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Receptor Mechanisms in the Metabolic Response

Much evidence suggests that membrane activation is influenced by the energetic status of the smooth muscle cell. Thus one or, more probably, several links in the membrane-associated activation sequence may be metabolically sensitive. Evidence has been reported for decreased agonist-stimulated formation of inositol [Pg.381]

5-trisphosphate (IP3) and diacylglycerol and for decreased levels of guanine nucleotides in contracting rabbit aorta during hypoxia (Coburn cf a/., 1988,1993). However, responses to receptor activation could still be elicited during metabolic depletion, indicating that G-protein-coupled activation mechanisms were operative. [Pg.381]

New interest has focused on the possibility that ATP-regulated K+ (K tp) channels might be involved in the membrane response to metabolic inhibition (Standen et al., 1989 Daut et al., 1990). These channels are blocked by ATP and activated by nucleoside diphosphates, and thus would be expected to increase their conductance as [ADP]/[ATP] increases, leading to hyperpolarization. This suggests an attractive hy- [Pg.381]

From an energetic point of view, a crucial aspect is whether ATP, ADP, and other nucleoside phosphates vary in the vicinity of the ion channels in such a way that the channel activity is influenced. Elucidation of this question requires knowledge of metabolic and electrophysiological alterations under given conditions in the same tissue. Such information is to some extent available for the rat portal vein. Noack et al. [Pg.382]

Lovgren and Hellstrand (1985) determined force, [ATP], and [PCr] during progressive hypoxia or respiratory inhibition in the rat portal vein (Fig. 1). When spontaneous activity was almost abolished using either intervention, ATP contents were unchanged, whereas PCr had declined to about 40% of the control value. Based on a [PCr]/[total creatine] ratio of 0.75 in relaxed normoxic portal vein (Hellstrand and Paul, [Pg.382]


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