Brain angiotensin receptor subtypes in the control of physiological and behavioral responses

Wright, John W.; Harding, Joseph W.

doi:10.1016/0149-7634(94)90034-5

Cited by 243 publications

(123 citation statements)

References 410 publications

Supporting

Mentioning

113

Contrasting

Unclassified

Order By: Relevance

“…It is widely accepted that the brain has its own reninangiotensin system that is distinct from that in the periphery (Wright & Harding, 1994). There are two major types of angiotensin II (AII) receptors in the brain, AT1 and AT2 (Wright & Harding, 1994;Saavedra, 1994;Aguilera et al 1995).…”

mentioning

confidence: 99%

Effects of targeted disruption of the mouse angiotensin II type 2 receptor gene on stress‐induced hyperthermia

Watanabe

Hashimoto

Okuyama

et al. 1999

The Journal of Physiology

View full text Add to dashboard Cite

; Aguilera et al. 1995). AT1 mediates all the well-known central actions of AII, including those involved in blood pressure regulation. By contrast, the physiological roles played by the AT2 receptor in the brain are as yet poorly defined. Recently, two laboratories developed mice deficient in AT2. These mice showed (i) increased pressor responses to AII and a lower resting body temperature (Hein et al. 1995;Ichiki et al. 1995) and (ii) attenuated exploratory behaviour and a reduction in spontaneous movements. These findings suggest that endogenous AII regulates central nervous functions via AT2. Animals exposed to stressors usually show activation of the sympathetic nervous system and the hypothalamopituitary adrenocortical axis, with consequent increases in body temperature, blood pressure, heart rate and the plasma concentration of adrenocorticotrophic hormone (McCubbin et al. 1991;Stanford & Samon, 1993). Recently, brain AII and its receptors have been shown to contribute to some stress-induced responses in rats. For example, we found that central administration of an AT2 antagonist, but not of an AT1 antagonist, attenuated the interleukin-1 (IL_1)-induced hyperthermic response . This suggests that AT2 in the brain may modulate (or mediate) the hyperthermia induced by immunological stress. On the other hand, to demonstrate inhibition of the hyperthermic, pressor and tachycardic responses to restraint stress required central injection of an AT1 antagonist (Saikiet al. 1997). Inhibition by an AT1 antagonist of the pressor response to heat or footshock stress has also been reported (Cierco & Israel, 1994;Kregel et al. 1994). Taken together, these findings suggest that brain AII and its receptors (AT1 and AT2) may play important roles in physiological reactions (such as body temperature increases) to several stress protocols in rats and they indicate the separate involvement of AT1 and AT2 in the effects induced by particular forms of stress. 1. We have previously reported that brain angiotensin II type 2 receptors (AT2) contribute to immunological stress-induced hyperthermia (fever) in rats. Now, in mice, we report the effect of AT2 gene disruption on the hyperthermia induced by immunological (interleukin-1 (IL_1) injection) and non-immunological (saline injection or cage switch) stress. 2. AT2-deficient and control mice both showed typical circadian rhythmicity in body temperature and physical activity. During the latter half of the dark period, AT2-deficient mice exhibited a lower body temperature than the controls. 3. By comparison with the controls, AT2-deficient mice exhibited: (i) a significantly smaller hyperthermia after intraperitoneal (i.p.) injection of IL-1â; (ii) significantly greater increases in body temperature and physical activity after i.p. saline; and (iii) a significantly greater hyperthermia (but a similar increase in activity) during cage-switch stress. 4. These results suggest that AT2, presumably in the brain, plays important roles in stressinduced hyperthermia in mice. 9055Keywords:

show abstract

mentioning

confidence: 99%

Effects of targeted disruption of the mouse angiotensin II type 2 receptor gene on stress‐induced hyperthermia

Watanabe

Hashimoto

Okuyama

et al. 1999

The Journal of Physiology

View full text Add to dashboard Cite

show abstract

“…A basic assumption of this view is that the formation of crab ANGIV involves successive cleavages of the N-terminus from ANGII to ANGIV, as also observed in mammals (58).…”

Section: Components Of the Renin-angiotensin System (Ras) Are Involvementioning

confidence: 99%

Long-term habituation (LTH) in the crab Chasmagnathus: a model for behavioral and mechanistic studies of memory

Maldonado¹,

Romano²,

Tomsic³

1997

Braz J Med Biol Res

View full text Add to dashboard Cite

A decade of studies on long-term habituation (LTH) in the crab Chasmagnathus is reviewed. Upon sudden presentation of a passing object overhead, the crab reacts with an escape response that habituates promptly and for at least five days. LTH proved to be an instance of associative memory and showed context, stimulus frequency and circadian phase specificity. A strong training protocol (STP) (≥15 trials, intertrial interval (ITI) of 171 s) invariably yielded LTH, while a weak training protocol (WTP) (≤10 trials, ITI = 171 s) invariably failed. STP was used with a presumably amnestic agent and WTP with a presumably hypermnestic agent. Remarkably, systemic administration of low doses was effective, which is likely to be due to the lack of an endothelial blood-brain barrier. LTH was blocked by inhibitors of protein and RNA synthesis, enhanced by protein kinase A (PKA) activators and reduced by PKA inhibitors, facilitated by angiotensin II and IV and disrupted by saralasin. The presence of angiotensins and related compounds in the crab brain was demonstrated. Diverse results suggest that LTH includes two components: an initial memory produced by spaced training and mainly expressed at an initial phase of testing, and a retraining memory produced by massed training and expressed at a later phase of testing (retraining). The initial memory would be associative, context specific and sensitive to cycloheximide, while the retraining memory would be nonassociative, context independent and insensitive to cycloheximide. Key wordsSimple and basic models to study memory Simple-system approaches using invertebrate species have led to considerable progress in our understanding of the mechanisms underlying learning and memory (e.g., the mollusks Aplysia (1,2) and Hermissenda (3,4), the fruit fly Drosophila (5), and the honey bee Apis (6)). A virtue usually attributed to invertebrates is that they are simple models though the use of this term has been highly controversial. Indeed, the CNS of invertebrates cannot be considered simple from the perspective of a neural network researcher since the amount of neurons involved in a current mnemonic process is assumed to be far larger than that required to obtain a satis-

show abstract

“…22 The aminopeptidases A and N sequentially remove amino acids from the N-terminus of Ang II to form the fragments Ang II(2-8), also known as Ang II, and Ang II (3)(4)(5)(6)(7)(8), also known as Ang IV. 23 Ang II(1-7) is another metabolite of Ang II 24 but may be cleaved directly from Ang I [24][25][26] by neutral endopeptidase 24.11 and prolyl endopeptidase.…”

Section: Ang II Metabolismmentioning

confidence: 99%

“…[2][3][4][5] In the kidney, for instance, Ang II acts on renal vessels, glomeruli, tubules and renomedullary interstitial cells, to alter renal blood flow, glomerular filtration rate and electrolyte reabsorption.…”

Section: Actions Of Ang IImentioning

confidence: 99%

See 1 more Smart Citation

Bioactive angiotensin peptides

et al. 1998

View full text Add to dashboard Cite

Angiotensin II is recognised as the principle active peptide of the renin-angiotensin system, exerting effects on fluid and electrolyte homeostasis, and cardiovascular control including neural and long term trophic effects. However, recent studies indicate that other angiotensin peptides such as angiotensin III, angiotensin II (1-7) and angiotensin IV, may have specific actions. Interestingly, recent work involving angiotensin IV demonstrates that this peptide binds to specific receptors and may be Keywords: angiotensin metabolites; angiotensin III; angiotensin II(1-7); angiotensin IV; globin Bioactive angiotensin peptidesThe renin-angiotensin system (RAS) was initially identified as a circulating humoral system with the effector peptide, angiotensin II (Ang II), generated by an enzymatic cascade. Angiotensinogen, which is synthesized in the liver, is cleaved by renin, a product of the juxtaglomerular cells of the kidney, to form Ang I, which in turn is cleaved by angiotensinconverting enzyme (ACE) to form Ang II. ACE is membrane bound and predominates on the endothelial cells of all vascular beds. Apart from the production of Ang II in plasma, Ang II, renin and ACE have all been described in tissues such as the brain, kidney, adrenal, vasculature, heart and ovaries. This suggests a separate and distinct RAS in these tissues and implies endocrine, paracrine and autocrine roles for Ang II. Actions of Ang IIAng II regulates blood pressure, fluid volume homeostasis and pituitary hormone release via AT 1 and AT 2 receptors located in the kidney, adrenal gland, and the cardiovascular and nervous systems. [2][3][4][5] In the kidney, for instance, Ang II acts on renal vessels, glomeruli, tubules and renomedullary interstitial cells, to alter renal blood flow, glomerular filtration rate and electrolyte reabsorption.6-9 Ang II also acts on the adrenal cortex to stimulate aldosterone secretion and hence renal sodium reabsorption. 10Ang II is a potent vasoconstrictor, acting directly on vascular smooth muscle and indirectly via facilitation of noradrenaline release from sympathetic terminals. 11,12 In the heart, Ang II exerts positive iono- tropic and chronotropic effects and facilitates sympathetic activity. 13Acting on the brain, Ang II induces fluid and salt ingestion, modulates neuroendocrine systems, including vasopressin and corticotropin releasing factor release, and interacts with the autonomic control of the cardiovascular system to influence blood pressure. 3,14,15 In many instances, these effects are complementary to those of the systemic peptide on peripheral target organs. Thus, systematic Ang II affects the brain through AT 1 receptors located in the circumventricular organs, regions with a deficient blood brain barrier. In addition, endogenous neurally derived Ang II appears to act at many central nervous system sites behind the blood brain barrier. [16][17][18] Most of the classical actions of Ang II are mediated via the AT 1 receptor whereas AT 2 receptor stimulation may cause opposing effects. This was o...

show abstract

Brain angiotensin receptor subtypes in the control of physiological and behavioral responses

Cited by 243 publications

References 410 publications

Effects of targeted disruption of the mouse angiotensin II type 2 receptor gene on stress‐induced hyperthermia

Effects of targeted disruption of the mouse angiotensin II type 2 receptor gene on stress‐induced hyperthermia

Long-term habituation (LTH) in the crab Chasmagnathus: a model for behavioral and mechanistic studies of memory

Bioactive angiotensin peptides

Contact Info

Product

Resources

About