Plasma angiotensin II levels and water intake following β-adrenergic stimulation, hypovolemia, cellular dehydration and water deprivation

Abdelaal, A. E.; Mercer, Paul F.; Mogenson, Gordon J.

doi:10.1016/0091-3057(76)90248-3

Cited by 45 publications

(23 citation statements)

References 27 publications

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“…To examine the role of thirst per se , we created “ATII-independent” thirst in mice expressing hM3Dq in NTS HSD2 neurons. Hyperosmotic stimuli, such as those produced with peripheral injections of 1 M NaCl or 1 M sucrose, cause thirst by directly activating osmosensors (Fitzsimons, 1961; Zimmerman et al, 2016), and do not increase peripheral ATII (Abdelaal et al, 1976). While injection of either NaCl or sucrose markedly increased H 2 O drinking, neither NaCl nor sucrose, unlike H 2 O restriction, enabled increased consumption of 3% NaCl in response to NTS HSD2 neuron stimulation (Figure 6J,K).…”

Section: Resultsmentioning

confidence: 99%

Aldosterone-Sensing Neurons in the NTS Exhibit State-Dependent Pacemaker Activity and Drive Sodium Appetite via Synergy with Angiotensin II Signaling

Resch

Fenselau

Madara

et al. 2017

Neuron

109

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Summary Sodium deficiency increases angiotensin II (ATII) and aldosterone, synergistically stimulating its retention and consumption. Recently, ATII-responsive neurons in the subfornical organ (SFO) and aldosterone-sensitive neurons in the nucleus of the solitary tract (NTSHSD2 neurons) were shown to drive sodium appetite. Here we investigate the basis for NTSHSD2 neuron activation, identify the circuit by which NTSHSD2 neurons drive appetite, and uncover an interaction between the NTSHSD2 circuit and ATII signaling. NTSHSD2 neurons respond to sodium deficiency with spontaneous pacemaker-like activity – the consequence of "cardiac" HCN and Nav1.5 channels. Remarkably, NTSHSD2 neurons are necessary for sodium appetite, and with concurrent ATII signaling their activity is sufficient to produce rapid consumption. Importantly, NTSHSD2 neurons stimulate appetite via projections to the vlBNST, which is also the effector site for ATII-responsive SFO neurons. The interaction between angiotensin signaling and NTSHSD2 neurons provides a neuronal context for the long-standing "synergy hypothesis" of sodium appetite regulation.

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Section: Resultsmentioning

confidence: 99%

Aldosterone-Sensing Neurons in the NTS Exhibit State-Dependent Pacemaker Activity and Drive Sodium Appetite via Synergy with Angiotensin II Signaling

Resch

Fenselau

Madara

et al. 2017

Neuron

109

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“…These deviations can include increases in plasma osmolality (P osmolality ) and sodium (P Na ), as well as decreases in plasma volume (P volume ) and pressure that stimulate renin secretion by the kidneys and, consequently, AngII production (P AngII ) in the blood 137 . These homeostatic circulating signals are translated by the brain into counter-regulatory responses, including thirst, anorexia, vasopressin (P AVP ) and oxytocin (P OXT ) secretion, and sympathetic nerve activation (SNA).…”

Section: Figurementioning

confidence: 99%

Neural circuits underlying thirst and fluid homeostasis

2017

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Thirst motivates animals to find and consume water. More than forty years ago, a set of interconnected brain structures known as the lamina terminalis (LT) was identified that governs thirst. However, due to the anatomical complexity of these brain regions, the structure and dynamics of their underlying neural circuitry has remained obscure. Recently, the emergence of new tools for neural recording and manipulation has reinvigorated the study of this circuit and prompted reexamination of longstanding questions about the neural origins of thirst. Here we review these advances, discuss what they teach us about the control of drinking behavior, and outline the key questions that remain unanswered.

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“…Intravenous or intracerebroventricular injection of All is a potent stimulus for vasopressin release in normal rats, but this release of vasopressin is blocked or attenuated in SFO-ablated rats (Knepel et al, 1982;Mangiapane et al, 1984). Dehydration, which causes a marked increase in plasma All concentration (Abdelaal et al, 1976;Mann et al, 1980), stimulates cellular metabolism in the SFO as determined by the 2-deoxyglucose technique (Gross et al, 1983).…”

mentioning

confidence: 99%

Subfornical organ. Does it protect against angiotensin II-induced hypertension in the rat?

Bruner

Mangiapane

Fink

1985

Circulation Research

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SUMMARY. The purpose of this study was to examine the contribution of the subfornical organ to the chronic hypertension produced by intravenous angiotensin II infusion in rats. Male rats were instrumented with permanent arterial and venous catheters and housed in metabolism cages for daily measurement of arterial pressure, heart rate, water intake, water balance, and urinary electrolyte excretion. Angiotensin II was infused intravenously at a rate of 10 ng/minute for 5 consecutive days, preceded by 2 control days, and followed by 2 recovery days. Normal rats with an intact subfornical organ (n = 7), and rats with an electrolytic lesion placed such that greater than 80% of the subfornical organ was destroyed (« = 9), were studied using this infusion protocol. An additional group of eight rats did not receive angiotensin II, and, thus, served as a time control. Both groups of rats receiving angiotensin II exhibited significant elevations in arterial pressure during the 5-day hormone infusion period, but pressure in rats with subfornical organ lesions (A23-29 mm Hg) was increased significantly more than that of intact rats (A14-20 mm Hg). Water intake was significantly increased on the 3rd, 4th, and 5th days of angiotensin II infusion only in rats with lesions in the subfornical organ. In contrast to previous studies showing that an intact subfornical organ is required for normal pressor and drinking responses to acute elevations in circulating angiotensin II in the rat, the current experiments indicate that the presence of the subfornical organ actually inhibits these same responses during more chronic increases in plasma angiotensin II levels. (Circ Res 56: 462-466, 1985)

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Plasma angiotensin II levels and water intake following β-adrenergic stimulation, hypovolemia, cellular dehydration and water deprivation

Cited by 45 publications

References 27 publications

Aldosterone-Sensing Neurons in the NTS Exhibit State-Dependent Pacemaker Activity and Drive Sodium Appetite via Synergy with Angiotensin II Signaling

Aldosterone-Sensing Neurons in the NTS Exhibit State-Dependent Pacemaker Activity and Drive Sodium Appetite via Synergy with Angiotensin II Signaling

Neural circuits underlying thirst and fluid homeostasis

Subfornical organ. Does it protect against angiotensin II-induced hypertension in the rat?

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