Hormonal Control of Cardiovascular Reflexes
Irving H. Zucker, Joseph P. Gilmore in Reflex Control of the Circulation, 2020
Expansion of the blood volume and increased atrial pressure leads to the release of ANP (Ballermann and Brenner, 1986). ANP, in turn, acts in the kidney to promote the loss of sodium and water, but it also relaxes vascular smooth muscle. The reflex responses to the hypotensive actions of ANP have been reported to be modulated by a neural effect of ANP (Ackermann, 1986; Thorén et al., 1986; Koyama et al., 1986). Early studies found that during pharmacological infusions of ANP, the decrease in blood pressure was not accompanied by an appropriate reflex increase in heart rate (Ackermann, 1986; Thorén et al., 1986; Seymour et al., 1985). In fact, heart rate often decreased. Ackermann et al. (1986) found that an atrial extract decreased heart rate and blood pressure in anesthetized rats. The bradycardic response was prevented by vagotomy but not atropine, suggesting that the atrial extract produced the bradycardia by activating cardiac vagal afferents. Although not tested in the Ackermann study, one would expect that activation of vagal afferents would also decrease peripheral sympathetic nerve activity and thus contribute to the depressor response. Indeed, Thorén et al. (1986) have shown that bolus doses of atriopeptin II and III produced marked decreases in blood pressure without a change in RSNA in anesthetized rats. In sinoaortic denervated rats, similar doses of atriopeptin II and III not only produced greater falls in blood pressure but also decreased RSNA. The decrease in RSNA was abolished by vagotomy.
Natriuretic Peptides and Cardiac Function
Malcolm J. Lewis, Ajay M. Shah in Endothelial Modulation of Cardiac Function, 2020
Bioactive human ANP consists of 28 amino acids (Figure 14-1) and is derived from the carboxy (C) –terminus of pro-ANP (Figure 14-2). Throughout this review the bioactive C-terminal ANP is referred to “ANP”. In normal adult heart ANP is predominantly produced in the atrium and the ventricular production of ANP is negligible. In the myocyte pro-ANP is stored and is cleaved to ANP and NH2 (N) –terminal ANP during exocytosis from the cell by an enzyme located on the plasma membrane (Inagami, 1989). ANP is rapidly cleared from plasma (half-life of 2.5 minutes) (Yandle et al., 1986). N-terminal ANP has a longer half-life and its plasma concentration is up to 50 times higher than that of ANP (Sundsfjord et al., 1988; Thibault et al., 1988).
Effects of an Active Lifestyle on Water Balance and Water Requirements
James M. Rippe in Lifestyle Medicine, 2019
Urine production is regulated by a number of hormones in response to changes in intravascular volume and osmolality: these include arginine vasopressin (AVP), aldosterone, and atrial natriuretic peptide (ANP). Secretion of AVP from the posterior pituitary is induced by an increase in plasma osmolality and a decrease in blood volume, increasing water reabsorption in the renal collecting ducts and the production of small volumes of concentrated urine. A one-mosm/kg increase in plasma osmolality results in a 0.41 pmol/L increase in plasma AVP concentration2 and a three-mosm/kg increase in plasma osmolality results in a 250-mosm/kg increase in urine osmolality.3 A change in blood volume of 7–10% is required for similar magnitudes of change in urine osmolality, making plasma osmolality the main determinant of AVP release.2 The renin-angiotensin aldosterone system is activated in response to decreases in blood volume with aldosterone acting on the collecting ducts of the kidney to increase sodium reabsorption which, in turn, leads to water reabsorption and the production of small volumes of concentrated urine. ANP is secreted from the right atrium in response to increases in blood pressure and leads to an increase in urine volume.
Biomarkers in patients with Takotsubo cardiomyopathy compared to patients with acute anterior ST-elevation myocardial infarction
Published in Biomarkers, 2020
Mathias Alexander Højagergaard, Christian Hassager, Thomas Emil Christensen, Lia Evi Bang, Jens Peter Gøtze, Sisse Rye Ostrowski, Lene Holmvang, Martin Frydland
Atrial natriuretic peptide (ANP) is a potent natriuretic and vasodilatory peptide hormone secreted from the myocardium by cardiomyocyte stretch (Maisel et al.2002) and ischaemia (Lindberg et al.2015). ProANP concentrations were increased in both TTC and STEMI patients compared to normal values, but we did not observe a difference between TTC and STEMI patients. This is in accordance with previous findings (Wu et al.2012). To the best of our knowledge, admission plasma concentrations of proANP in TTC patients have not been assessed before in a case-control study. In contrast, previous studies have found higher B-type natriuretic peptide concentrations in TTC patients compared to AMI patients (Madhavan et al.2009, Frohlich et al.2012). The variation may be explained by the fact that our blood samples were taken immediately on admission and/or that we had matched on LVEF, which potentially would lead to lower ANP concentrations due to decreased LVEF in TTC.
Acute myocardial infarction therapy: in vitro and in vivo evaluation of atrial natriuretic peptide and triphenylphosphonium dual ligands modified, baicalin-loaded nanoparticulate system
Published in Drug Delivery, 2021
Jie Wang, Shouwen Zhang, Lizhe Di
Surface-modification of nanocarriers such as conjugating specific ligands to nanocarrier surface can enhance the target efficacy of these nanocarriers and improve the drug efficiency (Ruckenstein & Li, 2005). Examples in MI therapy include that Yu et al. introduced an RGD modified alginate microspheres to repair the MI in the rat (Yu et al., 2010). Our previous study constructed a triphenylphosphonium (TPP) modified tanshinone-loaded nanocarriers for the target therapy of MI (Zhang et al., 2018), due to the ability of cationic TPP to pass through lipid bilayers and accumulate within mitochondria (Ong et al., 2017). Atrial natriuretic peptide (ANP) is a member of the natriuretic peptide family, which has been reported to inhibit IR injury, and reduces infarct size (Gaudin et al., 2014). In the present study, ANP and TPP dual ligands modified, BN loaded LPNs (ANP/TPP-BN-LPNs) were established, which has not been reported by other researchers.
Atrial natriuretic peptide inhibits epithelial-mesenchymal transition (EMT) of bronchial epithelial cells through cGMP/PKG signaling by targeting Smad3 in a murine model of allergic asthma
Published in Experimental Lung Research, 2019
Shuyuan Chu, Xiufeng Zhang, Yabing Sun, Yaxi Liang, Jingyi Sun, Minyan Lu, Jianwei Huang, Ming Jiang, Libing Ma
Asthma is a respiratory disease that imposes a great health burden in worldwide. It affected about 300 million people globally in 2011 and accounts for 250,000–345,000 death each year.1,2 In our previous work, we found that the level of atrial natriuretic peptide (ANP) in serum was higher in asthmatic patients than healthy controls, and was increased when asthma was aggravated.3 We also validated that finding in the murine model of allergic asthma.4 ANP is a polypeptide hormone that controls blood pressure via reducing water and sodium loads in circulatory system.5 It has been found to protect animal model against allergen-induced airway hyperresponsiveness,6,7 suggesting a protective role in allergic asthma. However, there is rare report on the precise mechanism how ANP plays a protective role in asthma. We further found that ANP could inhibit TGF-β1-induced epithelial-mesenchymal transition (EMT) in human bronchial epithelial cells.8 Airway EMT promotes mucosal remodeling, contributing to refractory asthma.9 Thus, we suppose that airway EMT of asthma may be interfered by ANP. In this study, we investigate the precise role of ANP in bronchial EMT of allergic asthma and its possible mechanism using bronchial epithelial cells from murine model of allergic asthma.
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