Abstract:SUMMARY1. The interaction between atrial natriuretic factor (ANF) and angiotensin II (Ang II) within the brain to influence renal function and blood pressure was studied in Inactin-anaesthetized male Sprague-Dawley rats.2. Central infusion of ANF produced a diuresis which was associated with a significant decrease in plasma arginine vasopressin (AVP) level. There was no change in sodium excretion rate over the 80 min of intracerebroventricular ANF infusion and ANF produced no detectable change in mean arterial… Show more
“…In several studies it was postulated that ANP acts in the brain by partially inhibiting the angiotensin II (ANG II) pathway. ANP injection prevented the pressor effect of centrally administered ANG II ( 46 , 51 ). On the behavioral level, centrally administered ANP was shown to inhibit water intake induced by ANG II or dehydration in rats ( 55 ).…”
Section: Natriuretic Peptidesmentioning
confidence: 93%
“…Numerous studies found no change in BP upon central administration of ANP ( 48 – 52 ) or BNP ( 53 ). However, there are reports describing a decrease in vasopressin secretion following central ANP infusion, suggesting that ANP and vasopressin may interact to attenuate the central pressor effects of vasopressin ( 49 , 51 – 54 ). Pretreatment of rats with i.c.v.…”
Natriuretic hormones (NH) include three groups of compounds: the natriuretic peptides (ANP, BNP and CNP), the gastrointestinal peptides (guanylin and uroguanylin), and endogenous cardiac steroids. These substances induce the kidney to excrete sodium and therefore participate in the regulation of sodium and water homeostasis, blood volume, and blood pressure (BP). In addition to their peripheral functions, these hormones act as neurotransmitters or neuromodulators in the brain. In this review, the established information on the biosynthesis, release and function of NH is discussed, with particular focus on their role in brain function. The available literature on the expression patterns of each of the NH and their receptors in the brain is summarized, followed by the evidence for their roles in modulating brain function. Although numerous open questions exist regarding this issue, the available data support the notion that NH participate in the central regulation of BP, neuroprotection, satiety, and various psychiatric conditions, including anxiety, addiction, and depressive disorders. In addition, the interactions between the different NH in the periphery and the brain are discussed.
“…In several studies it was postulated that ANP acts in the brain by partially inhibiting the angiotensin II (ANG II) pathway. ANP injection prevented the pressor effect of centrally administered ANG II ( 46 , 51 ). On the behavioral level, centrally administered ANP was shown to inhibit water intake induced by ANG II or dehydration in rats ( 55 ).…”
Section: Natriuretic Peptidesmentioning
confidence: 93%
“…Numerous studies found no change in BP upon central administration of ANP ( 48 – 52 ) or BNP ( 53 ). However, there are reports describing a decrease in vasopressin secretion following central ANP infusion, suggesting that ANP and vasopressin may interact to attenuate the central pressor effects of vasopressin ( 49 , 51 – 54 ). Pretreatment of rats with i.c.v.…”
Natriuretic hormones (NH) include three groups of compounds: the natriuretic peptides (ANP, BNP and CNP), the gastrointestinal peptides (guanylin and uroguanylin), and endogenous cardiac steroids. These substances induce the kidney to excrete sodium and therefore participate in the regulation of sodium and water homeostasis, blood volume, and blood pressure (BP). In addition to their peripheral functions, these hormones act as neurotransmitters or neuromodulators in the brain. In this review, the established information on the biosynthesis, release and function of NH is discussed, with particular focus on their role in brain function. The available literature on the expression patterns of each of the NH and their receptors in the brain is summarized, followed by the evidence for their roles in modulating brain function. Although numerous open questions exist regarding this issue, the available data support the notion that NH participate in the central regulation of BP, neuroprotection, satiety, and various psychiatric conditions, including anxiety, addiction, and depressive disorders. In addition, the interactions between the different NH in the periphery and the brain are discussed.
“…Furthermore, central injection of AT 1 receptor antagonist, Losartan, blocks AT 1 receptors and influences on central angiotensin mechanisms [24,26]. Infusion of Ang II into a lateral cerebral ventricle produce an increase in blood pressure [27,20,28], increase in mean arterial pressure [29,30], decrease in urine flow [27], regulate hydromineral balance [22], induce the pressor response [31], stimulate AVP and OT release [20,28] and elevate RSNA (renal sympathetic nerve activity) [32]. Losartan blocks water intake in intracellular and extracellular dehydrated conditions, inhibits the release of AVP and OT, reduces RSNA response and antidiuretic action [5,32].…”
Thirst, which provides the motivation to drink, is an important component of the coordinated sequence of physiological responses that maintain the volume and composition of body fluids. Special structures in the central nervous system like periventricular organs detect changes in these parameters continuously. The present study investigated the interaction between dopaminergic and angiotensinergic systems on water intake in adult male rats. Intracerebroventricular (ICV) injections were carried out in all experiments after 24 h deprivation of water intake. After the deprivation interval, the volume of consumed water was measured for 1 h. Administration the angiotensinergic (AT 1 ) receptor antagonist Losartan (45 µg/rat), and the dopaminergic antagonist Chlorpromazine (40 µg/rat) significantly decreased water intake when compared to saline-treated controls. In contrast, ICV microinjection of the dopaminergic agonist Bromocriptine (10 µg/rat) significantly increased water intake when compared to saline-treated controls. ICV injection of Bromocriptine 15 min after Losartan administration was able to attenuate the inhibitory effect of Losartan on water intake, whereas administration of Chlorpromazine 15 min after Losartan was unable to change the Losartan effect. These results suggest that the dopaminergic system interactions with the angiotensinergic system to regulate water intake through circumventricular organs. Dopaminergic and angiotensinergic neurons can monitor and regulate water intake via the stimulatory and inhibitory effects on each other, respectively.
“…Besides the important cardio-renal function of NPs, they also have vasorelaxant effects and they inhibit the renin–angiotensin-aldosterone system (RAAS) and the sympathetic nervous system (SNS) [ 108 , 109 ]. Circulating ANP and vasopressin can interact to attenuate the central pressor effects of vasopressin [ 36 , 110 , 111 , 112 , 113 , 114 ], and brain natriuretic peptide (BNP) suppresses the secretion of vasopressin [ 104 ]. All of these brain regions participate in the regulation of mood and CV responses.…”
Section: Psychiatric and Cardiometabolic Mediators That Could Be Umentioning
Corticotrophin releasing factor, vasopressin, oxytocin, natriuretic hormones, angiotensin, neuregulins, some purinergic substances, and some cytokines contribute to the long-term modulation and restructuring of cardiovascular regulation networks and, at the same time, have relevance in situations of comorbid abnormal stress responses. The synthesis, release, and receptor expression of these mediators seem to be under epigenetic control since early stages of life, possibly underlying the comorbidity to coronary artery disease (CAD) and stress-related disorders (SRD). The exposure to environmental conditions, such as stress, during critical periods in early life may cause epigenetic programming modifying the development of pathways that lead to stable and long-lasting alterations in the functioning of these mediators during adulthood, determining the risk of or resilience to CAD and SRD. However, in contrast to genetic information, epigenetic marks may be dynamically altered throughout the lifespan. Therefore, epigenetics may be reprogrammed if the individual accepts the challenge to undertake changes in their lifestyle. Alternatively, epigenetics may remain fixed and/or even be inherited in the next generation. In this paper, we analyze some of the common neuroendocrine functions of these mediators in CAD and SRD and summarize the evidence indicating that they are under early programming to put forward the theoretical hypothesis that the comorbidity of these diseases might be epigenetically programmed and modified over the lifespan of the individual.
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