Cardiovascular Journal of Africa: Vol 25 No 5 (September/October 2014)

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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 25, No 5, September/October 2014 202 AFRICA
factor-1 (TGF-1)-induced collagen production in cultured
fibroblasts.14 Recent reports have suggested that CNP has
cardio–renal protective effects via these humoral mechanisms
in the setting of stress injury, with suppression of pro-fibrotic
processes and a protective function.14-16
Furthermore, CNP has local regulatory functions via
the vascular renin–angiotensin system. CNP inhibits the
vasoconstrictor impact of angiotensin 1. Additionally, recent
reports suggest that CNP is an endogenous regulator of vascular
ACE activity. Higher CNP levels were demonstrated both in
renal failure patients who were on haemodialysis therapy and in
cardiac failure patients.15,16
In a recent study it was reported that CNP lacked renal action
but led to vasodilatation and inhibition of growth.19 These data
indicate that CNP is a non-cardiac regulator hormone that
regulates vascular tone according to cardio–renal interactions
via different mechanisms, such as the vascular renin–angiotensin
system.15-17
Natriuretic peptides are potent vasodilators during hypoxic
conditions. For example, Klinger et al. reported pulmonary vessel
vasodilation in response to natriuretic peptides in rats adapted
to hypoxic environments.9 Similarly, Zhao et al. described the
possible use of natriuretic peptides in maintaining pulmonary
vascular homeostasis in hypoxic patients.18
Hobbs et al. studied CNP in an experimental model of
myocardial ischaemia–reperfusion and found that CNP
had protective vasorelaxation properties.19 Ahluwalia et al.
demonstrated that hypoxia might directly induce the release of
CNP so that vascular homeostasis is maintained.20
It has been reported that CNP may contribute to the
regulation of blood flow with decreasing perfusion pressure and
also reduce the oxidative damage after reperfusion in ischaemic
conditions.19 Additionally, it was hypothesised that CNP was
upregulated in the presence of nitric oxide (NO) synthase
inhibition for compensation of the protective role of NO.19
In another study, it was shown that CNP led to an increment in
NO stimulation and suppression of the neo-intimal hyperplasia
and inflammatory process in an experimental carotid injury
model.21 Chun et al. demonstrated that oxidative stress could
modulate the endothelium-derived vasoactive substances such as
CNP.22 Yamahara et al. claimed that CNP enhanced angiogenesis
in ischaemic conditions in their experimental model.23 All these
studies identified a range of cellular and vascular interactions
that may clarify the role of elevated CNP levels due to oxidative
stress during mesenteric ischaemia after reperfusion.
Conclusion
CNP appears to regulate blood flow in the mesenteric vascular
bed. Clinically monitoring CNP levels may be useful in
estimating the duration over which the patient has sustained
mesenteric ischaemia and the severity of the injury due to acute
mesenteric artery occlusion. However, the exact mechanism of
the interaction between CNP and the mesenteric vessels must be
further elucidated in future clinical studies.
We thank the co-ordinator of scientific research at Dicle University for
language-editing the manuscript.
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