Interaction of vasopressin with area postrema during volume expansion

Hasser, Eileen M.; Undesser, K. P.; Bishop, Vernon S.

doi:10.1152/ajpregu.1987.253.4.r605

Cited by 12 publications

(15 citation statements)

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“…In particular, AP is a key center in regulation of baroreflex sensitivity. 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).…”

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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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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“…In the present study, we observed small increases in plasma AVP that were statistically significant in HT2. Several studies in animal models (3,14,15) suggest that circulating AVP has central sympathoinhibitory influences, involving interactions at circumventricular organs such as the area postrema (15). These influences include a decrease in gain of baroreflex control of SNA (3).…”

Section: Discussionmentioning

confidence: 99%

Interactions of plasma osmolality with arterial and central venous pressures in control of sympathetic activity and heart rate in humans

Charkoudian¹,

Eisenach²,

Joyner³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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. Interactions of plasma osmolality with arterial and central venous pressures in control of sympathetic activity and heart rate in humans. Am J Physiol Heart Circ Physiol 289: H2456 -H2460, 2005. First published September 30, 2005 doi:10.1152/ajpheart.00601.2005.-Plasma osmolality alters control of sympathetic activity and heart rate in animal models; however, it is unknown whether physiological increases in plasma osmolality have such influences in humans and what effect concurrent changes in central venous and/or arterial pressures may have. We tested whether physiological increases in plasma osmolality (similar to those during exercise dehydration) alter control of muscle sympathetic nerve activity (MSNA) and heart rate (HR) in humans. We studied 17 healthy young adults (7 women, 10 men) at baseline and during arterial pressure (AP) transients induced by sequential injections of nitroprusside and phenylephrine, under three conditions: control (C), after 1 ml/kg intravenous hypertonic saline (HT1), and after 2 ml/kg hypertonic saline (HT2). We continuously measured HR, AP, central venous pressure (CVP; peripherally inserted central catheter) and MSNA (peroneal microneurography) in all conditions. Plasma osmolality increased from 287 Ϯ 1 mosmol/kg in C to 290 Ϯ 1 mosmol/kg in HT1 (P Ͻ 0.05) but did not increase further in HT2 (291 Ϯ 1 mosmol/kg; P Ͼ 0.05 vs. C). Mean AP and CVP were similar between C and HT1, but both increased slightly in HT2. HR increased slightly but significantly during both HT1 and HT2 vs. C (P Ͻ 0.05). Sensitivity of baroreflex control of MSNA was significantly increased vs. C in HT1 [Ϫ7.59 Ϯ 0.97 (HT1) vs. Ϫ5.85 Ϯ 0.63 (C) arbitrary units (au) ⅐ beat Ϫ1 ⅐ mmHg Ϫ1 ; P Ͻ 0.01] but was not different in HT2 (Ϫ6.55 Ϯ 0.94 au ⅐ beat Ϫ1 ⅐ mmHg Ϫ1 ). We conclude that physiological changes in plasma osmolality significantly alter control of MSNA and HR in humans, and that this influence can be modified by CVP and AP. baroreflex; sympathetic nervous system; hydration; plasma volume CHANGES IN HYDRATION ELICIT important alterations in neural mechanisms controlling arterial pressure (AP) via the baroreflex (5, 6, 17). Influences of increased plasma osmolality, which can accompany decreases in volume seen with certain types of dehydration (such as with prolonged exercise), may also interact with changes in volume to alter autonomic mechanisms that have important implications for control of blood pressure in these conditions.Because increased plasma osmolality often accompanies dehydration, physiological responses to hyperosmolality are generally those that would tend to defend plasma volume and AP. In animal models, these have been shown to include sympathoexcitation (2, 7) and decreased urine output (20). Furthermore, hyperosmolality has been shown to alter arterial baroreflex control of both heart rate (HR) and sympathetic activity in rats (1, 7). Such influences of osmolality on baroreflex control mechanisms may also involve osmolality-induced increases in circulating volume-regulatory hormones ...

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“…It is well established in animal models that volume infusion causes reflex inhibition of sympathetic neural activity (1,11,24). This can occur via activation of either arterial or cardiopulmonary baroreflexes and occurs solely via the cardiopulmonary baroreflex in animals with sinoaortic denervation (1,24).…”

Section: Influences Of Cvp On Vascular Sympathetic Nerve Activitymentioning

confidence: 99%

“…In animal models, it has been demonstrated that volume expansion and/or increased CVP causes reflex inhibition of sympathetic nerve activity via activation of cardiopulmonary baroreceptors (1,11,24). In rabbits, increased right atrial pressure was associated with attenuated arterial baroreflex control of mean arterial pressure (MAP) (21).…”

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confidence: 99%

Influence of increased central venous pressure on baroreflex control of sympathetic activity in humans

Charkoudian¹,

Martin²,

Dinenno³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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Volume expansion often ameliorates symptoms of orthostatic intolerance; however, the influence of this increased volume on integrated baroreflex control of vascular sympathetic activity is unknown. We tested whether acute increases in central venous pressure (CVP) diminished subsequent responsiveness of muscle sympathetic nerve activity (MSNA) to rapid changes in arterial pressure. We studied healthy humans under three separate conditions: control, acute 10 degrees head-down tilt (HDT), and saline infusion (SAL). In each condition, heart rate, arterial pressure, CVP, and peroneal MSNA were measured during 5 min of rest and then during rapid changes in arterial pressure induced by sequential boluses of nitroprusside and phenylephrine (modified Oxford technique). Sensitivities of integrated baroreflex control of MSNA and heart rate were assessed as the slopes of the linear portions of the MSNA-diastolic blood pressure and R-R interval-systolic pressure relations, respectively. CVP increased approximately 2 mmHg in both SAL and HDT conditions. Resting heart rate and mean arterial pressure were not different among trials. Sensitivity of baroreflex control of MSNA was decreased in both SAL and HDT condition, respectively: -3.1 +/- 0.6 and -3.3 +/- 1.0 versus -5.0 +/- 0.6 units.beat(-1).mmHg(-1) (P < 0.05 for SAL and HDT vs. control). Sensitivity of baroreflex control of the heart was not different among conditions. Our results indicate that small increases in CVP decrease the sensitivity of integrated baroreflex control of sympathetic nerve activity in healthy humans.

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Interaction of vasopressin with area postrema during volume expansion

Cited by 12 publications

References 0 publications

Ghrelin modulates electrical activity of area postrema neurons

Ghrelin modulates electrical activity of area postrema neurons

Interactions of plasma osmolality with arterial and central venous pressures in control of sympathetic activity and heart rate in humans

Influence of increased central venous pressure on baroreflex control of sympathetic activity in humans

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