ArticleBritish journal of pharmacology1996
The mechanism of acidic pH-induced contraction in aortae from SHR and WKY rats enhanced by increasing blood pressure.
Article in British journal of pharmacology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 21 citations in OpenAlex.
- Article
- Acidosis-induced coronary constriction in the rat heart: evidence for the activation of L-type calcium channels.Heart and vessels · 1999Article
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4 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
1. Effect of pH on vascular smooth muscle contraction was analyzed by use of biochemical and pharmacological techniques. 2. In the aorta isolated from spontaneously hypertensive rats (SHR) decreasing extracellular pH (pH0) caused a rapid acidification of intracellular pH accompanied by a pH0-dependent increase in tension. The contraction of the SHR aorta was remarkable compared with that of the Wistar Kyoto rat (WKY) aorta. 3. Removal of NH4Cl caused a transient decrease in intracellular pH followed by a marked increase in tension. 4. Both contraction and intracellular Ca2+ mobilization induced by acidic pH0 were markedly inhibited by removal of extracellular Ca2+, verapamil and adenosine, whereas these were not affected by tetrodotoxin or Gd3+, a stretch-activated cation channel blocker. Furthermore, cromakalim (a K+ channel opener) inhibited acidic pH0-induced contraction (APIC). 5. Acidic pH0 induced a depolarization of cultured smooth muscle cells from SHR aorta. 6. Blood pressure elevated with increasing age of WKY and SHR accompanied by an increase in APIC. Feeding WKY with NG-nitro-L-arginine, an inhibitor of nitric oxide synthases caused a marked elevation of their blood pressure followed by an increase in APIC. 7. These results suggest that APIC is caused by Ca2+ influx mediated through the activation of voltage-sensitive Ca2+ channels mainly due to acidic pH0-induced depolarization of the plasma membrane of smooth muscle cells. It is also suggested that APIC is strengthened by the elevation of blood pressure.
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