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Titolo:
POSSIBLE MECHANISM OF THE POTENT VASOCONSTRICTOR ACTIONS OF RYANODINEON FEMORAL ARTERIES FROM SPONTANEOUSLY HYPERTENSIVE RATS
Autore:
ASANO M; KUWAKO M; NOMURA Y; ITO KM; ITO K; UYAMA Y; IMAIZUMI Y; WATANABE M;
Indirizzi:
NAGOYA CITY UNIV,SCH MED,DEPT PHARMACOL NAGOYA AICHI 467 JAPAN MIYAZAKI UNIV,FAC AGR,DEPT VET PHARMACOL MIYAZAKI 88921 JAPAN NAGOYA CITY UNIV,FAC PHARMACEUT SCI,DEPT CHEM PHARMACOL NAGOYA AICHI 467 JAPAN
Titolo Testata:
British Journal of Pharmacology
fascicolo: 4, volume: 118, anno: 1996,
pagine: 1019 - 1027
SICI:
0007-1188(1996)118:4<1019:PMOTPV>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
VASCULAR SMOOTH-MUSCLE; CYTOSOLIC FREE CALCIUM; SARCOPLASMIC-RETICULUM; CA-2+ RELEASE; CAFFEINE; AORTA; CONTRACTION; INHIBITION; CHANNELS; MEMBRANE;
Keywords:
SPONTANEOUSLY HYPERTENSIVE RATS (SHR); ARTERIAL MYOGENIC TONE; RYANODINE; SARCOPLASMIC RETICULUM; CYTOSOLIC CA2+ LEVEL; VOLTAGE-DEPENDENT CA2+ CHANNELS; CA2+ INFLUX; SUPERFICIAL BUFFER BARRIER HYPOTHESIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
42
Recensione:
Indirizzi per estratti:
Citazione:
M. Asano et al., "POSSIBLE MECHANISM OF THE POTENT VASOCONSTRICTOR ACTIONS OF RYANODINEON FEMORAL ARTERIES FROM SPONTANEOUSLY HYPERTENSIVE RATS", British Journal of Pharmacology, 118(4), 1996, pp. 1019-1027

Abstract

1 The Ca2+ buffering function of sarcoplasmic reticulum (SR) in the resting state of arteries from spontaneously hypertensive rats (SHR) was examined. Differences in the effects of ryanodine that removes the function of SR, on tension and cellular Ca2+ level were assessed in endothelium-denuded strips of femoral arteries from 13-week-old SHR and normotensive Wistar-Kyoto rats (WKY). 2 The addition of ryanodine to the resting strips caused a concentration-dependent contraction in SHR. This contraction was extremely small in WKY. In the presence of 10(-5)M ryanodine, caffeine (20 mM) failed to cause a further contraction in SHR, but it caused a small contraction in WKY. After washout of the strips with a Krebs solution, the resting tone was greatly elevated inSHR when compared with WKY. 3 The elevated resting tone in SHR stripswas abolished by 10(-7) M nifedipine. The ryanodine-induced contraction was also abolished by 10(-7) M nifedipine. Nifedipine itself causeda relaxation from the resting tone of SHR strips, suggesting the maintenance of myogenic tone. 4 In strips preloaded with fura-PE3, the addition of 10(-5) M ryanodine caused a large and moderate elevation of cytosolic Ca2+ level ([Ca2+](i)) in SHR and WKY, respectively. After washout, the resting [Ca2+](i) was greatly elevated in SHR. The ryanodine-induced elevation of [Ca2+](i) was decreased by 5x10(-6) M verapamilin SHR. Verapamil itself caused a decrease in resting [Ca2+](i) whichwas significantly greater in SHR than in WKY, and caused a relaxationonly in SHR. 5 The resting Ca2+ influx in arteries measured by a 5 min incubation with Ca-45 was significantly increased in SHR when compared with WKY. The resting Ca2+ influx was not increased by 10(-5) M ryanodine in both SHR and WKY. The net cellular Ca2+ uptake in arteries measured by a 30 min incubation with Ca-45 was decreased by 10(-5) M ryanodine in both strains. 6 The resting Ca2+ influx was decreased by 10(-7) M nifedipine in the SHR artery, but it was unchanged in the WKY artery. 7 These results suggest that (1) the Ca2+ influx via L-type voltage-dependent Ca2+ channels was increased in the resting state of theSHR femoral artery, (2) the greater part of the increased Ca2+ influxwas buffered by Ca2+ uptake into the SR and some Ca2+ reached the myofilaments resulting in the maintenance of the myogenic tone, and (3) therefore the functional removal of SR by ryanodine caused a potent contraction in this artery.

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Documento generato il 25/11/20 alle ore 17:19:27