Effect of individual or combined ablation of the nuclear  groups of the lamina terminalis on water drinking in sheep

McKinley, MJ; Mathai, Michael L.; Pennington, GL; Rundgren, Mats; Vivas, Laura

doi:10.1152/ajpregu.1999.276.3.r673

Cited by 55 publications

(57 citation statements)

References 34 publications

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“…Previous work in a number of species has shown the importance of the ventral lamina terminalis in other centrally mediated responses to Ang II or hypertonic saline such as drinking, vasopressin secretion, and natriuresis. [12][13][14]16,17 Ablation of more caudal midline tissue in the median eminence, which interrupts the AVP-containing axons of the hypothalamo-neurohypophysial tract, almost abolished the increase in plasma AVP concentration resulting from ICV infusion of Ang II. However, this infusion still reduced PRC considerably in these sheep with MEL, suggesting that increased AVP levels do not mediate the central influence of Ang II on PRC, as suggested previously.…”

Section: Discussionmentioning

confidence: 99%

“…These methods have been described previously. 14 After ablation of the lamina terminalis, sheep usually showed temporary reductions in daily fluid intake and were maintained with daily ruminal water loads.…”

Section: Methodsmentioning

confidence: 99%

“…In sheep with a brain lesion, the head was perfused with saline and fixative, and either coronal or sagittal sections of the hypothalamus were prepared as described previously. 14 The extent of lesions was mapped with a microfilm reader (Zeiss, Jena).…”

Section: Analysis Of Blood Samplesmentioning

confidence: 99%

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Neural Mechanisms Subserving Central Angiotensinergic Influences on Plasma Renin in Sheep

McBurnie

Mathai

2001

Hypertension

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Abstract-The mechanisms and brain regions subserving the suppression of plasma renin concentration caused by intracerebroventricular (ICV) infusion of angiotensin II were studied in sodium-depleted sheep. Infusion of angiotensin II (3 g/h for 1 hour) into the lateral ventricle reduced plasma renin from 4.3Ϯ0.4 to 1.6Ϯ0.2 pmol angiotensin I/mL per hour at 1 hour after the commencement of infusion. This change persisted for at least another 90 minutes and was blocked by concomitant ICV infusion of the AT 1 antagonist losartan (1 mg/h). Arterial pressure did not change, but plasma vasopressin secretion was increased. ICV infusion of losartan (1 mg/h) significantly increased plasma renin in sodium-depleted sheep. The reduction of plasma renin concentration in response to either ICV angiotensin II or hypertonic NaCl (0.75 mol/L at 1 mL/h) and the increase in response to ICV losartan was prevented in sheep in which the lamina terminalis of the brain had been ablated. Lesions in the median eminence (MEL), which blocked the increased plasma vasopressin levels, did not prevent suppression of plasma renin in response to ICV angiotensin II. However, bilateral renal denervation largely blocked this inhibition of plasma renin concentration but not the increased plasma renin resulting from ICV infusion of losartan in sodium-depleted sheep. The results show that AT 1 receptors, probably located in the lamina terminalis, mediate a central inhibitory influence of angiotensin II on renin secretion. This inhibition of renin release is probably due to a reduction in activity of renal sympathetic nerves innervating the juxtaglomerular apparatus of the kidney. Key Words: angiotensin Ⅲ renin Ⅲ receptors, angiotensin Ⅲ renal nerves T he secretion of renin by the kidney is influenced by several factors including the activity of the renal nerves, 1 and it is possible that several brain regions may contribute to the initiation of renal sympathetic drive 2 and therefore the control of renin release. However, the brain mechanisms controlling renin secretion are poorly understood. One of the factors that may influence renin secretion is the concentration of angiotensin (Ang) II in the brain. 3-8 Whereas intracerebroventricular (ICV) infusions of Ang II or renin reduce plasma renin concentration (PRC), arterial pressure also increases. [3][4][5][6][7][8] Thus, the inhibition of renin release may be mediated by renal or arterial baroreflexes secondary to the rise in pressure. ICV infusion of the angiotensin AT 1 receptor antagonist losartan elevates PRC in sodium-depleted sheep, suggesting that an angiotensinergic pathway in the brain may exert a tonic inhibitory influence on renin secretion in these animals. 8 We have observed that ICV infusion of either Ang II or hypertonic saline suppresses PRC in sodium-depleted sheep without increasing arterial pressure. 8,9 This contrasts with the pressor effects of such ICV infusions in sodium-replete sheep, 6 suggesting that the reduced plasma renin levels are not a reflex response to baroreceptor acti...

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Neural Mechanisms Subserving Central Angiotensinergic Influences on Plasma Renin in Sheep

McBurnie

Mathai

2001

Hypertension

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“…Adding NaCl to a hypertonic aCSF injection was a more potent dipsogen than if sucrose was used, so both osmosensitive and sodium-sensitive receptors may mediate polydipsia (87). Furthermore, ablation of the lamina terminalis, which includes the SFO, abolishes the induction of drinking and release of AVP that occurs upon intravenous hypertonic saline (88,89). These studies demonstrate that an elevation in osmolality can induce water intake through central mechanisms, which may in part involve the SFO.…”

Section: Stimulators Of the Brain Ras And Physiological Effects Of Sfmentioning

confidence: 99%

Mechanisms of brain renin angiotensin system-induced drinking and blood pressure: importance of the subfornical organ

Coble¹,

Grobe

Johnson³

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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Coble JP, Grobe JL, Johnson AK, Sigmund CD. Mechanisms of brain renin angiotensin system-induced drinking and blood pressure: importance of the subfornical organ. Am J Physiol Regul Integr Comp Physiol 308: R238 -R249, 2015. First published December 17, 2014 doi:10.1152/ajpregu.00486.2014.-It is critical for cells to maintain a homeostatic balance of water and electrolytes because disturbances can disrupt cellular function, which can lead to profound effects on the physiology of an organism. Dehydration can be classified as either intra-or extracellular, and different mechanisms have developed to restore homeostasis in response to each. Whereas the renin-angiotensin system (RAS) is important for restoring homeostasis after dehydration, the pathways mediating the responses to intra-and extracellular dehydration may differ. Thirst responses mediated through the angiotensin type 1 receptor (AT 1R) and angiotensin type 2 receptors (AT 2R) respond to extracellular dehydration and intracellular dehydration, respectively. Intracellular signaling factors, such as protein kinase C (PKC), reactive oxygen species (ROS), and the mitogen-activated protein (MAP) kinase pathway, mediate the effects of central angiotensin II (ANG II). Experimental evidence also demonstrates the importance of the subfornical organ (SFO) in mediating some of the fluid intake effects of central ANG II. The purpose of this review is to highlight the importance of the SFO in mediating fluid intake responses to dehydration and ANG II.angiotensin; blood pressure; barin; fluid; renin FLUID BALANCE is crucial for the homeostasis and survival of organisms because they have to properly maintain fluid and electrolyte concentrations for the normal function of all cells. Fluid balance can go awry in pathological states such as in chronic kidney disease and diabetes. Among its many roles in maintaining homeostasis, the renin-angiotensin system (RAS) is an important regulator of fluid balance. The RAS achieves this through the actions of its main effector peptide, angiotensin II (ANG II) through the ANG II type 1 (AT 1 R) and type 2 (AT 2 R) receptors. Activation of AT 1 R by blood-borne ANG II in target tissues causes increases in sodium and water retention, arginine vasopressin (AVP), and aldosterone release, vasoconstriction, increased sympathetic nervous system activity, and increased fluid intake. ANG II is produced by the consecutive enzymatic action of renin on its substrate angiotensinogen (AGT) and by angiotensin-converting enzyme (ACE) on its substrate angiotensin I (ANG I). The renin-AGT cleavage step is generally the rate-limiting step in the production of ANG II, and this is certainly true in the brain where the amount of renin is limiting. The RAS exists in two forms: a circulatory form where ANG II acts as an endocrine factor, and a tissue-specific form, where local production of ANG II acts in an autocrine or paracrine manner to induce AT 1 R signaling on ANG II producing or nearby cells (75). Intracrine, or intracellular forms of the RAS, hav...

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“…These include signals produced by osmoreceptors in the lamina terminalis (4)(5)(6), which respond to cellular dehydration and the resulting increase in sodium concentration within the cerebral spinal fluid (2), and signals produced in response to extracellular dehydration, such as those associated with the renin-angiotensin system, which is activated as a result of changes in vascular pressure and volume (7,8). In comparison, the mechanisms responsible for terminating drinking are less well understood.…”

mentioning

confidence: 99%

Overdrinking, swallowing inhibition, and regional brain responses prior to swallowing

Saker

Farrell

Egan

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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In humans, drinking replenishes fluid loss and satiates the sensation of thirst that accompanies dehydration. Typically, the volume of water drunk in response to thirst matches the deficit. Exactly how this accurate metering is achieved is unknown; recent evidence implicates swallowing inhibition as a potential factor. Using fMRI, this study investigated whether swallowing inhibition is present after more water has been drunk than is necessary to restore fluid balance within the body. This proposal was tested using ratings of swallowing effort and measuring regional brain responses as participants prepared to swallow small volumes of liquid while they were thirsty and after they had overdrunk. Effort ratings provided unequivocal support for swallowing inhibition, with a threefold increase in effort after overdrinking, whereas addition of 8% (wt/vol) sucrose to water had minimal effect on effort before or after overdrinking. Regional brain responses when participants prepared to swallow showed increases in the motor cortex, prefrontal cortices, posterior parietal cortex, striatum, and thalamus after overdrinking, relative to thirst. Ratings of swallowing effort were correlated with activity in the right prefrontal cortex and pontine regions in the brainstem; no brain regions showed correlated activity with pleasantness ratings. These findings are all consistent with the presence of swallowing inhibition after excess water has been drunk. We conclude that swallowing inhibition is an important mechanism in the overall regulation of fluid intake in humans.thirst | drinking | swallowing | inhibition | fMRI F luid depletion leads to drinking, an important evolutionary behavior that satisfies the physiological need to replenish lost fluid. The motivation to begin drinking is normally provided, in humans at least, by the presence of a subjective state of thirst. At some point after drinking has commenced, the sensation of thirst disappears and is replaced by the experience of satiation, along with the cessation of drinking. Studies performed in humans and animals indicate the regulatory mechanisms that have evolved to govern the cessation of drinking appear to be tightly calibrated, with the amount of fluid ingested commensurate with the degree of fluid depletion, even though some variation occurs between species regarding the time taken to conclude drinking (1-3).Several factors have been implicated in the regulation of fluid intake, with the majority relating to thirst and the initiation of drinking. These include signals produced by osmoreceptors in the lamina terminalis (4-6), which respond to cellular dehydration and the resulting increase in sodium concentration within the cerebral spinal fluid (2), and signals produced in response to extracellular dehydration, such as those associated with the renin-angiotensin system, which is activated as a result of changes in vascular pressure and volume (7,8). In comparison, the mechanisms responsible for terminating drinking are less well understood. Oropharyngeal metering ...

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Effect of individual or combined ablation of the nuclear groups of the lamina terminalis on water drinking in sheep

Cited by 55 publications

References 34 publications

Neural Mechanisms Subserving Central Angiotensinergic Influences on Plasma Renin in Sheep

Neural Mechanisms Subserving Central Angiotensinergic Influences on Plasma Renin in Sheep

Mechanisms of brain renin angiotensin system-induced drinking and blood pressure: importance of the subfornical organ

Overdrinking, swallowing inhibition, and regional brain responses prior to swallowing

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