Cardiovascular and respiratory actions of pituitary adenylate cyclase-activating polypeptides

Ishizuka, Y.; Kashimoto, Kazuhisa; Mochizuki, Tohru; Sato, Keigo; Ohshima, Keiich; Yanaihara, Noboru

doi:10.1016/0167-0115(92)90081-5

Cited by 69 publications

(35 citation statements)

References 11 publications

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“…For example, PACAP has various hormonal functions in all endocrine glands; it influences motility and secretion in the gastrointestinal and respiratory tracts and regulates urogenital physiology (Vaudry et al 2000 ;Cardell et al 1991 ;Cheng et al 1993 ;Ishizuka et al 1992 ;Botz et al 2013 ). In addition, it has been revealed that PACAP has potent vasomotor effects Nandha et al 1991 ;Hagi et al 2008 ).…”

Section: Pacap-induced Vasomotor Responses Of Various Tissuesmentioning

confidence: 99%

“…In vivo studies on beagle dogs described that intravenous infusion of very low doses (0.01-10 pmol/min) of PACAP induced a concentration-dependent increase in blood flow in human skin and a concomitant decrease in systemic blood pressure (Cardell et al 1991 ;Nandha et al 1991 ;Naruse et al 1993 ). High doses (>3 nmol) of PACAP elicited a biphasic effect: a transient hypotensive response, followed by a sustained period of hypertension (Ishizuka et al 1992 ;Cardell et al 1991 ). It was suggested that the action of PACAP on the vascular tone could be ascribed both to a direct relaxant effect and an indirect vasopressor action mediated through the release of endogenous catecholamines (Cardell et al 1991 ).…”

Section: Introductionmentioning

confidence: 99%

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Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP) Induces Relaxations of Peripheral and Cerebral Arteries, which are Differentially Impaired by Aging

et al. 2014

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Section: Pacap-induced Vasomotor Responses Of Various Tissuesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP) Induces Relaxations of Peripheral and Cerebral Arteries, which are Differentially Impaired by Aging

et al. 2014

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“…In rat intracardiac neurons, removal of extracellular Ca 2ϩ over a short period of time (minutes) not only prevents Ca 2ϩ conductance through the plasma membrane but also results in depletion of Ca 2ϩ from internal stores. 2 Thus, PACAPinduced [Ca 2ϩ ] i mobilization is blocked by washing the intracardiac neurons with Ca 2ϩ -free PSS. Fig.…”

Section: Pacap-and Vip-induced Excitability In Rat Intracardiacmentioning

confidence: 99%

“…ropeptides that belong to the glucagon/secretin/growth hormone-releasing factor family of peptides (1)(2)(3)(4). These neuropeptides have pronounced effects on the central nervous system as well as on neurons and effector targets of the autonomic nervous system.…”

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confidence: 99%

VPAC Receptor Modulation of Neuroexcitability in Intracardiac Neurons

DeHaven

Cuevas

2004

Journal of Biological Chemistry

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Pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal polypeptide (VIP) have been found within mammalian intracardiac ganglia, but the cellular effects of these neuropeptides remain poorly understood. Fluorometric calcium imaging and whole cell patch clamp recordings were used to examine the effects of PACAP and VIP on [ Pituitary adenylate cyclase-activating polypeptide (PACAP) 1 and vasoactive intestinal polypeptide (VIP) are pleiotropic neuropeptides that belong to the glucagon/secretin/growth hormone-releasing factor family of peptides (1-4). These neuropeptides have pronounced effects on the central nervous system as well as on neurons and effector targets of the autonomic nervous system. For example, in the central nervous system, PACAP is involved in hippocampal synaptic plasticity and associative learning in mice (5), whereas VIP has been shown to regulate intrathalamic rhythm activity and may modulate information transfer through the thalamocortical circuit (6). In the peripheral nervous system, PACAP and VIP appear to play a major role in autonomic regulation of the cardiovascular system. VIP has been shown to cause positive chronotropic and inotropic effects (7-9). In contrast, PACAP has been shown to cause a transient increase in sinus rate and atrial contractility that is followed by negative chronotropic and inotropic responses in isolated canine atria (10). Also, both PACAP and VIP are potent dilators of coronary arteries (11,12). Whereas these neuropeptides can directly influence cardiac tissues, the effects of PACAP and VIP on the heart are in part due to neuroregulatory effects on parasympathetic intracardiac ganglia (9,10,13,14).Mammalian intracardiac ganglia play a major role in neuronal control of the heart and are believed to be capable of independently monitoring and influencing cardiac function. A variety of neurotransmitters and neuromodulators, including PACAP and VIP, appear to be involved in the relaying of information within intracardiac ganglia and onto effector targets such as cardiac valves, coronary arteries, and cardiomyocytes. PACAP and VIP have been detected by immunocytochemistry in nerve fibers in the heart, coronary vasculature, and cardiac parasympathetic ganglia (15)(16)(17)(18)(19)(20). Although extrinsic fibers may be one source of these neuropeptides in the heart (21), PACAP and VIP are also found in cell bodies and nerve fibers of intrinsic cardiac neurons (15)(16)(17)(18)(19)(20). Despite the fact that data clearly demonstrate that these endogenous neuropeptides are potent regulators of the cardiovascular system, the cellular mechanisms mediating their effects remain poorly understood. There are also conflicting reports in the literature concerning the mechanisms by which PACAP and VIP regulate the function of intrinsic cardiac neurons. For example, it has been suggested that PACAP and VIP modulate neurotransmission

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“…PHI, VIP, peptide histidine valine (PHV), and peptide histidine methionine, among others, are processed from this precursor molecule. Prepro-VIPrelated peptides, including PHI, share a structural homology, as well as a certain degree of functional similarities, e.g., by having a stimulatory effect on the release and/or synthesis of glucagon (8), prolactin (20,28,40), and melatonin (21,37,49), and by affecting circadian rhythmicity (2,3), heart rate (38), vasomotor functions (15,19), and activation of the hypothalamic-pituitaryadrenal (HPA) axis (4,6).…”

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confidence: 99%

Effect of peptide histidine isoleucine on consummatory behavior in rats

Olszewski

Wirth

Shaw

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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. Effect of peptide histidine isoleucine on consummatory behavior in rats. Am J Physiol Regul Integr Comp Physiol 284: R1445-R1453, 2003. First published February 20, 2003 10.1152/ajpregu.00554.2002-Peptide histidine isoleucine (PHI) and VIP are derived from the same precursor. While central VIP decreases food intake, potential effects of PHI on feeding have not been studied. In the current study, we found that PHI administered intracerebroventricularly (ICV) or into the hypothalamic paraventricular nucleus (PVN) or central nucleus of the amygdala (CeA) decreased food consumption in overnight-deprived rats. The magnitude of an anorexigenic response to PHI differed depending on the injection route: ICV-infused peptide evoked the most potent effect. We determined that that only PVN-and CeA-injected PHI did not have aversive consequences. In addition, we infused anorexigenic doses of PHI via the same routes and assessed Fos immunoreactivity of PVN oxytocin (OT) and vasopressin (VP) neurons using double immunohistochemistry. OT and VP are thought to promote feeding termination. PHI increased the percentage of Fos-positive OT neurons regardless of the injection route. PVN-and ICV-infused PHI induced activation of VP cells. We conclude that central PHI has an inhibitory influence on food intake in rats. The PVN, with OT and VP neurons, and CeA may be involved in the mediation of anorexigenic effects of PHI. conditioned taste aversion; oxytocin; vasopressin; paraventricular nucleus of the hypothalamus; amygdala PEPTIDE HISTIDINE ISOLEUCINE (PHI) belongs to the pituitary adenylate cyclase-activating polypeptide (PACAP)/ glucagon family derived from a common precursor protein, prepro-VIP. PHI, VIP, peptide histidine valine (PHV), and peptide histidine methionine, among others, are processed from this precursor molecule. Prepro-VIPrelated peptides, including PHI, share a structural homology, as well as a certain degree of functional similarities, e.g., by having a stimulatory effect on the release and/or synthesis of glucagon (8), prolactin (20,28,40), and melatonin (21, 37, 49), and by affecting circadian rhythmicity (2, 3), heart rate (38), vasomotor functions (15, 19), and activation of the hypothalamic-pituitaryadrenal (HPA) axis (4, 6).PHI is widespread throughout the central and peripheral nervous systems (12). The presence of this peptide has been demonstrated in numerous central regions, where PHI often colocalizes in neurons with other products of prepro-VIP (13). Interestingly, PHIcontaining neuronal elements are encompassed in several brain sites involved in the regulation of consummatory behavior, including the hypothalamic paraventricular (PVN), supraoptic (SON), and arcuate (ARC) nuclei, central nucleus of the amygdala (CeA), and bed nucleus of the stria terminalis (17, 30).The abundance of receptors for PHI in these feedingrelated areas has also been confirmed. There are two well-described subtypes of receptors for PHI, termed VIP1 and VIP2 (18,24,45). These receptors do not seem to be selective to PHI al...

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Cardiovascular and respiratory actions of pituitary adenylate cyclase-activating polypeptides

Cited by 69 publications

References 11 publications

Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP) Induces Relaxations of Peripheral and Cerebral Arteries, which are Differentially Impaired by Aging

Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP) Induces Relaxations of Peripheral and Cerebral Arteries, which are Differentially Impaired by Aging

VPAC Receptor Modulation of Neuroexcitability in Intracardiac Neurons

Effect of peptide histidine isoleucine on consummatory behavior in rats

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