Area Postrema And Sympathetic Nervous System Effects Of Vasopressin And Angiotensin II

Hasser, Eileen M.; Cunningham, J. Thomas; Sullivan, Margaret J.; Curtis, Kathleen S.; Blaine, Edward H.; Hay, Meredith

doi:10.1046/j.1440-1681.2000.03261.x

Cited by 59 publications

(43 citation statements)

References 37 publications

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“…We conclude that the effect of AT 1 receptor antagonists in the expression of TH mRNA in the locus coeruleus may not be direct. Indirect effects may include inhibition of brain stem AT 1 receptors located in the nucleus of the solitary tract and the area postrema, as reported here, along with the blood pressure decrease and changes in the baroreflex that follow AT 1 receptor antagonism (Hasser et al 2000) and inhibition of the CRH mediation of the stress-induced stimulation of neuronal activity in this area (Porter 2000;Makino et al 2002;Zeng et al 2003).…”

Section: Effects Of Candesartan Treatment and Cold-restraint Stress Omentioning

confidence: 61%

Angiotensin II AT₁receptor blockade selectively enhances brain AT₂receptor expression, and abolishes the cold-restraint stress-induced increase in tyrosine hydroxylase mRNA in the locus coeruleus of spontaneously hypertensive rats

Bregonzio

Seltzer

Armando

et al. 2008

Stress

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Spontaneously hypertensive rats, a stress-sensitive strain, were pretreated orally for 14 days with the AT 1 receptor antagonist candesartan before submission to 2 h of cold-restraint stress. In non-treated rats, stress decreased AT 1 receptor binding in the median eminence and basolateral amygdala, increased AT 2 receptor binding in the medial subnucleus of the inferior olive, decreased AT 2 binding in the ventrolateral thalamic nucleus and increased tyrosine hydroxylase mRNA level in the locus coeruleus. In non-stressed rats, AT 1 receptor blockade reduced AT 1 receptor binding in all areas studied and enhanced AT 2 receptor binding in the medial subnucleus of the inferior olive. Candesartan pretreatment produced a similar decrease in brain AT 1 binding after stress, and prevented the stress-induced AT 2 receptor binding decrease in the ventrolateral thalamic nucleus. In the locus coeruleus and adrenal medulla, AT 1 blockade abolished the stress-induced increase in tyrosine hydroxylase mRNA level. Our results demonstrate that oral administration of candesartan effectively blocked brain AT 1 receptors, selectively increased central AT 2 receptor expression and prevented the stress-induced central stimulation of tyrosine hydroxylase transcription. The present results support a role of brain AT 1 and AT 2 receptors in the regulation of the stress response, and the hypothesis that AT 1 receptor antagonists may be considered as potential therapeutic compounds in stress related disorders in addition to their anti-hypertensive properties.

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Section: Effects Of Candesartan Treatment and Cold-restraint Stress Omentioning

confidence: 61%

Angiotensin II AT₁receptor blockade selectively enhances brain AT₂receptor expression, and abolishes the cold-restraint stress-induced increase in tyrosine hydroxylase mRNA in the locus coeruleus of spontaneously hypertensive rats

Bregonzio

Seltzer

Armando

et al. 2008

Stress

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“…A significant body of work has established that the circulating hormone arginine vasopressin acts directly on AP neurons, to inhibit sympathetic output and shift the baroreceptor reflex setpoint to lower arterial pressure (26,59; for a review, see also Ref. 25). Intriguingly, ghrelin is also reported to have cardiovascular effects by modulating baroreflex sensitivity.…”

Section: Examples Of Results From Nonresponding Neurons (A) Hyperpolmentioning

confidence: 99%

Ghrelin modulates electrical activity of area postrema neurons

Fry¹,

Ferguson²

2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Ghrelin, a peptide hormone secreted from the stomach, is known to have a potent appetite-stimulating activity. Recently, it has been shown that area postrema (AP), a caudal brain stem center that lacks a blood-brain barrier, is a key site of activity for ghrelin in stimulating appetite and regulating pancreatic protein secretion. In this study, we have examined the ability of ghrelin to regulate the electrical activity of area postrema neurons using patch-clamp electrophysiology. Using current-clamp configuration, we found that at a concentration of 10 nM, ghrelin caused inhibition in 19% of neurons tested, while a further 19% were excited by similar application of ghrelin. The remaining 62% of AP neurons were insensitive to ghrelin. These effects were concentration dependent, with an apparent EC 50 of 1.9 nM. Voltage-clamp recordings revealed that ghrelin caused a potentiation of voltage-gated K ϩ currents in neurons that exhibited a hyperpolarization and a potentiation of a depolarizing nonspecific cation current (NSCC) in those neurons that exhibited a depolarization of membrane potential. These are the first data showing that ghrelin exerts a direct effect on electrical activity of AP neurons and supports the notion that ghrelin can act via the AP to regulate energy homeostasis. patch clamp; action potential; sensory circumventricular organ; energy homeostasis GHRELIN IS AN ACYLATED 28-amino acid peptide hormone, which was discovered on the basis of its activity as an endogenous ligand for the growth hormone secretagogue receptor (GHSR) (35). Originally isolated from the stomach, ghrelin has also been shown to be expressed in various tissues, including the duodenum, adrenal gland, lung, and gonads (22), as well as in neurons in the hypothalamus (11). In addition to its role in the stimulation of growth hormone release in the pituitary, ghrelin is thought to play several roles in the regulation of energy balance. Circulating levels of ghrelin are increased in the fasting state and in anticipation of food (2, 12, 13). Conversely, ghrelin levels are attenuated by feeding and the presence of nutrients in the stomach (58), or by treatment with leptin (2). Administration of ghrelin potently stimulates food intake in rats (58, 64, 65), mice (2), and humans (63). These studies suggest a physiological role in initiation of feeding. Ghrelin is also suggested to play a role in long-term regulation of energy balance, as chronic administration of ghrelin causes weight gain by reducing fat utilization as an energy source (58). Lastly, ghrelin also plays a role in the digestion of food and the stimulation of gastric motility, acid secretion, and pancreatic protein secretion (38, 41).There is considerable interest as to the mechanism by which ghrelin exerts its appetite-stimulating effects, and, in particular, the site of action of ghrelin in the central nervous system (CNS). For example, the neuropeptide Y/Agouti-related peptide (NPY/AGRP) neurons within the arcuate nucleus of the hypothalamus (ARC) are suggested by many t...

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“…Past research has demonstrated that elevated levels of ANG II can act within the central nervous system to stimulate sympathetic outflow (27,34,42) and may attenuate baroreflex inhibition of sympathetic nerve activity (49). However, other research has shown that ANG II either had no effect (24) or attenuated (43) baroreflex-mediated sympathetic responses to hypotension.…”

Section: Discussionmentioning

confidence: 99%

Hypovolemia and neurovascular control during orthostatic stress

Kimmerly

Shoemaker

2002

American Journal of Physiology-Heart and Circulatory Physiology

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Humans exposed to real or simulated microgravity experience decrements in blood pressure regulation during orthostatic stress that may be related to autonomic dysregulation and/or hypovolemia. We examined the hypothesis that hypovolemia, without the deconditioning effects of bed rest or spaceflight, would augment the sympathoneural and vasomotor response to graded orthostatic stress. Radial artery blood pressure (tonometry), stroke volume (SV), brachial blood flow (Doppler ultrasound), heart rate (electrocardiogram), peroneal muscle sympathetic nerve activity (MSNA; microneurography), and estimated central venous pressure (CVP) were recorded during five levels (Ϫ5, Ϫ10, Ϫ15, Ϫ20 and Ϫ40 mmHg) of randomly assigned lower body negative pressure (LBNP) (n ϭ 8). Forearm (FVR) and total peripheral vascular resistance (TPR) were calculated. The test was repeated under randomly assigned placebo (normovolemia) or diuretic (spironolactone: 100 mg/day, 3 days) (hypovolemia) conditions. The diuretic produced an ϳ16% reduction in plasma volume. Compared with normovolemia, SV and cardiac output were reduced by ϳ12% and ϳ10% at baseline and during LBNP after the diuretic. During hypovolemia, there was an upward shift in the %⌬MSNA/⌬CVP, ⌬FVR/⌬CVP, and ⌬TPR/⌬CVP relationships during 0 to Ϫ20 mmHg LBNP. In contrast to normovolemia, blood pressure increased at Ϫ40 mmHg LBNP during hypovolemia due to larger gains in the %⌬MSNA/⌬CVP and ⌬TPR/⌬CVP relationships. It was concluded that acute hypovolemia augmented the neurovascular component of blood pressure control during moderate orthostasis, effectively compensating for decrements in SV and cardiac output.baroreflex; muscle sympathetic nerve activity; Doppler ultrasound; lower body negative pressure; vascular resistance; spironolactone EXPOSURE TO REAL OR SIMULATED MICROGRAVITY leads to cardiovascular deconditioning with the associated reductions in blood pressure regulation during orthostatic stress. The effect of this deconditioning on baroreflex neurovascular control in humans is not known, and the pathophysiology of postflight difficulties in blood pressure control remains a focus of debate.To maintain adequate blood pressure and cerebral perfusion during orthostatic stress, reflex adjustments occur to increase heart rate (HR) and peripheral vasoconstriction to compensate for a decreased venous return and stroke volume (SV). Primary contributors to the diminished ability to maintain blood pressure in many individuals after spaceflight or bed rest are believed to include reductions in plasma volume (PV) (3, 7, 10, 11), diminished baroreflex control of HR (10, 21), and/or vascular resistance (36,48). From these findings, two separate hypotheses have been proposed to explain difficulties in postural blood pressure control after spaceflight or bed rest.The first hypothesis recognizes the positive correlation between the duration of microgravity exposure and the degree of PV reduction reaching 12-15% or 350-500 ml (3). Hypovolemia leads to larger decreases in both venous return and ...

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Area Postrema And Sympathetic Nervous System Effects Of Vasopressin And Angiotensin II

Cited by 59 publications

References 37 publications

Angiotensin II AT₁receptor blockade selectively enhances brain AT₂receptor expression, and abolishes the cold-restraint stress-induced increase in tyrosine hydroxylase mRNA in the locus coeruleus of spontaneously hypertensive rats

Angiotensin II AT₁receptor blockade selectively enhances brain AT₂receptor expression, and abolishes the cold-restraint stress-induced increase in tyrosine hydroxylase mRNA in the locus coeruleus of spontaneously hypertensive rats

Ghrelin modulates electrical activity of area postrema neurons

Hypovolemia and neurovascular control during orthostatic stress

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Area Postrema And Sympathetic Nervous System Effects Of Vasopressin And Angiotensin II

Cited by 59 publications

References 37 publications

Angiotensin II AT1receptor blockade selectively enhances brain AT2receptor expression, and abolishes the cold-restraint stress-induced increase in tyrosine hydroxylase mRNA in the locus coeruleus of spontaneously hypertensive rats

Angiotensin II AT1receptor blockade selectively enhances brain AT2receptor expression, and abolishes the cold-restraint stress-induced increase in tyrosine hydroxylase mRNA in the locus coeruleus of spontaneously hypertensive rats

Ghrelin modulates electrical activity of area postrema neurons

Hypovolemia and neurovascular control during orthostatic stress

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Product

Resources

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Angiotensin II AT₁receptor blockade selectively enhances brain AT₂receptor expression, and abolishes the cold-restraint stress-induced increase in tyrosine hydroxylase mRNA in the locus coeruleus of spontaneously hypertensive rats

Angiotensin II AT₁receptor blockade selectively enhances brain AT₂receptor expression, and abolishes the cold-restraint stress-induced increase in tyrosine hydroxylase mRNA in the locus coeruleus of spontaneously hypertensive rats