2 Receptor Antagonists in Rat Aorta

“…Secondly, rat aortic contractions evoked by 5-HT depend on Ca 2 in¯ux (Okoro & Marwood 1997b) and the current data indicate that the resulting contractions are sensitive to blockade by a series of L-type Ca 2 -channel antagonists as documented previously (Gouw et al 1989;Iwanov & Mould 1991). The current IC50 values (Table 1) are, however, different from those reported by the investigators cited above.…”

“…The current IC50 values (Table 1) are, however, different from those reported by the investigators cited above. It should be noted that our method of assessing antagonist potency against 5-HT-induced contractions was similar to those of Gouw et al (1989) but different from those of Iwanov & Mould (1991). Further, many of these studies were undertaken on aorta derived from different rat strains, and tissue contact time with antagonist drugs was brief, often less than 20 min, compared with 45 min or more in this study.…”

LOE 908: A Specific Blocker of Nonselective Cation Channel

“…6a and 6b), whereas higher concentrations of Cardiovascular Drug Reviews, Vol. 18 ET-1 induced a biphasic increase in [Ca 2+ ] i consisting of an initial transient phase and a subsequent sustained phase ( Fig. 6c) (16,17,38).…”

“…However, subsequent studies have shown that the agonist-induced contractions and increases in [Ca 2+ ] i are virtually resistant to or only partially sensitive to specific blockers of L-type voltage-operated Ca 2+ channels (VOCCs) such as dihydropyridines (6)(7)(8)14,18,19,28,33,35,39). Thus, it is now clear that Ca 2+ entry through ion channels other than VOCCs plays a critical role in the agonists-induced contractions and increases in [Ca 2+ ] i .…”

“…Vasoconstricting agonists, such as endothelin-1 (ET-1), norepinephrine and vasopressin exert, their action by inducing an increase in the intracellular free Ca 2+ concentration ([Ca 2+ ] i ) in vascular smooth muscle cells (VSMCs), which depends entirely on the entry of extracellular Ca 2+ (19,28,30,31,39). However, subsequent studies have shown that the agonist-induced contractions and increases in [Ca 2+ ] i are virtually resistant to or only partially sensitive to specific blockers of L-type voltage-operated Ca 2+ channels (VOCCs) such as dihydropyridines (6)(7)(8)14,18,19,28,33,35,39). Thus, it is now clear that Ca 2+ entry through ion channels other than VOCCs plays a critical role in the agonists-induced contractions and increases in [Ca 2+ ] i .…”