Central cardiovascular effects of acetylcholine in the conscious dog

Brefel, Christine; Lazartigues, Eric; Tran, Marie-Antoinette; Gauquelin, G.; Geelen, G.; Gharib, Claude; Jl, Montastruc; Montastruc, P; Rascol, Olivier

doi:10.1111/j.1476-5381.1995.tb15051.x

Cited by 14 publications

(6 citation statements)

References 42 publications

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“…Vasopressin and electrolytes. Urine from NSE-AT1A transgenic (n ϭ 30) and control littermates (n ϭ 36) was analyzed for vasopressin levels using radioimmunoassay, as described (7). In addition, urines were diluted (1:4), and osmolality was determined using a vapor pressure osmometer (Wescor Instruments).…”

Section: Methodsmentioning

confidence: 99%

Enhanced water and salt intake in transgenic mice with brain-restricted overexpression of angiotensin (AT₁) receptors

Lazartigues

Sinnayah²,

Augoyard³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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(AT 1A) to blood pressure and volume homeostasis, we generated a transgenic mouse model [neuron-specific enolase (NSE)-AT 1A] with brain-restricted overexpression of AT1A receptors. These mice are normotensive at baseline but have dramatically enhanced pressor and bradycardic responses to intracerebroventricular ANG II or activation of endogenous ANG II production. Here our goal was to examine the water and sodium intake in this model under basal conditions and in response to increased ANG II levels. Baseline water and NaCl (0.3 M) intakes were significantly elevated in NSE-AT 1A compared with nontransgenic littermates, and bolus intracerebroventricular injections of ANG II (200 ng in 200 nl) caused further enhanced water intake in NSE-AT 1A. Activation of endogenous ANG II production by sodium depletion (10 days low-sodium diet followed by furosemide, 1 mg sc) enhanced NaCl intake in NSE-AT 1A mice compared with wild types. Fos immunohistochemistry, used to assess neuronal activation, demonstrated sodium depletion-enhanced activity in the anteroventral third ventricle region of the brain in NSE-AT 1A mice compared with control animals. The results show that brain-selective overexpression of AT 1A receptors results in enhanced salt appetite and altered water intake. This model provides a new tool for studying the mechanisms of brain AT 1A -dependent water and salt consumption. thirst; sodium appetite; transgenic mice; circumventricular organs; volume homeostasis; anteroventral third ventricle THERE IS SUBSTANTIAL EVIDENCE that activation of the reninangiotensin system (RAS) is involved in water and sodium intake. Thirst and sodium depletion are monitored by osmoreceptors and/or sodium receptors located at the periphery and in the brain (5). Although several candidates have been identified (6,27,28,49), the nature and mechanism of action of these receptors remain unclear. However, it is well known that systemically and brain-generated angiotensin II (ANG II) can act directly or indirectly on ANG II receptor type 1 (AT 1 ) receptors located in the lamina terminalis to produce water and salt intake (20,36). While the role and independence of centrally vs. peripherally generated ANG II in these responses still remain unclear, the pivotal involvement of central AT 1 receptors was established by studies where intracerebroventricular (ICV) administration of RAS antagonists reduced sodium appetite of sodium-depleted intact rats (41) and adrenalectomized rats (42). Furthermore, the exaggerated salt appetite observed in spontaneously hypertensive rats was reduced by central treatment with angiotensin-converting enzyme inhibitors, suggesting a role for the brain RAS in the exaggerated salt appetite in this model of hypertension (14).In rodents, water deprivation upregulates the AT 1 receptor in various areas of the brain, including the subfornical organ (SFO) and the anterior pituitary (43), as well as in the periphery (19). In addition, water and sodium intake can be abolished by pretreatment with selective antagonists ...

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Section: Methodsmentioning

confidence: 99%

Enhanced water and salt intake in transgenic mice with brain-restricted overexpression of angiotensin (AT₁) receptors

Lazartigues

Sinnayah²,

Augoyard³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Centrally administered ACh or cholinergic agents increase arterial BP [53] because of the increase in sympathetic nerve tone and the acceleration of vasopressin release [53][54][55]. Systemic injection of ChE inhibitor increases systolic and diastolic BP [27,56].…”

Section: Effect Of Inhibition Of Cholinesterase On Arterial Blood Prementioning

confidence: 99%

Cardiac Effect of Cholinesterase Inhibitors Used in Alzheimers Disease - from Basic Research to Bedside

Masuda

2004

CAR

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In this review, the basic mechanism of the parasympathetic nervous effect on the heart is discussed. This is expanded to clinical situations to clarify what can happen to patients after cholinesterase (ChE) inhibitor is administered and to avoid unnecessary adverse effects. The parasympathetic nervous system can affect heart as well as brain function, and its effect on the heart is more complicated than is generally thought. The best-known effect is the cardioinhibitory effect, i.e. slowing of the heart rate. Its effect is also very sensitive to the time at which the stimulus falls within the cardiac cycle (phase-dependent effect). On some occasions, a cardiostimulatory effect can be observed. The parasympathetic nervous system also interacts with the sympathetic nervous system (sympathetic-parasympathetic interaction). ChE inhibitors or acetylcholinesterase inhibitors are often being administered to improve cognitive function of patients with Alzheimer's disease. The heart is naturally rich with ChE, and its inhibition may affect cardiac function, especially in elderly patients, many of whom have concomitant cardiovascular disease. Inhibition of ChE retards ACh degradation and potentiates the cardioinhibitory effect. However, the effect of ChE inhibitor is only slight in patients that receive a typical dose. After administration of ChE inhibitor in humans, the phase-dependent effect is reduced because the parasympathetic nervous effect is potentiated and saturated (saturation mechanism). Beat-by-beat fluctuation is reduced. ChE inhibitor increases arterial blood pressure through central M1 and M2 subtypes of muscarinic receptors (Br J Pharmacol 127:1657-1665, 1999). However, diastolic blood pressure increases slightly.

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“…Among factors affecting electrophysiological properties of vasopressinergic neurons and release of vasopressin are noradrenaline, gamma-aminobutyric acid (GABA) and glutamate. It has been shown that neurosecretory cells of SON and PVN nuclei receive inputs from A1 noradrenergic, GABAergic and glutamatergic neurons of the brain stem and forebrain [44][45][46][47][48][49][50][51]. Effectiveness of these neurotransmitters is modulated by several locally acting neuropeptides and by gasotransmitters, specifically by angiotensin II, cytokines, and nitric oxide, and by some other local factors [52][53][54][55][56][57].…”

Section: Central and Peripheral Vasopressin Systemsmentioning

confidence: 99%

Vasopressin: a possible link between hypoxia and hypertension

Szczepañska‐Sadowska

Żera

2022

Exploration of Medicine

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Cardiovascular and respiratory diseases are frequently associated with transient and prolonged hypoxia, whereas hypoxia exerts pro-hypertensive effects, through stimulation of the sympathetic system and release of pressor endocrine factors. This review is focused on the role of arginine vasopressin (AVP) in dysregulation of the cardiovascular system during hypoxia associated with cardiovascular disorders. AVP is synthesized mainly in the neuroendocrine neurons of the hypothalamic paraventricular nucleus (PVN) and supraoptic nucleus (SON), which send axons to the posterior pituitary and various regions of the central nervous system (CNS). Vasopressinergic neurons are innervated by multiple neuronal projections releasing several neurotransmitters and other regulatory molecules. AVP interacts with V1a, V1b and V2 receptors that are present in the brain and peripheral organs, including the heart, vessels, lungs, and kidneys. Release of vasopressin is intensified during hypernatremia, hypovolemia, inflammation, stress, pain, and hypoxia which frequently occur in cardiovascular patients, and blood AVP concentration is markedly elevated in cardiovascular diseases associated with hypoxemia. There is evidence that hypoxia stimulates AVP release through stimulation of chemoreceptors. It is suggested that acting in the carotid bodies, AVP may fine-tune respiratory and hemodynamic responses to hypoxia and that this effect is intensified in hypertension. There is also evidence that during hypoxia, augmentation of pro-hypertensive effects of vasopressin may result from inappropriate interaction of this hormone with other compounds regulating the cardiovascular system (catecholamines, angiotensins, natriuretic peptides, steroids, nitric oxide). In conclusion, current literature indicates that abnormal mutual interactions between hypoxia and vasopressin may significantly contribute to pathogenesis of hypertension.

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Central cardiovascular effects of acetylcholine in the conscious dog

Cited by 14 publications

References 42 publications

Enhanced water and salt intake in transgenic mice with brain-restricted overexpression of angiotensin (AT₁) receptors

Enhanced water and salt intake in transgenic mice with brain-restricted overexpression of angiotensin (AT₁) receptors

Cardiac Effect of Cholinesterase Inhibitors Used in Alzheimers Disease - from Basic Research to Bedside

Vasopressin: a possible link between hypoxia and hypertension

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Central cardiovascular effects of acetylcholine in the conscious dog

Cited by 14 publications

References 42 publications

Enhanced water and salt intake in transgenic mice with brain-restricted overexpression of angiotensin (AT1) receptors

Enhanced water and salt intake in transgenic mice with brain-restricted overexpression of angiotensin (AT1) receptors

Cardiac Effect of Cholinesterase Inhibitors Used in Alzheimers Disease - from Basic Research to Bedside

Vasopressin: a possible link between hypoxia and hypertension

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Product

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Enhanced water and salt intake in transgenic mice with brain-restricted overexpression of angiotensin (AT₁) receptors

Enhanced water and salt intake in transgenic mice with brain-restricted overexpression of angiotensin (AT₁) receptors