Why the study?
Does a maternal high salt diet alter adenosine-mediated vasodilatation in the coronary arteries of offspring rats?
Does a maternal high salt diet alter adenosine-mediated vasodilatation in the coronary arteries of offspring rats?
Prenatal high salt exposure impairs adenosine-mediated coronary vasodilatation in offspring via the cAMP/PKA/BK channel pathway, suggesting a mechanism for increased cardiovascular risk.
Warrants caution on prenatal salt intake; leaves open translation to human offspring coronary risk.
Scope High salt (HS) diets are related to cardiovascular diseases, and prenatal HS was suggested to increase risks of coronary artery diseases in the offspring. This study tested the hypothesis that prenatal HS may influence Adenosine‐induced vasodilatation via protein kinase A (PKA) pathway in coronary arteries. Methods and results Sprague–Dawley rats were fed with 8% salt diet for gestation, the control was fed with 0.3% salt diet. Coronary arteries from male adult offspring were tested for K + channels and Adenosine signal pathways. Adenosine‐mediated vasodilatation was reduced in coronary arteries in HS. There was no difference in gene expression of A 2A receptors between the two groups. After pretreatment with PKA inhibitor, vasodilatation to Adenosine was decreased to a smaller extent in HS than that in control. Forskolin (activator of adenylate cyclase)‐mediated vasodilatation was decreased in HS. Iberiotoxin (large‐conductance Ca 2+ ‐activated K + channel [BK channel] inhibitor) attenuated Forskolin‐induced vasodilatation in control, not in HS group. Currents of BK channels decreased in coronary artery smooth muscle cells, and PKA‐modulated BK channel functions were declined. Protein levels of BK β1 and PKA C‐subunits in coronary arteries of HS offspring were reduced. Conclusions Prenatal HS diets altered Adenosine‐mediated coronary artery vasodilatation in the offspring, which was linked to downregulation of cAMP/PKA/BK channel pathway.
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Wu et al. (2017) studied this question.
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