Ca Antagonists (ca + antagonist)

Distribution by Scientific Domains
Medical Sciences100%

Selected Abstracts

The actions of azelnidipine, a dihydropyridine-derivative Ca antagonist, on voltage-dependent Ba2+ currents in guinea-pig vascular smooth muscle

BRITISH JOURNAL OF PHARMACOLOGY, Issue 6 2006
H-L Zhu
Background and purpose: Although azelnidipine is used clinically to treat hypertension its effects on its target cells, Ca2+ channels, in smooth muscle have not been elucidated. Therefore, its effects on spontaneous contractions and voltage-dependent L-type Ca2+ channels were investigated in guinea-pig portal vein. Experimental approach: The inhibitory potency of azelnidipine on spontaneous contractions in guinea-pig portal vein was compared with those of other dihydropyridine (DHP)-derived Ca antagonists (amlodipine and nifedipine) by recording tension. Also its effects on voltage-dependent nifedipine-sensitive inward Ba2+ currents (IBa) in smooth muscle cells dispersed from guinea-pig portal vein were investigated by use of a conventional whole-cell patch-clamp technique. Key results: Spontaneous contractions in guinea-pig portal vein were reduced by all of the Ca antagonists (azelnidipine, Ki=153 nM; amlodipine, Ki=16 nM; nifedipine, Ki=7 nM). In the whole-cell experiments, azelnidipine inhibited the peak amplitude of IBa in a concentration- and voltage-dependent manner (-60 mV, Ki=282 nM; ,90 mV, Ki=2 ,M) and shifted the steady-state inactivation curve of IBa to the left at ,90 mV by 16 mV. The inhibitory effects of azelnidipine on IBa persisted after 7 min washout at ,60 mV. In contrast, IBa gradually recovered after being inhibited by amlodipine, but did not return to control levels. Both azelnidipine and amlodipine caused a resting block of IBa at -90 mV. Only nifedipine appeared to interact competitively with S(-)-Bay K 8644. Conclusions and implications: These results suggest that azelnidipine induces long-lasting vascular relaxation by inhibiting voltage-dependent L-type Ca2+ channels in vascular smooth muscle. British Journal of Pharmacology (2006) 149, 786,796. doi:10.1038/sj.bjp.0706919 [source]

High incidence of newly-developed gastroesophageal reflux disease in the Japanese community: A 6-year follow-up study

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 3 2008
Masaki Miyamoto
Abstract Background and Aim:, We conducted a community-based study to assess the incidence of newly-developed gastroesophageal reflux disease (GERD). We also analyzed the risk factors of GERD occurrence. Methods:, A total of 322 patients without acid suppression therapy (135 men, mean age: 59.8 years), who lived in the Japanese community, took a QUEST questionnaire (a self-administered questionnaire for the screening of GERD) in 1998. Blood samples were taken for the measurement of an anti- Helicobacter pylori antibody and pepsinogen (PG) I/II to assess the grade of gastric atrophy. Of these patients, 289 scored less than six points and were diagnosed as non-GERD. Two-hundred-and-forty-one patients (95 men, mean age: 67.0 years) took the QUEST questionnaire again in 2004 (after 6 years). The incidence of newly-developed GERD was analyzed. These patients were categorized into three groups based on their initial PG I/II (group A: less than three, group B: three to six, and group C: more than six). The risk factors of GERD occurrence were evaluated. Results:, Of the 241 non-GERD patients, 37 patients (15.4%) developed GERD after 6 years. The incidence of newly-developed GERD in group C was significantly higher than both groups A and B (group A: 3.8% [three of 79], group B: 11.8% (11/93), group C: 33.3% (26/69), P < 0.01, respectively). The prevalence of H. pylori negativity, constipation, and medication of Ca antagonists in newly-developed GERD were significantly higher than in those who did not develop GERD. [Correction added after online publication on 1 July 2007: the preceding sentence has replaced one that read ,The prevalence of H. pylori negativity, constipation, and medication of Ca antagonists in newly-developed GERD were significantly higher than in those who did develop GERD.'] Conclusion:, The incidence of newly-developed GERD in the Japanese community was 16.5% for 6 years. The incidence of newly-developed GERD patients who scored a PG I/II over six was significantly higher than those who scored lower. H. pylori negativity, constipation, and medication of Ca antagonists might be risk factors of GERD occurrence. [source]

The actions of azelnidipine, a dihydropyridine-derivative Ca antagonist, on voltage-dependent Ba2+ currents in guinea-pig vascular smooth muscle

BRITISH JOURNAL OF PHARMACOLOGY, Issue 6 2006
H-L Zhu
Background and purpose: Although azelnidipine is used clinically to treat hypertension its effects on its target cells, Ca2+ channels, in smooth muscle have not been elucidated. Therefore, its effects on spontaneous contractions and voltage-dependent L-type Ca2+ channels were investigated in guinea-pig portal vein. Experimental approach: The inhibitory potency of azelnidipine on spontaneous contractions in guinea-pig portal vein was compared with those of other dihydropyridine (DHP)-derived Ca antagonists (amlodipine and nifedipine) by recording tension. Also its effects on voltage-dependent nifedipine-sensitive inward Ba2+ currents (IBa) in smooth muscle cells dispersed from guinea-pig portal vein were investigated by use of a conventional whole-cell patch-clamp technique. Key results: Spontaneous contractions in guinea-pig portal vein were reduced by all of the Ca antagonists (azelnidipine, Ki=153 nM; amlodipine, Ki=16 nM; nifedipine, Ki=7 nM). In the whole-cell experiments, azelnidipine inhibited the peak amplitude of IBa in a concentration- and voltage-dependent manner (-60 mV, Ki=282 nM; ,90 mV, Ki=2 ,M) and shifted the steady-state inactivation curve of IBa to the left at ,90 mV by 16 mV. The inhibitory effects of azelnidipine on IBa persisted after 7 min washout at ,60 mV. In contrast, IBa gradually recovered after being inhibited by amlodipine, but did not return to control levels. Both azelnidipine and amlodipine caused a resting block of IBa at -90 mV. Only nifedipine appeared to interact competitively with S(-)-Bay K 8644. Conclusions and implications: These results suggest that azelnidipine induces long-lasting vascular relaxation by inhibiting voltage-dependent L-type Ca2+ channels in vascular smooth muscle. British Journal of Pharmacology (2006) 149, 786,796. doi:10.1038/sj.bjp.0706919 [source]