Review: AT1-receptors in the central nervous system

Allen, Andrew M.; Giles, Michelle; Lee, JooHyung; Oldfield, Brian J.; Mendelsohn, Frederick A.O.

doi:10.1177/14703203010020011701

Cited by 13 publications

(16 citation statements)

References 120 publications

(136 reference statements)

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“…22 Excitation of the rostral ventrolateral medulla produces an increase in blood pressure due to activation of sympathetic vasoconstrictor nerves, tachycardia and the release of catecholamines from the adrenal medulla. [22][23][24][25][26] An overactive brain RAS has been implicated in the development and maintenance of high blood pressure in spontaneously hypertensive rats (SHR). In SHR, the central RAS is activated, as demonstrated by increased formation of angiotensin II and increased AT 1 receptor expression in the brain.…”

Section: The Brain Ras: Cardiovascular Effects and Hypertensionmentioning

confidence: 99%

The renin-angiotensin system in the brain: possible therapeutic implications for AT1-receptor blockers

et al. 2002

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Section: The Brain Ras: Cardiovascular Effects and Hypertensionmentioning

confidence: 99%

The renin-angiotensin system in the brain: possible therapeutic implications for AT1-receptor blockers

et al. 2002

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“…While the exact location in the brain for ANG II mediation of thermoregulation remains to be elucidated, hypothalamic sites expressing AT 1 receptors, such as the median preoptic nucleus or the paraventricular nucleus, could be possible sites of AT 1 antagonist influences on thermoregulation (1). The fact that candesartan-treated animals fail to cool themselves while pregnant, while reverting to a higher temperature during lactation, indicates that there is a specific cooling mechanism during pregnancy that is not activated or is impaired when central angiotensin is blocked.…”

Section: Discussionmentioning

confidence: 99%

Influence of brain angiotensin on thermoregulation and hydromineral balance during pregnancy in rats

Cairns

Burns

Nicolantonio

et al. 2005

Journal of Applied Physiology

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. Influence of brain angiotensin on thermoregulation and hydromineral balance during pregnancy in rats. J Appl Physiol 98: 1813-1819, 2005. First published December 3, 2004 doi:10.1152/japplphysiol.00842.2004.-During mammalian pregnancy, body temperature decreases and there are changes in fluid and electrolyte balance. Angiotensin signaling mechanisms in the brain have been shown to influence thermoregulation and body fluid balance in the nonpregnant state. We hypothesized that brain angiotensin is also implicated in adjusting these physiological systems in the pregnant rat. We compared core temperature and fluid regulation in three groups of pregnant rats: untreated rats, rats receiving continuous infusion of an AT1 antagonist candesartan (5 g ⅐ kg Ϫ1 ⅐ day Ϫ1 ) into a lateral cerebral ventricle to block brain AT1 receptors, and rats receiving vehicle [artificial cerebrospinal fluid (aCSF)] vehicle. Untreated and aCSF-treated rats showed a decrease in colonic temperature (Ϫ0.5 and Ϫ0.8°C respectively) by day 20 of gestation. However, rats treated with candesartan had increased colonic temperature compared with baseline (ϩ0.9°C), and their temperature was significantly higher on days 7 (P Ͻ 0.05), 17 (P Ͻ 0.05), and 20 (P Ͻ 0.001) compared with the other groups (aCSF and untreated). Daily food and water intakes and body weight were not different between the three groups. Similarly, litter sizes and pup weights were equal in all groups. Finally, the expected decreases in plasma Na ϩ and osmolality during pregnancy were equivalent in all groups. This study suggests that brain angiotensin mediates the progressive decrease in body temperature that occurs during pregnancy. However, the changes in fluid balance associated with pregnancy are not dependent on brain angiotensin. gestational hypothermia; candesartan; osmoregulation; lactation DURING PREGNANCY, REVERSIBLE changes occur in maternal homeostasis that alter body weight, temperature, and hydromineral balance (25). In several mammalian species that have been investigated, there is a 0.5-1°C reduction in maternal temperature toward the end of pregnancy (13,19,26). In late-pregnant rats studied in a thermocline (temperature gradient between 12 and 36°C), environmental temperature preference was unchanged between pregnant and nonpregnant animals (12), indicating that the reduction in maternal temperature is under thermoregulatory control rather than an inability to maintain a higher temperature. Similarly, the threshold temperature for cooling mechanisms such as skin vasodilation and salivary evaporative heat loss are reduced compared with nonpregnant rats (32), indicating that pregnant rats defend a lower body temperature. Fetal temperature in sheep has been shown to be higher than maternal temperature, which may indicate that the mother functions as a heat sink for its offspring to maintain optimal physiological temperature in utero (19). This reduction has been proposed to be both a neuroprotective mechanism against induction of hyperthermic stress in developing...

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“…Thus, circulating levels of AngII impact the baroreceptor reflex by a pathway from the AP to the NTS [22,23]. In addition, AngII activation of the AT 1 R subtype in the anterior ventral medulla increases blood pressure by activation of the sympathetic nervous system, tachycardia, and catecholamine released from the adrenal medulla [22,[24][25][26][27].…”

Section: Formation Of Angiotensin Ligands and Their Receptorsmentioning

confidence: 99%

New insights into the importance of aminopeptidase A in hypertension

et al. 2007

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The renin-angiotensin system (RAS) plays an important role in the maintenance of normal blood pressure and the etiology of hypertension; however, minimal attention has been paid to the degradation of the effector peptide, angiotensin II (AngII). Since aminopeptidase A (APA)-deficient mice develop hypertension APA appears to be an essential enzyme in the control of blood pressure via degradation of AngII. The robust hypertension seen in the spontaneously hypertensive rat (SHR) is due to activation of the RAS, and an accompanying decrease in kidney APA. Changes in APA have also been measured during the activation of the RAS in the Goldblatt hypertension model and Dahl salt-sensitive (DSS) rat. The DSS rat shows an elevation in renal APA activity at the onset of hypertension suggesting a protective role against elevations in circulating AngII, followed by decreased APA activity with advancing hypertension. Changes seen in human maternal serum APA activity during preeclampsia are similar to changes measured in renal APA in the DSS rat model. APA activity is higher than during normal pregnancy at the onset of preeclampsia, and with advancing preeclampsia (severe preeclampsia) declines below that seen during normal pregnancy. Serum APA activity is also increased during hormone replacement therapy (HRT), perhaps in reaction to elevated levels of AngII. Thus, it appears important to consider the relationship among activation of the RAS, circulating levels of AngII, and the availability of APA in hypertensive disorders.

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Review: AT1-receptors in the central nervous system

Cited by 13 publications

References 120 publications

The renin-angiotensin system in the brain: possible therapeutic implications for AT1-receptor blockers

The renin-angiotensin system in the brain: possible therapeutic implications for AT1-receptor blockers

Influence of brain angiotensin on thermoregulation and hydromineral balance during pregnancy in rats

New insights into the importance of aminopeptidase A in hypertension

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