The Biochemical Pharmacology of Atrial Peptides

Needleman, Philip; Blaine, Edward H.; Greenwald, James E.; Michener, Marshall L.; Saper, Clifford B.; Stockmann, Paul T.; Tolunay, Hatice

doi:10.1146/annurev.pa.29.040189.000323

Cited by 172 publications

(53 citation statements)

References 88 publications

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“…CNP is somewhat selectively predominant in the central nervous system [5,6], hence it is possible that it acts as a neurotransmitter and/or participates in the centrally-related fluid secretion and blood pressure regulation. One important second messenger of these hormones is cyclic GMP (reviewed in [2][3][4]). The receptors for ANF (ANF-RGC) [7-l 31 and CNP (CNP-RGC) [ 14,151 have been characterized; both are guanylate cyclases and are structurally similar.…”

Section: Introductionmentioning

confidence: 99%

The glycine residue of ATP regulatory module in receptor guanylate cyclases that is essential in natriuretic factor signaling

1993

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Atrial natriuretic factor (ANF) and C-type natriuretic peptide (CNP)-activated guanylate cyclases are single-chain transmembrane-spanning proteins, containing both ligand binding and catalytic activities. In both proteins, ligand binding to the extracellular receptor domain activates the cytosolic catalytic domain, generating the second messenger cyclic GMP. Obligatory in this activation process is an ATP-dependent step. ATP directly binds to a deBned ATP-regulatory module (ARM) sequence motif in the cyclases and through ARM bridges the events of ligand binding and signal transduction. These ARM sequence motifs are respectively represented by GlySo'-Xa-Gl$05-Xa-Xa-Xa-Gly509 and Gly@-Xa-Xa-XaGly"' in the case of ANF receptor guanylate cyclase (ANF-RGC) and CNP receptor guanylate cyclase (CNP-RGC). Through genetic remodeling techniques, we now show that ARM-GlJo5 in ANF-RGC and the corresponding ARM-Gly"% in CNP-RGC are critical for ANF and CNP signaling, and other ARM-Gly residues have minimal effect in the respective signaling processes.Guanylate cyclase; ATP-regulatory module; Atrial natriuretic factor receptor; Type C natriuretic peptide receptor

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Section: Introductionmentioning

confidence: 99%

The glycine residue of ATP regulatory module in receptor guanylate cyclases that is essential in natriuretic factor signaling

1993

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“…The major site of ANP biosynthesis is the atria of the heart, where it constitutes 1-3% of the total messenger RNA (mRNA) (Needleman et al, 1989). Recent evidence shows that biosynthesis of ANP also occurs in extra-atrial tissues, particularly in cardiac ventricles (Bloch et al, 1986;Gardner et al, 1986a;Needleman et al, 1989). In tissue culture, ventricular as well as atrial cardiocytes secrete ANP into the culture medium (Bloch et al, 1986).…”

Section: Introductionmentioning

confidence: 99%

Release of atrial natriuretic peptide from rat myocardium in vitro: effect of minoxidil‐induced hypertrophy

Kinnunen

Taskinen

Leppäluoto

et al. 1990

British J Pharmacology

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1 Ventricular hypertrophy is characterized by stimulation of ventricular synthesis of atrial natriuretic peptide (ANP). To examine the role of ventricular ANP levels in the secretion of ANP into the circulation, atrial and ventricular levels of immunoreactive-ANP (IR-ANP) as well as ANP messenger RNA (mRNA), and the release of IR-ANP from isolated perfused hearts, both before and after atrialectomy, were measured simultaneously in control and minoxidil-treated Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats. 2 IR-ANP levels in the ventricles of untreated, 12 month-old SHR with severe ventricular hypertrophy were increased when compared to age-matched WKY rats. Minoxidil treatment for 8 weeks in both strains resulted in a decrease in mean arterial pressure and increases in ventricular weight to body weight ratios, plasma IR-ANP concentrations (in WKY from 133 + 20 to 281 + 34pgml-1, P < 0.01; in SHR from 184 + 38 to 339 + 61 pgml-', P < 0.05), and in ventricular IR-ANP contents (in WKY: 53%; in SHR: 41%). A highly significant correlation was found between ventricular IR-ANP content and ventricular weight to body weight ratio (r = 0.59, P < 0.001, n = 26). 3 When studied in vitro, in isolated perfused heart preparations, the hypertrophied ventricular tissue after atrialectomy secreted more ANP into the perfusate than ventricles of the control hearts; ventricles contributed 28%, 22%, 18% and 15% of the total ANP release to perfusate in the minoxidil-treated SHR, control SHR, minoxidil-treated WKY and control WKY, respectively. A significant correlation was found between the IR-ANP release from ventricles and ventricular weight to body weight ratio (r = 0.56, P < 0.01, n = 24). 4 These studies demonstrate that the ventricles contribute substantially to the circulating level of ANP, and that the amount released depends on the degree of ventricular hypertrophy.

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“…Both NO and ANP re lax vascular smooth muscles (1,2). ANP activates the particulate guanylate cyclase in smooth muscle (3), while NO activates soluble guanylate cyclase (4).…”

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confidence: 99%

“…ANP activates the particulate guanylate cyclase in smooth muscle (3), while NO activates soluble guanylate cyclase (4). Since ANP has a potent diuretic action (2), it has been sug gested that ANP might have a role in regulating blood volume (5). Several investigators have reported that administered atriopeptin (rat ANP) increases the hema tocrit in rats (6,7).…”

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Effects of Nitric Oxide-Related Compounds and Carperitide on Hemodynamics and Hematocrit in Anesthetized Rats

Aisaka

Miyazaki

Hidaka

et al. 1992

Japanese Journal of Pharmacology

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ABSTRACT-Sodium nitroprusside, nitroglycerin and carperitide (a-human ANP) all reduced mean blood pressure, but only carperitide increased the hematocrit in rats with bilateral renal artery and ureter-ligation. Nc-Monomethyl L-arginine, a selective inhibitor of nitric oxide synthesis, elevated the mean blood pressure but did not change the hematocrit significantly. These findings suggest that ANP has a physiological role in regulating circulatory blood volume distinct from that of NO, although both increase intracellular cyclic GMP in the vasculature. Nitric oxide (NO) is produced in vascular endothelial cells, and atrial natriuretic peptide (ANP) is produced in and released from atrial cells. Both NO and ANP re lax vascular smooth muscles (1, 2). ANP activates the particulate guanylate cyclase in smooth muscle (3), while NO activates soluble guanylate cyclase (4). Since ANP has a potent diuretic action (2), it has been sug gested that ANP might have a role in regulating blood volume (5). Several investigators have reported that administered atriopeptin (rat ANP) increases the hema tocrit in rats (6, 7). However, the increase in hemato crit has not been totally explained by fluid loss due to the diuretic action of ANP. Almedia et al. (6) have hypothesized that the rat ANP-induced increase in hematocrit may be due to an increase in the fluid efflux from capillaries, which thereby causes a decrease in plasma volume. On the other hand, kidney function has also been reported to be regulated by NO (8), but to our knowledge, the effect of NO on hematocrit is not known yet. To assess whether exogenous NO and ANP can modulate the hematocrit, we have examined the effect of NO-generating drugs and carperitide (a-hu man ANP) on the hematocrit by concomitantly moni toring arterial blood pressure and heart rate in anesthe tized rats.Male Wistar rats weighing 200 290 g were used (Shizuoka Agr. Coop., Hamamatsu, Japan). Each of the drug-treatment groups consisted of 5 rats. Rats were anesthetized with urethane plus a -chloralose (500 mg/kg and 100 mg/kg, i.p., respectively). The bilateral renal arteries, veins and ureters exposed by a dorsal approach were ligated concomitantly. A tracheotomy was performed to keep good ventilation. Polyethylene catheters (PE 50) were inserted into the left juglar vein for infusion of drugs and into the right common carotid artery for measurement of systemic blood pressure and withdrawal of blood sample for determination of hemato crit. Blood pressure (BP) was measured by a pressure transducer (MPU-0.5A, Nihon Kohden, Tokyo), and heart rate (HR) was measured with a heart rate counter (AT-600T, Nihon Kohden) triggered by the BP pulse. Changes in BP and HR were continuously recorded on a polygraph recorder (RM-6200, Nihon Kohden). At first, the effect of physiological saline solution (vehicle) given intravenously in a volume of 80 p1/kg/min for 30 min was studied in all animals used, and then each of the test drugs was cumulatively in fused by increasing the concentration in a stepwise fashion at ...

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The Biochemical Pharmacology of Atrial Peptides

Cited by 172 publications

References 88 publications

The glycine residue of ATP regulatory module in receptor guanylate cyclases that is essential in natriuretic factor signaling

The glycine residue of ATP regulatory module in receptor guanylate cyclases that is essential in natriuretic factor signaling

Release of atrial natriuretic peptide from rat myocardium in vitro: effect of minoxidil‐induced hypertrophy

Effects of Nitric Oxide-Related Compounds and Carperitide on Hemodynamics and Hematocrit in Anesthetized Rats

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