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. 1992 Aug;106(4):859–864. doi: 10.1111/j.1476-5381.1992.tb14425.x

Noradrenaline-stimulated inositol phosphate accumulation in arteries from spontaneously-hypertensive rats.

S B Guild 1, S Jenkinson 1, T C Muir 1
PMCID: PMC1907654  PMID: 1393285

Abstract

1. The effects of noradrenaline upon polyphosphoinositide (PPI) breakdown was investigated by measuring the accumulation of inositol phosphates (IPs) in tail arteries from normo- (WKY) and spontaneously-hypertensive (SHR) rats. 2. Noradrenaline (10(-7)-10(-3) M) evoked a concentration-dependent increase in total IP accumulation in both WKY and SHR rats but no significant differences between the populations were detected. 3. In contrast, significant differences in the accumulation of the individual IPs, which contributed to the total IP, occurred. A significantly greater noradrenaline-stimulated accumulation of inositol trisphosphate (IP3) was observed in tissues from SHR compared with those from WKY rats at each effective concentration of noradrenaline. This was paralleled by an equivalent reduction in inositol monophosphate (IP1) accumulation, consistent with the lack of a significant difference in noradrenaline-stimulated total IP accumulation between the two populations. 4. In time course studies, an enhanced noradrenaline-induced accumulation of IP3, in SHR compared to WKY rats, occurred from the earliest time point studied after the addition of the catecholamine both in the presence and absence of LiCL (10 mM). In the presence of LiCl (10 mM) no significant difference in noradrenaline-evoked total IP accumulation between SHR and WKY rats was observed; in the absence of LiCl noradrenaline-evoked a greater total IP accumulation in SHR than in WKY rats at all time points investigated. 5. These studies suggest that the main reason for the enhanced noradrenaline-induced accumulation of IP3 in arteries from SHR rats is a reduced rate of dephosphorylation of both IP3 and inositol bisphosphate (IP2) rather than a greater formation of IP3 from PPIs.(ABSTRACT TRUNCATED AT 250 WORDS)

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Selected References

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  1. Abdel-Latif A. A. Calcium-mobilizing receptors, polyphosphoinositides, and the generation of second messengers. Pharmacol Rev. 1986 Sep;38(3):227–272. [PubMed] [Google Scholar]
  2. Akhtar R. A., Abdel-Latif A. A. Carbachol causes rapid phosphodiesteratic cleavage of phosphatidylinositol 4,5-bisphosphate and accumulation of inositol phosphates in rabbit iris smooth muscle; prazosin inhibits noradrenaline- and ionophore A23187-stimulated accumulation of inositol phosphates. Biochem J. 1984 Nov 15;224(1):291–300. doi: 10.1042/bj2240291. [DOI] [PMC free article] [PubMed] [Google Scholar]
  3. Bao J. X., Eriksson I. E., Stjärne L. Neurogenic contractions in the tail artery of normotensive rats are mediated by noradrenaline and ATP via post-junctional alpha 1- and alpha 2-adrenoceptors and P2x-purinoceptors. Acta Physiol Scand. 1989 May;136(1):139–140. doi: 10.1111/j.1748-1716.1989.tb08642.x. [DOI] [PubMed] [Google Scholar]
  4. Batty I. H., Nahorski S. R. Rapid accumulation and sustained turnover of inositol phosphates in cerebral-cortex slices after muscarinic-receptor stimulation. Biochem J. 1989 May 15;260(1):237–241. doi: 10.1042/bj2600237. [DOI] [PMC free article] [PubMed] [Google Scholar]
  5. Berridge M. J., Irvine R. F. Inositol phosphates and cell signalling. Nature. 1989 Sep 21;341(6239):197–205. doi: 10.1038/341197a0. [DOI] [PubMed] [Google Scholar]
  6. Berridge M. J. Rapid accumulation of inositol trisphosphate reveals that agonists hydrolyse polyphosphoinositides instead of phosphatidylinositol. Biochem J. 1983 Jun 15;212(3):849–858. doi: 10.1042/bj2120849. [DOI] [PMC free article] [PubMed] [Google Scholar]
  7. Brodde O. E., Michel M. C. Disease states can modify both receptor number and signal transduction pathways. Trends Pharmacol Sci. 1989 Oct;10(10):383–384. doi: 10.1016/0165-6147(89)90176-4. [DOI] [PubMed] [Google Scholar]
  8. Brodde O. E., Zerkowski H. R., Borst H. G., Maier W., Michel M. C. Drug- and disease-induced changes of human cardiac beta 1- and beta 2-adrenoceptors. Eur Heart J. 1989 Jun;10 (Suppl B):38–44. doi: 10.1093/eurheartj/10.suppl_b.38. [DOI] [PubMed] [Google Scholar]
  9. Ekas R. D., Jr, Lokhandwala M. F. Sympathetic nerve function and vascular reactivity in spontaneously hypertensive rats. Am J Physiol. 1981 Nov;241(5):R379–R384. doi: 10.1152/ajpregu.1981.241.5.R379. [DOI] [PubMed] [Google Scholar]
  10. Fouda A. K., Marazzi A., Boillat N., Sonnay M., Guillain H., Atkinson J. Changes in the vascular reactivity of the isolated tail arteries of spontaneous and renovascular hypertensive rats to endogenous and exogenous noradrenaline. Blood Vessels. 1987;24(1-2):63–75. doi: 10.1159/000158672. [DOI] [PubMed] [Google Scholar]
  11. Holman M. E., Surprenant A. An electrophysiological analysis of the effects of noradrenaline and alpha-receptor antagonists on neuromuscular transmission in mammalian muscular arteries. Br J Pharmacol. 1980;71(2):651–661. doi: 10.1111/j.1476-5381.1980.tb10986.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  12. Muir T. C., Wardle K. A. Vascular smooth muscle responses in normo- and hypertensive rats to sympathetic nerve stimulation and putative transmitters. J Auton Pharmacol. 1989 Feb;9(1):23–34. doi: 10.1111/j.1474-8673.1989.tb00193.x. [DOI] [PubMed] [Google Scholar]
  13. Shears S. B., Storey D. J., Morris A. J., Cubitt A. B., Parry J. B., Michell R. H., Kirk C. J. Dephosphorylation of myo-inositol 1,4,5-trisphosphate and myo-inositol 1,3,4-triphosphate. Biochem J. 1987 Mar 1;242(2):393–402. doi: 10.1042/bj2420393. [DOI] [PMC free article] [PubMed] [Google Scholar]

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