Brain angiotensinergic mediation of enhanced water  consumption in lactating rats

Speth, Robert C.; Smith, M. Susan; Grove, Kevin L.

doi:10.1152/ajpregu.00432.2001

Cited by 5 publications

(3 citation statements)

References 39 publications

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“…However, it should be noted that AT 1A receptor-deficient mice do not respond to intracerebroventricular injections of ANG II (8,9). 3) Recent studies, coupled with the present results, suggest that ANG II may not be an agonist in the brain and thus may be an antagonist (40). 4) Perhaps the brain RAS is designed to provide at least two active ligands, ANG III and ANG IV (49), and both ANG I and ANG II are precursor molecules.…”

Section: Discussionsupporting

confidence: 49%

Conversion of brain angiotensin II to angiotensin III is critical for pressor response in rats

Wright

Tamura-Myers²,

Wilson³

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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The present investigation measured the relative pressor potencies of intracerebroventricularly infused ANG II, ANG III, and the metabolically resistant analogs d-Asp(1)ANG II and d-Arg(1)ANG III in alert freely moving rats. The stability of these analogs was further facilitated by pretreatment with the specific aminopeptidase A inhibitor EC33 or the aminopeptidase N inhibitor PC18. The results indicate that the maximum elevations in mean arterial pressure (MAP) were very similar for each of these compounds across the dose range 1, 10, and 100 pmol/min during a 5-min infusion period. However, d-Asp(1)ANG II revealed significantly extended durations of pressor effects before return to base level MAP. Pretreatment intracerebroventricular infusion with EC33 blocked the pressor activity induced by the subsequent infusion of d-Asp(1)ANG II, whereas EC33 had no effect on the pressor response to subsequent infusion of d-Arg(1)ANG III. In contrast, pretreatment infusion with PC18 extended the duration of the d-Asp(1)ANG II pressor effect by about two to three times and the duration of d-Arg(1)ANG III's effect by approximately 10 to 15 times. Pretreatment with the specific AT(1) receptor antagonist losartan blocked the pressor responses induced by the subsequent infusion of both analogs indicating that they act via the AT(1) receptor subtype. These results suggest that the brain AT(1) receptor may be designed to preferentially respond to ANG III, and ANG III's importance as a centrally active ligand has been underestimated.

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Section: Discussionsupporting

confidence: 49%

Conversion of brain angiotensin II to angiotensin III is critical for pressor response in rats

Wright

Tamura-Myers²,

Wilson³

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

Self Cite

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“…After the film was developed, the signal on the film was quantified using densimetric analysis (AIS, Imaging Research, St. Catherines, Ontario, Canada) according to a previously reported method (39). Briefly, to quantify, an analog camera was used to capture and magnify the image of each section, with the lighting and magnification kept constant for the entire study.…”

Section: In Situ Hybridizationmentioning

confidence: 99%

Basomedial Hypothalamic Injections of Neuropeptide Y Conjugated to Saporin Selectively Disrupt Hypothalamic Controls of Food Intake

Bugarith

Dinh

et al. 2005

Endocrinology

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Neuropeptide Y (NPY) conjugated to saporin (NPY-SAP), a ribosomal inactivating toxin, is a newly developed compound designed to selectively target and lesion NPY receptor-expressing cells. We injected NPY-SAP into the basomedial hypothalamus (BMH), just dorsal to the arcuate nucleus (ARC), to investigate its neurotoxicity and to determine whether ARC NPY neurons are required for glucoprivic feeding. We found that NPY-SAP profoundly reduced NPY Y1 receptor and alpha MSH immunoreactivity, as well as NPY, Agouti gene-related protein (AGRP), and cocaine and amphetamine-related transcript mRNA expression in the BMH. NPY-SAP lesions were localized to the injection site with no evidence of retrograde transport by hindbrain NPY neurons with BMH terminals. These lesions impaired responses to intracerebroventricular (icv) leptin (5 microg/5 microl x d) and ghrelin (2 microg/5 microl), which are thought to alter feeding primarily by actions on ARC NPY/AGRP and proopiomelanocortin/cocaine and amphetamine-related transcript neurons. However, the hypothesis that NPY/AGRP neurons are required downstream mediators of glucoprivic feeding was not supported. Although NPY/AGRP neurons were destroyed by NPY-SAP, the lesion did not impair either the feeding or the hyperglycemic response to 2-deoxy-D-glucose-induced blockade of glycolysis use. Similarly, responses to glucagon-like peptide-1 (GLP-1, 5 microg/3 microl icv), NPY (5 microg/3 microl icv), cholecystokinin octapeptide (4 microg/kg ip), and beta-mercaptoacetate (68 mg/kg ip) were not altered by the NPY-SAP lesion. Thus, NPY-SAP destroyed NPY receptor-expressing neurons in the ARC and selectively disrupted controls of feeding dependent on those neurons but did not disrupt peptidergic or metabolic controls dependent upon circuitry outside the BMH.

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“…Lactating rats have increased dipsogenic responsivity to intracerebroventricular ANG II. An AT 1 antagonist reduced drinking in lactating rats, but not in control rats, again pointing to a central role for ANG II in the control of thirst (33). In mice lacking the AT 1a receptor, dehydration caused a smaller increase in plasma vasopressin concentration than in control mice.…”

mentioning

confidence: 93%

Body sodium and volume homeostasis

Skøtt

2003

American Journal of Physiology-Regulatory, Integrative and Comp

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MAINTENANCE OF A "MILIEU INTERIEUR," which allows our cells to function away from the ancient sea, is one of the most important functions of the body. Maintenance of constant extracellular osmolarity and sodium concentration depends on a precise balance between intake and excretion of sodium and water. Intakes of water and sodium are governed by an urge driven by the lack of these substances, by habit, or by more or less wellfounded recommendations (43). Regulated excretion of the substances takes place mainly in the kidney.The aim of this "In Focus" article is to give a short overview of the regulation of body sodium and volume homeostasis, with an emphasis on recent developments, and focus on papers published in the American Journal of Physiology-Regulatory, Integrative and Comparative Physiology.Regulation of water and sodium intake. Variations in the composition of blood plasma are picked up in the brain by the small areas that lack a blood-brain barrier. These areas, the circumventricular organs, surround the ventricular system. Three of these are involved in body fluid homeostasis: the subfornical organ (SFO) and organum vasculosum laminae terminalis (OVLT), which are located in the anteroventral third ventricle, and the area postrema (AP), which is located at the transition of the fourth ventricle and the central canal of the spinal cord (12).Thirst. Hyperosmolarity is a strong stimulus for water intake. When exposed to hyperosmolality, osmoreceptor cells in the SFO and OVLT activate neurons projecting to the paraventricular nucleus (PVN) and supraoptic nucleus (SON) in the hypothalamus to stimulate thirst. The protooncogene c-Fos is an immediateearly response gene, which has become an excellent mapping tool to identify active cells in the nervous system. It is activated in response to a wide range of stimuli and its expression is barely detectable under basal conditions (18). Consistent with this, dehydration increased the expression of c-Fos in the OVLT, SFO, and SON in rats (11).Thirst is also induced by profound volume contraction, which is probably detected by stretch receptors in the heart (39). A fall in arterial blood pressure increases thirst in response to intracerebroventricular ANG II (41). Conversely, thirst is inhibited by increased arterial blood pressure, which is detected by arterial baroreceptors (36) and inhibits thirst induced by ANG II infusion, hypovolemia, or hyperosmolarity (35).ANG II is a strong dipsogenic agent. Circulating ANG II stimulates AT 1 receptors in the SFO of rats (39), and intracerebroventricular injection of ANG II stimulates c-Fos expression in median preoptic nucleus (MnPO), SFO, PVN, and SON (21). On repetitive stimulation, there is desensitization to this response, which is associated with an increase in AT 1 receptor protein expression (21). Thirst induced by intracerebroventricular hypertonic saline in sheep is inhibited by administration of intracerebroventricular losartan, which is an AT 1 receptor antagonist (44). Upregulation of AT 1 receptors in most regio...

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Brain angiotensinergic mediation of enhanced water consumption in lactating rats

Cited by 5 publications

References 39 publications

Conversion of brain angiotensin II to angiotensin III is critical for pressor response in rats

Conversion of brain angiotensin II to angiotensin III is critical for pressor response in rats

Basomedial Hypothalamic Injections of Neuropeptide Y Conjugated to Saporin Selectively Disrupt Hypothalamic Controls of Food Intake

Body sodium and volume homeostasis

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