Effect of arterial pressure on drinking and urinary responses to angiotensin II

Evered, Mark; Robinson, Marilyn M.; Rose, Patricia A.

doi:10.1152/ajpregu.1988.254.1.r69

Cited by 29 publications

(38 citation statements)

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“…The previously reported failure of peripherally administered ANG II to stimulate drinking in mice may be due to a presumed ANG II-induced elevation in blood pressure (3,9). Although water consumption in hypotensive rats is at least partly dependent upon ANG II (3,5,9,17), water drinking in mice seems to be independent of ANG II. On the basis of the present finding that salt appetite is inhibited by losartan, salt appetite in mice is dependent upon AT1 receptor signaling.…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, Fos-ir in the PVN was further elevated with the addition of losartan to the PEG treatment. PEG has a very modest hypotensive action in rats (3,16); presumably, the ANG II generated helps to prevent a drop in arterial pressure. Blood pressure during elevated renin states is reduced by losartan (19), so we infer that losartan should exacerbate hypotension in PEG-treated rodents.…”

Section: Discussionmentioning

confidence: 99%

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Role of angiotensin in body fluid homeostasis of mice: effect of losartan on water and NaCl intakes

Crews¹,

Rowland²

2005

American Journal of Physiology-Regulatory, Integrative and Comp

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Crews, Emily C., and Neil E. Rowland. Role of angiotensin in body fluid homeostasis of mice: effect of losartan on water and NaCl intakes. Am J Physiol Regul Integr Comp Physiol 288: R638 -R644, 2005. First published November 4, 2004 doi:10.1152/ajpregu. 00525.2004.-It is known that mice injected peripherally with ANG II do not show a drinking response but that cFos immunoreactivity (ir) is induced in brain regions similar to those in rats. We now show in Crl:CD1(ICR) mice that peripheral injection of the ANG II type 1 receptor antagonist losartan was sufficient to prevent this induction of Fos-ir in the subfornical organ (SFO). Injection of ANG II into the lateral cerebral ventricle produced a robust water intake in mice and induced Fos-ir in SFO, as well as in median preoptic (MnPO) and paraventricular (PVN) nuclei. Peripheral injection of losartan blocked this drinking response and prevented the induction of Fos-ir in each of these brain regions. Hypovolemia produced by polyethylene glycol (PEG) produced a robust water intake but no evidence of sodium appetite, and it induced Fos-ir in SFO, MnPO, and PVN. Peripheral injection of losartan did not affect this drinking response. Fos-ir induced by PEG in SFO and MnPO was reduced by treatment with losartan, while that induced in the PVN was further increased by losartan. Sodium depletion with furosemide and low-sodium diet produced a strong sodium appetite and induced Fos-ir in SFO and MnPO. Treatment with losartan completely blocked the sodium appetite, as well as the induction of Fos-ir in these brain regions. These data indicate that endogenous production of ANG II and action at forebrain receptors is critically involved in depletion-related sodium appetite in mice. The absence of an effect of losartan on PEG-induced drinking suggests the critical involvement of other factor(s) such as arterial or venous baroreceptor input, and we discuss how this factor could also explain why peripheral ANG II is not dipsogenic in mice.hypovolemia; sodium depletion; subfornical organ; baroreceptors; Fos immunoreactivity THE RENIN-ANGIOTENSIN CASCADE has important signaling functions in many tissues, including an integrative role in the regulation of hydromineral homeostasis by the brain (4, 5). Most of the studies that have led to this knowledge, especially in regard to neural mechanisms, have been performed in a few strains of rats. Contemporary interest in the use of mouse transgenic models has made it important to understand whether and how this rat-based model applies to mice. In particular, studies from this laboratory (12), as well as others (1, 4, 18), performed over a decade ago suggested that mice of several strains did not use ANG II as a signal molecule in precisely the same way as rats. Most prominent among the findings was that mice drank neither water nor NaCl solution when injected peripherally with ANG II (6, 12, 14, 18).There are two general classes of potential explanations for that finding. The first is that ANG II is not dipsogenic because it does not hav...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Role of angiotensin in body fluid homeostasis of mice: effect of losartan on water and NaCl intakes

Crews¹,

Rowland²

2005

American Journal of Physiology-Regulatory, Integrative and Comp

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“…In vitro experiments on rat mesenteric arterial beds have shown an estrogen-induced increase in pressor responses to AVP and an increase in AVP receptors [50]. Increases in blood pressure have been shown to attenuate responses to AngII-induced water intake [51]and may explain, in part, the attenuated water intake observed following estradiol treatment. However, the consequences of estradiol action on AVP-induced pressor responses are less clear in the in vivo situation.…”

Section: Discussionmentioning

confidence: 99%

Estrogen Increases Angiotensin II-Induced c-Fos Expression in the Vasopressinergic Neurons of the Paraventricular Nucleus in the Female Rat

Kisley¹,

Sakai

Flanagan‐Cato

et al. 2000

Neuroendocrinology

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Previous studies in female rats have shown that estrogen treatment attenuates angiotensin II (AngII)-induced water intake. The mechanism underlying this attenuation may be decreased responsiveness to AngII, as revealed by a reduction in AngII binding to the angiotensin type 1 (AT₁) receptor in the subfornical organ (SFO). It has not been determined whether these changes in receptor binding translate into changes in neuronal activity that, in turn, may influence behavior. Therefore, an estrogen-modulated change in neuronal pathways relevant to AngII-induced water intake was tested in ovariectomized (OVX) female rats using immunohistochemistry for the immediate early gene c-Fos as a marker for neuronal activation. Third cerebroventricular injection of AngII (6 ng) induced intense c-Fos immunoreactivity in forebrain regions associated with fluid intake, including the organum vasculosum of the lamina terminalis, the median preoptic nucleus, the SFO, the supraoptic nucleus and the paraventricular nucleus (PVN). Forty-eight-hour estradiol (10 µg) administration to OVX female rats increased AngII-induced c-Fos labeling in the lateral magnocellular neurons of the PVN by 30% as compared to vehicle-treated controls. Double labeling neurons in the PVN with c-Fos and either vasopressin or oxytocin antisera revealed that estrogen increased AngII-induced c-Fos expression by 28%, specifically in vasopressinergic neurons. Such changes in neuronal activation may explain the estrogen modulation of AngII-induced water intake that has been previously reported; it may be due to increased water retention to maintain plasma osmolality or to induction of a pressor response.

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“…Old rats secrete considerably less renin in response to most stimuli than younger animals (4 -6, 25) and therefore may not generate dipsogenic levels of ANG II during hypotension. Additionally, it is possible that old rats do not adequately sense the levels of ANG II that are produced during thirst challenges and may have elevated levels of factors such as atrial natriuretic peptide that are known to inhibit drinking (15).The administration of exogenous ANG II, whether by subcutaneous bolus or intravenous infusion, produces drinking in rats (8,19,(23)(24)(25)28). In addition, administration of exogenous ANG II produces a marked pressor response that is capable of inhibiting drinking (8,23,28).…”

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confidence: 99%

“…The administration of exogenous ANG II, whether by subcutaneous bolus or intravenous infusion, produces drinking in rats (8,19,(23)(24)(25)28). In addition, administration of exogenous ANG II produces a marked pressor response that is capable of inhibiting drinking (8,23,28).…”

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confidence: 99%

Drinking and arterial blood pressure responses to ANG II in young and old rats

Thunhorst

Beltz²,

Johnson

2010

American Journal of Physiology-Regulatory, Integrative and Comp

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We investigated water drinking and arterial blood pressure responses to intravenous infusions of ANG II in young (4 mo), middle-aged adult (12 mo), and old (29 mo) male Brown Norway rats. Infusions of ANG II began with arterial blood pressure either at control levels or at reduced levels following injection of the vasodilator minoxidil. Under control conditions, mean arterial pressure (MAP) in response to ANG II rose to the same level for all groups, and middle-aged and old rats drank as much or more water in response to ANG II compared with young rats, depending on whether intakes were analyzed using absolute or body weight-adjusted values. When arterial blood pressure first was reduced with minoxidil, MAP in response to ANG II stabilized at significantly lower levels compared with control conditions for all groups. Young rats drank significantly more water under reduced pressure conditions compared with control conditions, while middle-aged and old rats did not. Urine volume in response to ANG II was lower, while water balance was higher, under conditions of reduced pressure compared with control conditions. Baroreflex control of heart rate was substantially reduced in old rats compared with young and middle-aged animals. In summary, young rats appear to be more sensitive to the inhibitory effects of increased arterial blood pressure on water drinking than are older animals.

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Effect of arterial pressure on drinking and urinary responses to angiotensin II

Cited by 29 publications

References 0 publications

Role of angiotensin in body fluid homeostasis of mice: effect of losartan on water and NaCl intakes

Role of angiotensin in body fluid homeostasis of mice: effect of losartan on water and NaCl intakes

Estrogen Increases Angiotensin II-Induced c-Fos Expression in the Vasopressinergic Neurons of the Paraventricular Nucleus in the Female Rat

Drinking and arterial blood pressure responses to ANG II in young and old rats

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