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Intranasal Angiotensin II Directly Influences Central Nervous Regulation of Blood Pressure Inge Derad, Karen Willeke, Reinhard Pietrowsky, Jan Born, and Horst L. Fehm
Intranasal administration of some peptides has been shown to directly influence central nervous functions, thus pointing to a nose– brain pathway for these substances in humans. The present study investigated whether intranasal administration of angiotensin II (ANG II) affects central nervous functions of cardiovascular control in a different way from intravenously administered ANG II. In a balanced cross-over design 12 healthy men were treated with ANG II intravenously (2.5 mg), ANG II intranasally (400 mg), and placebo. Angiotensin II, vasopressin, norepinephrine, and epinephrine plasma levels were assessed every 10 min; blood pressure, heart rate, and systemic vascular resistance were measured by a Dinamap, and by continuous, noninvasive body plethysmography. Also, feelings of activation and mood were measured. Intranasal and intravenous administration invoked equivalent increases in plasma levels of ANG II, and induced an acute rise in blood pressure of comparable size and duration. However, subsequent blood pressure profiles
differed dependent on intravenous and intranasal ANG II administration; after intravenous ANG II administration blood pressure remained enhanced at an intermediate level, but it returned to normal or even decreased below normal levels after intranasal ANG II administration. Intranasal ANG II also counteracted the decrease in norepinephrine levels observed after intravenous administration of ANG II. Intranasal but not intravenous ANG II enhanced plasma concentrations of vasopressin. This diverging pattern of effects bears similarities with effects of intracerebroventricular administration of ANG II in animals, suggesting that the effects after intranasal administration reflect a direct central nervous action of ANG II. Am J Hypertens 1998;11:971–977 © 1998 American Journal of Hypertension, Ltd.
he peptide hormone angiotensin II (ANG II) displays a wide range of regulatory actions on the cardiovascular system. On the one hand, these actions include effects in the body periphery, such as systemic vasoconstriction1
and multiple paracrine effects.2,3 On the other hand, ANG II acts as a neuropeptide in various brain structures controlling cardiovascular activity. Brain and peripheral functions of ANG II differ as indicated by different neurohormonal and cardiovascular re-
Received August 13, 1997. Accepted March 9, 1998. From the Departments of Internal Medicine (ID, KW, HLF) and Clinical Neuroendocrinology (RP, JB), University of Lu¨beck, Lu¨beck, Germany.
Address correspondence and reprint request to Dr. Inge Derad, Medizinische Klinik I, Medizinische Universita¨t zu Lu¨beck, Ratzeburger Allee 160, 23538 Lu¨beck, Germany; e-mail: [email protected] t-online.de
© 1998 by the American Journal of Hypertension, Ltd. Published by Elsevier Science, Inc.
Angiotensin II, vasopressin, blood pressure, central nervous system, intranasal administration.
0895-7061/98/$19.00 PII S0895-7061(98)00095-8
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sponses to ANG II after systemic versus central nervous administration in animal models.4 –7 A discrimination of central and peripheral actions of ANG II seems also important for the understanding of cardiovascular regulation and the development of essential hypertension in humans.8 After systemic administration in humans, ANG II has been reported to induce an acute as well as a chronic increase in blood pressure (lasting for hours and days), and a decrease in norepinephrine plasma levels, whereas effects on plasma vasopressin concentrations remained nonsignificant.1,6,9 In contrast, transiently intracerebroventricular administration of ANG II in animals increased or decreased blood pressure, depending on the site of ANG II administration, strongly enhanced release of vasopressin and drinking behavior, and increased norepinephrine turnover in various brain regions.10 –15 The present study examined whether intranasal administration of ANG II in humans invokes similar effects like those observed after direct central nervous administration of the peptide in animals. Animal studies have provided converging evidence that, after intranasal administration, larger molecules such as horseradish peroxidase and viruses reach the extracellular compartment of the brain within 45 to 90 min through intercellular junctions of the olfactory epithelia.16,17 Moreover, in humans synthetic peptides such as 1-desamino-8d-arginine-vasopressin (DDAVP) have been shown to accumulate in liquor after intranasal administration.18 There are also coherent functional data indicating a direct access of peptides to brain functions through the nose.19,20 Here, we compared effects of different doses of ANG II after intranasal versus intravenous administration on plasma vasopressin and catecholamine concentrations, blood pressure, heart rate, and systemic vascular resistance. Also associated changes in subjective feelings of activation and mood were evaluated. With equivalent systemic plasma concentrations of ANG II after intranasal and intravenous administration, changes in these variables after intranasal administration diverging from those after intravenous ANG II would be indicative for a central nervous action of the peptide. METHODS Subjects Twelve normotensive, healthy male students (age 25.8 6 3 years; body weight 76.6 6 8 kg; height 182 6 8 cm) participated in the study. All subjects were nonsmokers and did not take any medication at the time of the experiments. Before the experiment, all had a general medical examination including blood pressure control. The participants were instructed to abstain from caffeine and alcohol at least 16 hours before experimental sessions, and were examined in the postabsorptive state (last meal at least
6 h before the experiment). Women were not examined to avoid interferences of hormonal changes related to their menstrual cycle. One subject had to be excluded because of a history of listeriosis 5 years ago, another subject, a body builder, was excluded due to an extreme exerciseinduced bradycardia, so that the final number of subjects was 10. The study had been approved by the local ethics committee. After comprehensive information about possible side effects of a single administration of ANG II, each subject gave written consent before the experiments. Procedure, Design, and Recordings The experiments were conducted as a blind, within-subject crossover comparison according to a Latin square-type design. Each subject participated in five test sessions starting either at 8:00 or 14:30, balanced across subjects. The sessions of each individual subject were separated by an interval of 1 week. The order of treatments was randomized across subjects. The subjects received ANG II (Hypertensin®, Ciba, diluted in sterile NaCl 0.9%). ANG II was administered intravenously at a low (0.625 mg) and high dose (2.5 mg) as an infusion for 15 min, or intranasally at a low (100 mg) and high dose (400 mg) with four single intranasal puffs of 100 mL within 15 min. Placebo (NaCl 0.9%) was administered intravenously and intranasally. Throughout the test sessions the subject remained in a supine position. At the beginning a cannula was placed into the right cubital vein for drug administration and another into the left cubital vein for blood sampling. After a 15-min baseline period, substances were administered within 15 min either by infusion or by four intranasal puffs. Measurements continued for 165 min after the end of the infusion period. Blood samples for determination of plasma concentrations of ANG II, vasopressin, and the catecholamines (norepinephrine, epinephrine) were collected every 10 min, starting 10 min before and ending 145 min after the initiation of treatments, thereafter blood samples were collected every 30 min. Blood pressure was measured according to Korotkoff’s method by a Dinamap (Critikon, Norderstedt, Germany) on the left arm. For noninvasive continuous monitoring of hemodynamics by body plethysmography (NCCOM3-R7, Dr. Osypka GmbH, Grenzach-Wyhlen, Germany), the electrodes (Ag/AgCl) were placed on the thorax and neck. Blood pressure (systolic and diastolic) was automatically recorded every minute. These results were fed into the hemodynamic measurement program, evaluating online the continuous data from thoracic body plethysmography to assess heart rate (HR) and systemic vascular resistance (SVR).21 Values were determined at a sampling rate of 300 Hz. Immediately before and after the 195-min recording
AJH–AUGUST 1998 –VOL. 11, NO. 8, PART 1
INTRANASAL ADMINISTRATION OF ANGIOTENSIN II
session, the subject’s feelings of activation and mood were assessed using a standardized adjective checklist (Eigenschaftswoerterliste, EWL).22 Data Analysis Plasma concentrations of vasopressin and ANG II were determined by a commercially available radioimmunoassay kit (RIA) (DPC, Bad Manheim, Germany), with a detection level of 0.06 pg/mL, range of twofold standard deviation (2s): 1 to 7.8 pg/mL for vasopressin; and a detection level of ANG II of 0.7 pg/mL, 2s: 0 to 12.7 pg/mL. All samples were assessed in duplicate. For further evaluation, data were averaged across three successive blood samples, resulting in average values for subsequent 30-min periods. Recordings of systolic, diastolic, and mean arterial blood pressure, mean HR and SVR were averaged offline. Mean HR and SVR recordings were inspected visually to exclude artifact contaminated periods and to correct escape beats. The statistical evaluation of effects of intravenous and intranasal ANG II administration on hormone concentrations, blood pressure, HR, and SVR made use of an analysis of covariance (ANCOVA) including the repeated measures factors “treatment” (intravenous, intranasal, placebo) and “time” after treatment. The average value during the baseline served as covariate. After the overall analysis, significant main effects were specified by pairwise comparisons between the effects of any two treatment conditions for each point in time. Greenhouse-Geisser corrections were calculated if necessary. Effects of the treatments on self-reported measures of activation and mood were evaluated statistically by nonparametric tests (Wilcoxon’s t test). RESULTS At the low dose, both intravenous and intranasal administration of ANG II did not exert any significant effects on plasma concentrations of angiotensin and vasopressin, blood pressure, hemodynamics, or mood and feelings of activation. Therefore, this report will be restricted to the effects of the higher, intravenously and intranasally administered doses of ANG II. Plasma Levels of Angiotensin II, Vasopressin, and Catecholamines While subjects rested in a supine position, in the placebo condition, ANG II plasma concentrations remained within the physiologic range throughout the session. The high doses of ANG II after both intravenous and intranasal administration induced discernible plasma ANG II peaks, which were of comparable magnitude for both routes of administration (Table 1). Vasopressin plasma concentrations were significantly enhanced by intranasal administration of ANG II and appeared to be slightly, although not signifi-
TABLE 1. PLASMA ANGIOTENSIN II (ANG II) CONCENTRATIONS AFTER ADMINISTRATION OF PLACEBO, INTRAVENOUS ANG II (IVAN), AND INTRANASAL ANG II (INANG) ANG II Administration at: 0–30 30–60 60–90 90–120 120–180
min min min min min
Placebo (mean 6 SEM)
IVANG (mean 6 SEM)
INANG (mean 6 SEM)
9.7 6 3.1 13.7 6 6.9 8.9 6 3.2 9.9 6 3.9 12.8 6 3.8
25.1 6 7.2* 12.0 6 1.8 10.5 6 1.7 14.2 6 2.6 10.2 6 2.5
28.9 6 10.8* 14.9 6 4.3 13.5 6 2.6 11.3 6 2.9 10.0 6 2.6
* P , .05 for pairwise comparison with respective placebo value. Means are baseline adjusted as derived from ANCOVA.
cantly enhanced after intravenous administration of ANG II, as compared to the effects of placebo (Figure 1A). After intranasal ANG II, the increase in plasma vasopressin concentrations reached significance between 75 and 145 min after administration. Thereafter (ie, 120 to 180 min after intranasal intake), vasopressin levels dropped below the concentrations observed after placebo and intravenous ANG II administration (P , .05, Figure 1A). Plasma concentrations of norepinephrine were lowered after the intravenous administration of ANG II only. The decrease reached significance 75 to 105 min after the start of peptide administration, compared with the effect of placebo as well as compared with the effects of intranasal ANG II. In contrast, intranasal ANG II tended to increase norepinephrine plasma concentrations toward the end of the session (Figure 1B). Plasma concentrations of epinephrine remained at a low level after placebo administration and were not changed by intravenous or intranasal ANG II administration. Blood Pressure and Hemodynamics Systolic and diastolic blood pressure changed in parallel after both routes of drug administration. Therefore, results from mean arterial pressure (MAP) are reported (Figure 2A). The intravenous administration of ANG II induced a prompt increase in MAP (up to 10 mm Hg compared with placebo) lasting until 20 min after the end of drug administration (P , .01). Thereafter, MAP remained at a moderately elevated level until 3 h after the start of intravenous ANG II administration (P , .05; Figure 2A). The intranasal administration of ANG II also induced an acute rise in MAP that was of similar magnitude as that after intravenous ANG II. After this acute rise, MAP gradually declined to reach the level of the placebo condition (or slightly lower). Thus, during the remaining period (ie, between 30 and 180 min after intranasal ANG II administration), MAP was substantially lower compared to the MAP levels
DERAD ET AL
AJH–AUGUST 1998 –VOL. 11, NO. 8, PART 1
creased, but still remained significantly above levels observed during the placebo session. After intranasal ANG II administration SVR also acutely increased for about 30 min (as compared with the effects of placebo), but then declined toward placebo values. Hence, during the later period after intranasal ANG II administration, SVR was significantly lower than after intravenous ANG II administration. Feelings of activation and mood, as assessed by the EWL were not altered by ANG II. DISCUSSION
FIGURE 1. Adjusted mean (6 SEM) plasma concentrations of vasopressin (A) and norepinephrine (B) after placebo (open bars), intravenous administration of ANG II (2.5 mg, gray bars), and intranasal administration of ANG II (400 mg, hatched bars), as derived from the statistical analysis. Administration of substances started at 0 min and for the intravenous route lasted 15 min. Plasma concentrations were averaged across intervals of 30 and 60 min, respectively. Asterisks indicate significant (P , .05) differences between the effects of any two of the treatments.
after intravenous ANG II, which during that time were still elevated (P , .05). Changes in blood pressure after ANG II administration were not accompanied by significant changes in HR, except for a slight, transient (,1 min) HR deceleration (of about 4 beats/ min) associated with the immediate increase in MAP after intravenous ANG II administration. Changes in SVR after ANG II paralleled those in MAP (Figure 2B). After intravenous ANG II, SVR displayed an acute and highly significant increase during the time of ANG II infusion. Then, SVR de-
This study compared effects of ANG II on plasma concentrations of vasopressin and norepinephrine, and on cardiovascular parameters. It was hypothesized that intranasal administration would reflect more direct actions of the peptide on the brain, as compared to the effects of intravenous administration mediated predominantly through binding to peripheral ANG II receptors but also to ANG II receptors in the circumventricular organs. Although peak and average increases in plasma ANG II concentrations after the intranasal administration of 400 mg of ANG II and after the intravenous administration of 2.5 mg of ANG II were highly comparable, the pattern of changes differed in essential aspects: 1) intranasal but not intravenous ANG II significantly increased plasma vasopressin concentrations, ie, induced an increased vasopressin release via the neurohypophysis; 2) plasma norepinephrine concentrations were reduced by intravenous ANG II, but not by intranasal ANG II administration; and 3) although both routes of ANG II administration induced an acute rise in blood pressure, subsequent blood pressure profiles after intravenous and intranasal administration differed in spite of similarly raised blood ANG II levels. In particular, the induction of vasopressin release and the increase in sympathetic noradrenergic tone, after intranasal ANG II administration as compared with intravenous ANG II administration, suggest a prevalence of central nervous actions after the intranasal route of ANG II administration. In fact, substantial increases in plasma vasopressin have been observed so far only after intracerebroventricular administration of ANG II in animals.4,5,15,23,24 Like in previous studies in men, changes toward increasing plasma levels of vasopressin remained nonsignificant after intravenous administration of ANG II.9 With regard to norepinephrine, only the direct central nervous administration of ANG II in animals has been found to activate central nervous catecholaminergic pathways,25,26 although these effects did not express themselves in enhanced norepinephrine plasma concentrations. In men, the infusion of ANG II led to reduced plasma levels of norepinephrine.6,27
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FIGURE 2. Means (6 SEM) of mean arterial blood pressure (A) and systemic vascular resistance (B) after placebo (dotted line), intravenous administration of ANG II (2.5 mg, thin solid line), and after intranasal administration of ANG II (400 mg, thick solid line) for subsequent 1-min intervals (SEM are shown every 5 min). Administration of substances started at 0 min and for the intravenous route lasted 15 min (hatched horizontal bar). Asterisks and bars at the bottom indicate periods of significant differences between the effects of any two of the treatments (**thick bar, P , .01; *thin bar, P , .05).
The intravenous administration of ANG II acutely induced a pronounced increase in systolic and diastolic blood pressures, followed by a prolonged phase of moderately elevated systolic and diastolic blood pressures. These changes resulting from an increased SVR, are in accordance with previous findings in men and animals after systemic ANG II administration.1,9,28,29 The prolonged elevation of blood pressure is considered to involve an activation of ANG II receptors within circumventricular organs, ie, the area
postrema.9 These receptors probably serve as an interface gating effects of blood-borne ANG II to hypothalamic nuclei regulating tonic blood pressure levels through a modulation of baroreceptor reflex activity and the sympathetic nervous activity.1,6,23 Interestingly, plasma norepinephrine concentrations after intravenous ANG II administration were reduced,9,27 and the source of this finding, be it negative feedback regulation or another mechanism, remains to be elucidated.
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Although an action via receptor sites in the area postrema is known to mediate the persisting elevation of blood pressure after intravenous administration of ANG II, the blockade of this elevation was a prominent feature of intranasal ANG II administration. Because the systemic increase in plasma ANG II concentrations was comparable with the intravenous and intranasal routes of administration, this finding suggests a direct, central nervous blood pressure reduction developing about 40 to 50 min after intranasal administration of the peptide. Yet, the locus of the effect of intranasal ANG II remains unclear at present. Pressor effects of ANG II after direct central nervous administration in animals have been found to be variable depending on dose and location of the administration. Injection of high doses of ANG II into the third ventricle of rats increased blood pressure.1,13 Moreover, in spontaneously hypertensive rats, inhibition of ANG II synthesis by intracerebroventricular administration of antisense oligodesoxynucleotides to angiotensinogen mRNA inhibited hypertension.30 Those findings argue against the view that effects of ANG II after intranasal administration mimic a diffuse stimulatory influence on the brain’s ANG II receptor system. Rather an effect mediated through a localized stimulation of ANG II receptors near the olfactory bulb and neighboring structures seems likely. With regard to the principle mechanisms responsible for central nervous actions of peptides after intranasal administration various pathways through which brain barriers may be circumvented have been demonstrated in animals. Large tracer molecules, such as native horseradish peroxidase, pass freely through intercellular junctions of the olfactory epithelia to reach the olfactory bulbs of the central nervous system extracellularly within 45 to 90 min. Signals can be transferred from the nose to the brain also by an intraaxonal transport of the whole substance or of centrally active fragments of the substance derived from degradation in the nasal epithelium.31 Although the exact mechanisms mediating the effects of ANG II after the intranasal administration remains to be specified, the effects of intranasal ANG II, ie, the modulation of vasopressin release, norepinephrine release, and the normalization of elevated blood pressure levels clearly differed from those after intravenous ANG II administration. Simultaneously they bear similarity with changes observed after intracerebroventricular administration in animals. On these grounds it seems justified to conclude that these effects reflect a direct action of ANG II on central nervous mechanisms of blood pressure regulation by way of the intranasal route.
S. Baxmann for technical assistance. This research was supported by the Deutsche Forschungsgemeinschaft.
Peach MJ: Physiological roles of angiotensin, in Meyerhofer J (ed): Chemistry of Biological Peptides: Proceedings of the Third American Peptide Symposium. Ann Arbor Science Publishers, Ann Arbor, MI, 1972, pp 477– 493.
Dzau VJ, Ingelfinger JR, Pratt RE: Regulation of tissue renin and angiotensin gene expression. J Cardiovasc Pharmacol 1986;8(suppl 10):S11–S16.
Linz W, Wiemer G, Gohlke P, et al: Contribution of kinins to the cardiovascular actions of angiotensin-converting enzyme inhibitors. Pharmacol Rev 1995;47:25– 49.
Ho¨hle S, Blume A, Lebrun C, et al: Angiotensin receptors in the brain. Pharmacol Toxicol 1995;77:306 –315.
Unger T, Chung O, Csikos T, et al: Angiotensin receptors. J Hypertens 1996;14:S95–S103.
Guo GB, Abboud FM: Angiotensin II attenuates baroreflex control of heart rate and sympathetic activity. Am J Physiol 1984;246:H80 –H89.
Reid I: Interactions between ANG II, sympathetic nervous system, and baroreceptor reflexs in regulation of blood pressure. Am J Physiol 1992;262:E763–E778.
Phillips M, Wielbo D, Gyurko R: Antisense inhibition of hypertension: a new strategy for renin-angiotensin candidate genes. Kidney Int 1994;46:1554 –1556.
Goldsmith SR, Dodge-Brown D, Pentel P: Effects of infused norepinephrine and angiotensin-II on vasopressin levels in humans. Am J Med Sci 1988;295:513– 516.
Unger T, Badoer E, Ganten D, et al: Brain angiotensin: pathways and pharmacology. Circulation 1988;77 (suppl I):I40 –I54.
Steckelings U, Bottari S, Unger T: Angiotensin receptor subtypes in the brain. Trends Pharmacol Sci 1992;13: 365–368.
MacGregor DP, Murone C, Song K, et al: Angiotensin II receptor subtypes in the human central nervous system. Brain Res 1995;675:231–240.
Badoer E, Unger T, Ganten D: Role of endocrine brain in the control of hypertension. Angiotensin II and atrial natriuretic peptide in the brain, in Motta M (ed): Brain Endocrinology, 2nd ed. Raven Press, New York, 1991, pp 403– 430.
Ferguson AV, Wall KM: Central actions of angiotensin in cardiovascular control: multiple roles for a single peptide. Can J Physiol Pharmacol 1991;70:779 –785.
Culman J, Ho¨hle S, Quadri F, et al: Angiotensin as neuromodulator/neurotransmitter in central control of body fluid and electrolyte homeostasis. Clin Exp Hypertens 1995;17:281–293.
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ACKNOWLEDGMENTS We thank Dr. C. Niederstadt and Dr. W. Guenther for helpful advice. We gratefully thank A. Otterbein, C. Zinke, and
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tral nervous system in mouse, rat, and squirrel monkey. J Comp Neurol 1986;251:260 –280. 18.
Riekkinen P, Legros J-J, Sennef C, et al: Penetration of DGAVP (Org 5667) across the blood-brain barrier in human subjects. Peptides 1987;8:261–265.
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Pietrowsky R, Stru¨ben C, Mo¨lle M, et al: Brain potential changes after intranasal vs. intravenous administration of vasopressin: evidence for a direct nose-brain pathway for peptide effects in humans. Biol Psychiatry 1996;39:332–340.
Linde M, Halabi A, Hinrichsen H, et al: Impedance cardiography in clinical pharmacology-advantages and limitations, in Winter UJ, Klocke RK, Kubicek WG, Niederlag W (eds): Thoracic Impedance Measurements in Clinical Cardiology. Thieme Verlag, Stuttgart, 1994, pp 81– 84. Janke W, Debus G: Die Eigenschaftswo¨rterliste EWL. Eine mehrdimensionale Methode zur Beschreibung von Aspekten des Befindens. Verlag fu¨r Psychologie Hogrefe, Go¨ttingen, 1988. Veltmar A, Culman J, Qadri F, et al: Involvement of adrenergic and angiotensinergic receptors in the paraventricular nucleus in the angiotensin II-induced vaso-
pressin release. J Pharmacol Exp Ther 1992;263:1253– 1260. Steckelings U, Lebrun C, Qadri F, et al: Role of brain angiotensin in cardiovascular regulation. J Cardiovasc Pharmacol 1992;19(suppl 6):S72–S79. Qadri F, Badoer E, Stadler T, et al: Angiotensin IIinduced noradrenaline release from anterior hypothalamus in conscious rats: a brain microdialysis study. Brain Res 1991;563:137–141. Stadler T, Veltmar A, Qadri F, et al: Angiotensin II evokes noradrenaline release from the paraventricular nucleus in conscious rats. Brain Res 1992;569:117–122. Mendelsohn FAO, Doyle AE, Gray GW: Lack of response of sympathetic nervous system to angiotensin infusion. Lancet 1980;i:492– 493. Mace PJE, Watson RDS, Skan W, et al: Inhibition of the baroreceptor heart reflex by angiotensin II in normal man. Cardiovasc Res 1985;19:525–527. Seidelin PH, Coutie WJR, Struthers AD: The effect of angiotensin II on endogenous noradrenaline release in man. Br J Clin Pharm 1987;24:699 –704. Phillips P, Bretherton M, Risvanis J, et al: Effects of drinking on thirst and vasopressin in dehydrated elderly men. Am J Physiol 1993;264:R877– 881. Dahl A, Hadley W: Nasal cavity enzymes involved in xenobiotic metabolism effects on the toxicity of inhalants. Crit Rev Toxicol 1991;21:345–372.
Free download or read online Blood Song pdf (ePUB) book. The first edition of the novel was published in 2011, and was written by Anthony Ryan. The book was published in multiple languages including English, consists of 591 pages and is available in Kindle Edition format. The main characters of this fantasy, fantasy story are Vaelin Al Sorna, Caenis. The book has been awarded with , and many others.
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Blood Song PDF Details
|Original Title:||Blood Song|
|Book Format:||Kindle Edition|
|Number Of Pages:||591 pages|
|First Published in:||2011|
|Latest Edition:||January 22nd 2012|
|Series:||Ravens Shadow #1|
|Main Characters:||Vaelin Al Sorna, Caenis, Princess Lyrna, Lord Vernier, Master Sollis|
|category:||fantasy, fantasy, epic fantasy, fiction, fantasy, high fantasy|
|Formats:||ePUB(Android), audible mp3, audiobook and kindle.|
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