Brain Angiotensin

Lang, R.; Unger, Thomas; Rascher, Wolfgang; Ganten, Detlev

doi:10.1007/978-1-4613-3515-3_5

Cited by 21 publications

(9 citation statements)

References 168 publications

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“…28 The enhanced salt preference of SHR was reported to be suppressed by ICV infusion of an angiotensin-converting enzyme inhibitor, captoril. 23 These findings suggest the role of enhanced brain RAS in SHR in manifesting the development of hypertension and the exaggerated salt appetite.…”

Section: Discussionmentioning

confidence: 99%

Centrally infused atrial natriuretic polypeptide attenuates exaggerated salt appetite in spontaneously hypertensive rats.

Itoh¹,

Nakao²,

Katsuura³

et al. 1986

Circulation Research

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Section: Discussionmentioning

confidence: 99%

Centrally infused atrial natriuretic polypeptide attenuates exaggerated salt appetite in spontaneously hypertensive rats.

Itoh¹,

Nakao²,

Katsuura³

et al. 1986

Circulation Research

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“…The main structures of the forebrain angiotensin-I1 system are the two circumventricular organs (subfornical organ and the organum vasculosum of the lamina terminalis), the nucleus medianus (a structure continuous with the subfornical organ dorsally and the lamina terminalis ventrally), and the hypothalamic magnocellular nuclei, with major projections to and from brain-stem cardiovascular centers (73)(74)(75). All these regions contain angiotensin-I1 receptors and possess the biochemical machinery necessary for local production of angiotensin-I1 (76)(77)(78).…”

Section: Relaxin and The Forebrain Angiotensin-ll Systemmentioning

confidence: 99%

The Emerging Concept of Relaxn as a Centrally Actng Peptide Hormone with Hemodynamic Actions

Geddes

Summerlee

1995

J Neuroendocrinology

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The novel finding that relaxin has an action on the brain was first published in 1984. Since then, it has been shown that exogenous relaxin affects the release of a number of hypothalamo-pituitary hormones and has a robust pressor action. In this paper, we review the accumulating evidence that relaxin affects the release of oxytocin and vasopressin by an action at the level of the brain. The potential mechanisms of this central action are discussed and the evidence presented for the interaction between relaxin and the forebrain angiotensin-ll system. Furthermore, we articulate the possible physiological influences of relaxin on the changes in cardiovascular function that occur during pregnancy.F. L. Hisaw ( I ) discovered an ovarian substance that caused relaxation of the pelvic ligament of a variety of species in 1926 but it was not until 1930 that the first crude extract of the substance was obtained and named relaxin (2). Initial work focused on the role of relaxin on the birth canal and it was not until 1957 that an effect on the cardiovascular system was first reported (3). Miller and colleagues (3) showed that an extract of ovary caused a short hypotensive episode in dogs and suggested that relaxin had a direct action on peripheral blood vessels. Since that time. a number of hemodynamic actions of relaxin have been described (4, 5). The balance of the data, however, suggests that relaxin is hypertensive and exerts this effect through an action at the level of the brain (6-9) and on the heart (10, 11). RelaxinRelaxin is a peptide hormone produced primarily by the corpus luteum, placenta, uterus and possibly brain. It is present in detectable quantities in the peripheral circulation only during pregnancy. There are considerable species differences in the site and pattern of release of the hormone, hormone structure, and the putative role the hormone plays in the preparturient period. These differences have been extensively reviewed by Sherwood (4). Most research into the physiological actions of relaxin has been carried out using porcine relaxin obtained by the method described by Sherwood and O'Byrne (12). The classic actions of relaxin in pregnancy include softening of the cervix (13), separation of the pelvic symphysis (14). and maintenance of myornetrial quiescence towards the end of pregnancy ( 15).In the rat, relaxin is produced almost entirely within the corpora lutea of pregnancy (16) although there is some evidence that the hormone may also be produced by the endometrium (17). Levels of hormone are below the limit of detectability, by radioimmunoassay. during the first 7/12 days of pregnancy and start to increase from day 7 onwards. The levels increase steadily until day 16 when they begin to plateau. In the 48 h before birth, in association with the collapse of the corpora lutea, relaxin levels show a sharp peak then fall to low levels before birth starts (18). Sherwood et al. (18) also reported that there were peaks of relaxin in parturition. Although these data have not been confirmed by ...

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“…These include stimulation of drinking, increased salt appetite, elevation of blood pressure (1)(2)(3), and release of several pituitary hormones, including vasopressin, corticotropin (3)(4)(5), and prolactin (6). All components of the renin-angiotensin system (3), including renin (7,8), angiotensin-converting enzyme (9)(10)(11)(12)(13), and the polypeptide precursor angiotensinogen (14), have been identified in the brain.…”

mentioning

confidence: 99%

Autoradiographic localization of angiotensin II receptors in rat brain.

Mendelsohn¹,

Quirion²,

Saavedra³

et al. 1984

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

442

209

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The 125I-labeled agonist analog [1-sarcosine]-angiotensin II ([Sar']AII) bound with high specificity and affinity (Ka = 2 x 109 M-1) to a single class of receptor sites in rat brain. This ligand was used to analyze the distribution of All receptors in rat brain by in vitro autoradiography followed by computerized densitometry and color coding. A very high density of All receptors was found in the subfornical organ, paraventricular and periventricular nuclei of the hypothalamus, nucleus of the tractus solitarius, and area postrema. A high concentration of receptors was found in the suprachiasmatic nucleus of the hypothalamus, lateral olfactory tracts, nuclei of the accessory and lateral olfactory tracts, triangular septal nucleus, subthalamic nucleus, locus coeruleus, and inferior olivary nuclei. Moderate receptor concentrations were found in the organum vasculosum of the lamina terminalis, median preoptic nucleus, medial habenular nucleus, lateral septum, ventroposterior thalamic nucleus, median eminence, medial geniculate nucleus, superior colliculus, subiculum, preand parasubiculum, and spinal trigeminal tract. Low concentrations of sites were seen in caudate-putamen, nucleus accumbens, amygdala, and gray matter of the spinal cord. These studies have demonstrated that All receptors are distributed in a highly characteristic anatomical pattern in the brain. The high concentrations of All receptors at numerous physiologically relevant sites are consistent with the emerging evidence for multiple roles of All as a neuropeptide in the central nervous system.

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Brain Angiotensin

Cited by 21 publications

References 168 publications

Centrally infused atrial natriuretic polypeptide attenuates exaggerated salt appetite in spontaneously hypertensive rats.

Centrally infused atrial natriuretic polypeptide attenuates exaggerated salt appetite in spontaneously hypertensive rats.

The Emerging Concept of Relaxn as a Centrally Actng Peptide Hormone with Hemodynamic Actions

Autoradiographic localization of angiotensin II receptors in rat brain.

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