Abstract:.2010.-We investigated the effect of the intravenous infusion of atrial natriuretic peptide (ANP) on the response of plasma arginine vasopressin (AVP) levels to intravenous infusion of angiotensin II (ANG II) in healthy individuals. Intravenous infusion of ANP (10 ng·kg Ϫ1 ·min Ϫ1 ) slightly but significantly decreased plasma AVP levels, while intravenous infusion of ANG II (10 ng·kg Ϫ1 ·min Ϫ1 ) resulted in slightly increased plasma AVP levels. ANG II infused significant elevations in arterial blood pressure … Show more
“…Whereas great attention has been placed on V2‐related effects on hyponatraemia in advanced HF, much less is known about the role of vascular and myocardial V1a effects. Finally, little is known about the relationship between ANP and AVP levels, despite its well‐known physiological cross‐regulation …”
Section: Discussionmentioning
confidence: 99%
“…In particular, whether increased AVP levels are associated with LV remodelling in HFpEF and HFrEF is unknown. Similarly, little is known about the association between AVP levels and atrial natriuretic peptide (ANP) levels, which are released in response to increased atrial stretch and inhibit AVP release …”
AimsThe arginine vasopressin (AVP) pathway has been extensively studied in heart failure (HF) with reduced ejection fraction (HFrEF), but less is known about AVP in HF with preserved EF (HFpEF). Furthermore, the association between AVP and atrial natriuretic peptide (ANP, a well‐known inhibitor of AVP secretion) in HF is unknown.Methods and resultsWe studied subjects with HFpEF (n = 28) and HFrEF (n = 25) and without HF (n = 71). Left ventricular (LV) mass and left atrial (LA) volumes were measured with cardiac magnetic resonance imaging. Arginine vasopressin and ANP were measured with enzyme‐linked immunosorbent assay. Arginine vasopressin levels were significantly greater in HFpEF [0.96 pg/mL; 95% confidence interval (CI) = 0.83–1.1 pg/mL] compared with subjects without HF (0.69 pg/mL; 95% CI = 0.6–0.77 pg/mL; P = 0.0002). Heart failure with preserved ejection fraction (but not HFrEF) was a significant predictor of higher AVP after adjustment for potential confounders. Arginine vasopressin levels were independently associated with a greater LA volume and also paradoxically, with lower ANP levels. Key independent correlates of higher AVP were the presence of HFpEF (standardized β = 0.32; 95% CI = 0.09–0.56; P = 0.0073) and the ANP/LA volume ratio (standardized β = −0.23; 95% CI = −0.42 to −0.04; P = 0.0196). Arginine vasopressin levels were independently associated with LV mass (β = 0.26; 95% CI = 0.09–0.43; P = 0.003) and with an increased risk of death or HF admissions during follow‐up (hazard ratio = 1.61; 95% CI = 1.13–2.29; P = 0.008).ConclusionsArginine vasopressin is increased in HFpEF and is associated with LV hypertrophy and poor outcomes. Higher AVP is associated with the combination of LA enlargement and paradoxically low ANP levels. These findings may indicate that a relative deficiency of ANP (an inhibitor of AVP secretion) in the setting of chronically increased LA pressure may contribute to AVP excess.
“…Whereas great attention has been placed on V2‐related effects on hyponatraemia in advanced HF, much less is known about the role of vascular and myocardial V1a effects. Finally, little is known about the relationship between ANP and AVP levels, despite its well‐known physiological cross‐regulation …”
Section: Discussionmentioning
confidence: 99%
“…In particular, whether increased AVP levels are associated with LV remodelling in HFpEF and HFrEF is unknown. Similarly, little is known about the association between AVP levels and atrial natriuretic peptide (ANP) levels, which are released in response to increased atrial stretch and inhibit AVP release …”
AimsThe arginine vasopressin (AVP) pathway has been extensively studied in heart failure (HF) with reduced ejection fraction (HFrEF), but less is known about AVP in HF with preserved EF (HFpEF). Furthermore, the association between AVP and atrial natriuretic peptide (ANP, a well‐known inhibitor of AVP secretion) in HF is unknown.Methods and resultsWe studied subjects with HFpEF (n = 28) and HFrEF (n = 25) and without HF (n = 71). Left ventricular (LV) mass and left atrial (LA) volumes were measured with cardiac magnetic resonance imaging. Arginine vasopressin and ANP were measured with enzyme‐linked immunosorbent assay. Arginine vasopressin levels were significantly greater in HFpEF [0.96 pg/mL; 95% confidence interval (CI) = 0.83–1.1 pg/mL] compared with subjects without HF (0.69 pg/mL; 95% CI = 0.6–0.77 pg/mL; P = 0.0002). Heart failure with preserved ejection fraction (but not HFrEF) was a significant predictor of higher AVP after adjustment for potential confounders. Arginine vasopressin levels were independently associated with a greater LA volume and also paradoxically, with lower ANP levels. Key independent correlates of higher AVP were the presence of HFpEF (standardized β = 0.32; 95% CI = 0.09–0.56; P = 0.0073) and the ANP/LA volume ratio (standardized β = −0.23; 95% CI = −0.42 to −0.04; P = 0.0196). Arginine vasopressin levels were independently associated with LV mass (β = 0.26; 95% CI = 0.09–0.43; P = 0.003) and with an increased risk of death or HF admissions during follow‐up (hazard ratio = 1.61; 95% CI = 1.13–2.29; P = 0.008).ConclusionsArginine vasopressin is increased in HFpEF and is associated with LV hypertrophy and poor outcomes. Higher AVP is associated with the combination of LA enlargement and paradoxically low ANP levels. These findings may indicate that a relative deficiency of ANP (an inhibitor of AVP secretion) in the setting of chronically increased LA pressure may contribute to AVP excess.
“…Activation of ANG II receptors in the brain increases sympathetic outputs, which increases cardiac output and total peripheral resistance, thus contributing to the elevation of blood pressure [31]. ANG II also boosts release of vasopressin from the posterior pituitary gland, which is inhibited by ANP [31,33].…”
Section: Physiological Background Of the Hypothesismentioning
confidence: 99%
“…Against the effect of aldosterone, ANP induces water diuresis by inhibiting the release of vasopressin from the posterior pituitary gland [31,33].…”
Section: Physiological Background Of the Hypothesismentioning
“…The AVP receptor is regulated, in part, by angiotensin II (AngII), a peptide hormone that induces vasoconstriction (5). AngII is formed by the conversion of angiotensin I (AngI) by angiotensin-converting enzyme (ACE) (6).…”
Renal aquaporin-2 (AQP2) is critical for maintaining water balance and is associated with hypertension. Anti-hypertensive drugs, including imidapril, improve kidney function; however, it remains unclear whether these effects are mediated through the regulation of AQP2. In this study, the effects of imidapril on AQP2 expression in the kidneys and excretion in urine were assessed in hypertensive rats. Hypertension was induced in 24 rats, which were randomized into a control group, treated with water only, and an imidapril treatment group (n=12 per group). Blood and urine samples were collected from all rats to determine blood pressure (BP), serum Na+, urine volume and urine osmolality after 8 weeks of treatment. Molecular and immunological techniques were used to measure the expression of AQP2 in the kidneys. Urine AQP2 concentration was detected by indirect enzyme-linked immunosorbent assay (ELISA). The concentration of plasma arginine vasopressin (AVP), a regulator of AQP2 was detected by radioimmunoassay (RIA). Hypertensive rats treated with imidapril exhibited reduced BP and 24-h urine osmolality, with a concomitant increase in 24-h urine volume, compared with control hypertensive rats (P<0.05). Additionally, the expression of Aqp2 mRNA, detected by RT-PCR, and AQP2 protein, detected by immunohistochemistry and western blotting, in renal tissue significantly decreased (P<0.05). Finally, urine AQP2 concentration increased while plasma AVP concentration decreased following imidapril treatment (P<0.05). These findings indicate that imidapril reduces the expression level of AQP2 in renal tissue and accelerates its excretion.
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