Reverse mode of the Na+-Ca2+ exchange after myocardial stretch: Underlying mechanism of the slow force response

Néstor G. Pérez, María C.Camilión De Hurtado, Horacio E. Cingolani

Research output: Contribution to journalArticlepeer-review

Abstract

This study was designed to gain additional insight into the mechanism of the slow force response (SFR) to stretch of cardiac muscle. SFR and changes in intracellular Na+ concentration ([Na+]i) were assessed in cat papillary muscles stretched from 92% to ≈98% of Lmax. The SFR was 120±0.6% (n=5) of the rapid initial phase and coincided with an increase in [Na+]i. The SFR was markedly depressed by Na+-H+ exchanger inhibition, AT1 receptor blockade, nonselective endothelin-receptor blockade and selective ETA-receptor blockade, extracellular Na+ removal and inhibition of the reverse mode of the Na+-Ca2+ exchange by KB-R7943. KB-R7943 prevented the SFR but not the increase in [Na+]i. Inhibition of endothelin-converting enzyme activity by phosphoramidon suppressed both the SFR and the increase in [Na+]i. The SFR and the increase in [Na+]i after stretch were both present in muscles with their endothelium (vascular and endocardial) made functionally inactive by Triton X-100. In these muscles, phosphoramidon also suppressed the SFR and the increase in [Na+]i. The data provide evidence that the last step of the autocrine-paracrine mechanism leading to the SFR to stretch is Ca2+ entry through the reverse mode of Na+-Ca2+ exchange.

Original languageEnglish (US)
Pages (from-to)376-382
Number of pages7
JournalCirculation research
Volume88
Issue number4
DOIs
StatePublished - Mar 2 2001
Externally publishedYes

Keywords

  • Angiotensin II
  • Endothelin
  • Myocardial stretch
  • Na-Ca exchange
  • Na-H exchange

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

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