Key result
Uncontrolled SBP in volume-dependent hypertension is linked to lower ANP and blunted volume overload indices.
Why the study?
It was unknown whether systolic blood pressure control in sustained volume-dependent primary hypertension is associated with blunted ANP relationships with indexes of volume load.
Does uncontrolled systolic blood pressure attenuate the relationship between ANP and indexes of volume overload in volume-dependent primary hypertension?
Observational (n=772)
Does uncontrolled systolic blood pressure attenuate the relationship between ANP and indexes of volume overload in volume-dependent primary hypertension?
Uncontrolled systolic blood pressure in volume-dependent primary hypertension is associated with a blunted ANP response to volume overload, suggesting impaired compensatory mechanisms.
Answers are grounded in this paper and cite their sources.
Uncontrolled SBP may blunt ANP response to volume overload; leaves open whether ANP pathways merit interventional study in primary hypertension.
Background: Whether systolic blood pressure (SBP) control in sustained volume-dependent primary hypertension is associated with blunted ANP (atrial natriuretic peptide) relationships with indexes of volume load is unknown. Methods: Systemic hemodynamics (central pressure, echocardiographic aortic velocity and diameter measurements in the outflow tract), circulating ANP concentrations (ELISA assays) and glomerular and tubular function (24-hour urine collections [n=519]) were determined in a community of African ancestry (n=772). Results: As compared with those with a controlled SBP, those with an uncontrolled SBP (n=198) showed lower ANP concentrations ( P <0.005) despite higher stroke volume and cardiac output ( P <0.0001) and renal differences consistent with enhanced fluid retention. In those with a controlled SBP, fractional Na + excretion (FeNa + ; P <0.0005) and creatinine clearance (glomerular filtration rate; P <0.005) were inversely associated with ANP concentrations independent of confounders. Moreover, in those with a controlled SBP, stroke volume and cardiac output ( P <0.0001) were independently and positively associated with ANP concentrations. In addition, in those with a controlled SBP, ANP concentrations were independently and inversely associated with systemic vascular resistance (SVR; P <0.0001) and aortic characteristic impedance (Zc; P <0.005). By contrast, in those with uncontrolled SBP, no relationships between either stroke volume ( P >0.25), cardiac output ( P >0.29), FeNa + ( P >0.77), or glomerular filtration rate ( P >0.47) and ANP concentrations were noted. Furthermore, in those with an uncontrolled SBP, no relationships between ANP concentrations and SVR or Zc were observed ( P >0.34). Conclusions: In a population where primary hypertension is strongly volume-dependent, those with an uncontrolled SBP have an attenuated relationship between ANP and both renal and hemodynamic indexes of volume overload and the vascular effects of ANP.
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Yusuf et al. (2022) conducted an observational in Sustained volume-dependent primary hypertension (n=772). Uncontrolled systolic blood pressure vs. Controlled systolic blood pressure was evaluated on ANP concentrations (p=<0.005). Uncontrolled systolic blood pressure in volume-dependent primary hypertension was associated with lower ANP concentrations (P<0.005) and blunted relationships between ANP and volume overload indexes.
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