Hypoxia induces release of atrial natriuretic peptide in rat atrial tissue: a role for this peptide during low oxygen stress

Abstract

A variety of different factors have been shown to induce release of atrial natriuretic peptide from atrial tissue. Among these, stretching of atrial myocytes is considered the most important. In a recent study we showed that atrial natriuretic peptide increased cGMP and reduced lactate accumulation during hypoxia in rat ventricular myocardium. This suggests that atrial natriuretic peptide has a beneficial metabolic effect during hypoxia and raises the question whether hypoxia alone induces release of atrial natriuretic peptide. The right atrium and pieces of the right ventricle, from rats, were incubated in polyethylene vials containing 3 ml Krebs bicarbonate buffer equilibrated with 75% N2 + 20% O2 + 5% CO2 (= hypoxic conditions) or 95% O2 + 5% CO2 (= normoxic conditions). After 10 min, the ventricular tissues and aliquots of the buffer were frozen. Cyclic GMP was analyzed in the ventricular tissue and atrial natriuretic peptide was analyzed in the buffer samples. The results show that the release of atrial natriuretic peptide during hypoxia significantly exceeds the release under normoxic conditions. The hypoxia-induced release of atrial natriuretic peptide over time is characterized by an s-shaped curve with the steepest slope after about 10 min. In the presence of atrial tissue the intracellular level of cGMP in ventricular myocardium increased from 0.3 +/- 0.1 to 2.6 +/- 0.9 pmol/g w wt (P = 0.033, n = 6). We conclude that ANP is released from atrial tissue and induces increased formation of cGMP in ventricular myocardium when oxygen tension is low.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain natriuretic peptide and acute hypobaric hypoxia in humans

“…Isolated rat hearts increase ANP and BNP with an acute (30 min) exposure to normobaric hypoxic [2]. Indeed, even just 10 min of normobaric hypoxia can induce ANP release in both anaesthetized rats [3] and rat atrial and ventricular tissue [4], with the steepest rise in ANP after the first 10 min of exposure [4]. In humans, ANP has been found to rise acutely after breathing a hypoxic gas mixture (10% O 2 ) for only 10 min [5].…”

Hypoxia exposure and B‐type natriuretic peptide release from Langendorff heart of rats

“…1996, Zhang et al . 2004) and from isolated cell lines of human cardiac origin (Ljusegren & Andersson 1994, Klinger et al . 2001, Hopkins et al .…”

“…hypoxia has also proved to be a powerful stimulus for the release of natriuretic peptides from the rodent heart (Baertschi et al 1986, Lew & Baertschi 1989, Uusimaa et al 1992a,b, Chen et al 1993, Arad et al 1994, T oth et al 1994, Focaccio et al 1995, Svorak et al 1996, Zhang et al 2004) and from isolated cell lines of human cardiac origin (Ljusegren & Andersson 1994, Klinger et al 2001, Hopkins et al 2004, Casals et al 2009). Also, both the A-and B-type peptides have a hypoxia-responsive element in the promoter sequence of their respective genes (Chun et al 2003, Luo et al 2006 and hypoxia has been shown to be a direct and sufficient stimulus for the transcription of the gene encoding B-type peptide (Weidemann et al 2008).…”

Endocrine Aspects of High Altitude Acclimatization and Acute Mountain Sickness

“…Isolated rat hearts increase ANP and BNP with an acute (30 minutes) hypoxic exposure [27]. Indeed, even just 10 minutes of hypoxic exposure can induce ANP release in both isolated rat atrial tissue [28] and in anaesthetized rats [29].…”