Synthesis and Excretion of Atrial Natriuretic Peptide in Secretory Cardiomyocytes in Experimental Hypertension

Bugrova, Marina L.; Галкина, М.В.

doi:10.1007/s10517-020-04849-y

Cited by 1 publication

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“…In RV model, the increase in gene expression was not sufficient to increase plasma levels on ANP at 12 weeks. A recent study also showed that the accumulation and release of ANP from myocyte granules depends on the pathogenesis of hypertension, and described a higher number of ANP secretory granules in a salt loading model compared to two-kidney 1-clip hypertension, providing a possible explanation for the lack of increase in plasma ANP in our RV model ( Bugrova and Galkina, 2020 ). Another possible explanation is a differential regulation of the tissue cleavage enzymes and clearance receptors, which we have not addressed in this study.…”

Section: Discussionsupporting

confidence: 58%

Cardiac Natriuretic Peptide Profiles in Chronic Hypertension by Single or Sequentially Combined Renovascular and DOCA-Salt Treatments

et al. 2021

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The involvement of natriuretic peptides was studied during the hypertrophic remodeling transition mediated by sequential exposure to chronic hemodynamic overload. We induced hypertension in rats by pressure (renovascular) or volume overload (DOCA-salt) during 6 and 12 weeks of treatment. We also studied the consecutive combination of both models in inverse sequences: RV 6 weeks/DS 6 weeks and DS 6 weeks/RV 6 weeks. All treated groups developed hypertension. Cardiac hypertrophy and left ventricular ANP gene expression were more pronounced in single DS than in single RV groups. BNP gene expression was positively correlated with left ventricular hypertrophy only in RV groups, while ANP gene expression was positively correlated with left ventricular hypertrophy only in DS groups. Combined models exhibited intermediate values between those of single groups at 6 and 12 weeks. The latter stimulus associated to the second applied overload is less effective than the former to trigger cardiac hypertrophy and to increase ANP and BNP gene expression. In addition, we suggest a correlation of ANP synthesis with volume overload and of BNP synthesis with pressure overload-induced hypertrophy after a prolonged treatment. Volume and pressure overload may be two mechanisms, among others, involved in the differential regulation of ANP and BNP gene expression in hypertrophied left ventricles. Plasma ANP levels reflect a response to plasma volume increase and volume overload, while circulating BNP levels seem to be regulated by cardiac BNP synthesis and ventricular hypertrophy.

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Section: Discussionsupporting

confidence: 58%