Angiotensin receptors in the nervous system

Allen, Andrew M.; Moeller, Ingrid; Jenkins, Trisha A.; Zhuo, Jia L.; Aldred, G.Peter; Chai, Siew Yeen; Mendelsohn, Frederick A.O.

doi:10.1016/s0361-9230(98)00039-2

Cited by 217 publications

(177 citation statements)

References 121 publications

Supporting

Mentioning

171

Contrasting

Unclassified

Order By: Relevance

“…44,45 Although the role of the brain angiotensins in humans remains to be fully explored, experimental studies have demonstrated that intracerebroventricular administration of AII and its fragments facilitated acquisition in active conditioning trials and retention in a passive avoidance situation. [46][47][48] The facilitatory effects of angiotensins on memory has been connected mainly with the recently discovered AT4 receptors, which preferentially bind AIV and AII [3][4][5][6][7] and are found in brain areas distinct from those possessing AT1 and AT2 receptors (mainly in the neocortex, hippocampus, dentate gyrus, thalamus and cerebellum).…”

Section: Discussionmentioning

confidence: 99%

Influence of losartan and atenolol on memory function in very elderly hypertensive patients

et al. 2003

View full text Add to dashboard Cite

The aim of this study was to compare the effect of the beta-adrenergic blocker atenolol and the Angiotensin II type 1 (AT1) receptor antagonist losartan on cognitive function in very elderly hypertensive patients. A total of 120 mild to moderate essential hypertensive (DBP 490 and o105 mmHg) patients, aged 75-89 years, were studied. After a 4-week wash-out period on placebo, they were randomized to receive atenolol 50 mg or losartan 50 mg for 24 weeks according to a parallel arm design. At the end of the placebo period and of each active treatment period, BP was measured (by mercury sphygmomanometer, Korotkoff I and V) and cognitive function was evaluated through three different tests (word list memory, word list recall and word list fluency). Both atenolol and losartan were equally effective in reducing SBP (À22.1 and À23.1 mmHg, respectively, Po 0.01 vs baseline) and DBP (À10.3 and À11.2 mmHg, respectively, Po 0.01 vs baseline). Atenolol treatment did not induce significant changes in any test score, whereas losartan significantly increased the score of both the word list memory (+2.2, Po0.05 vs baseline) and the word list recall test (+2.1, Po0.05 vs baseline). The comparison between losartan and atenolol was significant (Po0.05) for both memory tests. These data suggest that in very elderly hypertensive patients, chronic AT1 receptor blockade by losartan could improve cognitive function, in particular immediate and delayed memory.

show abstract

Section: Discussionmentioning

confidence: 99%

Influence of losartan and atenolol on memory function in very elderly hypertensive patients

et al. 2003

View full text Add to dashboard Cite

show abstract

“…The lamina terminalis, which comprises the subfornical organ, median preoptic nucleus, and OVLT, is rich in angiotensin receptors in all mammalian species studied, including sheep. 10 In addition, ICV infusion of Ang II has been shown to result in the activation of neurons (as indicated II (3 g/h, n‫)6؍‬ or Losartan (1 mg/h, n‫) by Fos production) throughout the lamina terminalis of the rat. 16 Therefore, it seems likely that the suppression of PRC resulting from ICV infusion of Ang II is due to activation of neural pathways that originate in the lamina terminalis.…”

Section: Discussionmentioning

confidence: 99%

“…4 In regard to the brain regions mediating effects of ICV Ang II on PRC, the lamina terminalis may be crucial. This region of the brain is rich in AT 1 receptors, 10 and transsynaptic neural tracing studies with pseudorabies virus show that the lamina terminalis is neurally linked to the renal nerves. 11 Moreover, high levels of PRC result if the lamina terminalis is ablated, 12,13 suggesting the disruption of an inhibitory influence on renin secretion.…”

mentioning

confidence: 99%

Neural Mechanisms Subserving Central Angiotensinergic Influences on Plasma Renin in Sheep

McBurnie

Mathai

2001

Hypertension

View full text Add to dashboard Cite

Abstract-The mechanisms and brain regions subserving the suppression of plasma renin concentration caused by intracerebroventricular (ICV) infusion of angiotensin II were studied in sodium-depleted sheep. Infusion of angiotensin II (3 g/h for 1 hour) into the lateral ventricle reduced plasma renin from 4.3Ϯ0.4 to 1.6Ϯ0.2 pmol angiotensin I/mL per hour at 1 hour after the commencement of infusion. This change persisted for at least another 90 minutes and was blocked by concomitant ICV infusion of the AT 1 antagonist losartan (1 mg/h). Arterial pressure did not change, but plasma vasopressin secretion was increased. ICV infusion of losartan (1 mg/h) significantly increased plasma renin in sodium-depleted sheep. The reduction of plasma renin concentration in response to either ICV angiotensin II or hypertonic NaCl (0.75 mol/L at 1 mL/h) and the increase in response to ICV losartan was prevented in sheep in which the lamina terminalis of the brain had been ablated. Lesions in the median eminence (MEL), which blocked the increased plasma vasopressin levels, did not prevent suppression of plasma renin in response to ICV angiotensin II. However, bilateral renal denervation largely blocked this inhibition of plasma renin concentration but not the increased plasma renin resulting from ICV infusion of losartan in sodium-depleted sheep. The results show that AT 1 receptors, probably located in the lamina terminalis, mediate a central inhibitory influence of angiotensin II on renin secretion. This inhibition of renin release is probably due to a reduction in activity of renal sympathetic nerves innervating the juxtaglomerular apparatus of the kidney. Key Words: angiotensin Ⅲ renin Ⅲ receptors, angiotensin Ⅲ renal nerves T he secretion of renin by the kidney is influenced by several factors including the activity of the renal nerves, 1 and it is possible that several brain regions may contribute to the initiation of renal sympathetic drive 2 and therefore the control of renin release. However, the brain mechanisms controlling renin secretion are poorly understood. One of the factors that may influence renin secretion is the concentration of angiotensin (Ang) II in the brain. 3-8 Whereas intracerebroventricular (ICV) infusions of Ang II or renin reduce plasma renin concentration (PRC), arterial pressure also increases. [3][4][5][6][7][8] Thus, the inhibition of renin release may be mediated by renal or arterial baroreflexes secondary to the rise in pressure. ICV infusion of the angiotensin AT 1 receptor antagonist losartan elevates PRC in sodium-depleted sheep, suggesting that an angiotensinergic pathway in the brain may exert a tonic inhibitory influence on renin secretion in these animals. 8 We have observed that ICV infusion of either Ang II or hypertonic saline suppresses PRC in sodium-depleted sheep without increasing arterial pressure. 8,9 This contrasts with the pressor effects of such ICV infusions in sodium-replete sheep, 6 suggesting that the reduced plasma renin levels are not a reflex response to baroreceptor acti...

show abstract

“…Angiotensin II (angio II) is an octapeptide most familiar for its role in the renin-angiotensin-aldosterone system that helps to maintain blood volume and pressure 2) . In addition, angiotensin is also involved in local functions through the activity of tissue renin-angiotensin systems that occur in many organs, including the brain, adrenal gland, vascular wall, reproductive organs, and heart 2) .…”

Section: Introductionmentioning

confidence: 99%

Angiotensin II-induced depolarizations in hamster submandibular ganglion neurons.

Ikegami

Yamada

Suzuki

2000

Bull. Tokyo Dent. Coll.

View full text Add to dashboard Cite

Angiotensin II acts as an excitatory neurotransmitter of the sympathetic ganglia. In the parasympathetic neurons, however, angiotensin II (angio II)-induced responses have not been recorded. In this study, we investigated the effects of angio II in the hamster submandibular ganglion (SMG) neurons using a intracellular recording technique. Approximately 70% of these ganglion cells responded with persistent depolarization (3-6 mV, 5-9min) at a concentration of 10M. The angio II-induced depolarizations were caused by the combination of an increase in Na ‫ם‬ conductance and a decrease in K ‫ם‬conductance. An involvement of K ‫ם‬ channels such as M channels and SK channels in the electrogenesis mechanism was suggested by an inhibitory effect of Ba ‫ם2‬ ion on the component of the increased membrane input resistance during the angio II-induced depolarization. In addition, the angio II-induced depolarizations were mediated through angio II type I (AT 1 ) receptors. Thus angio II is probably a neurotransmitter that increases their excitability in most of the neurons in parasympathetic ganglia.

show abstract

Angiotensin receptors in the nervous system

Cited by 217 publications

References 121 publications

Influence of losartan and atenolol on memory function in very elderly hypertensive patients

Influence of losartan and atenolol on memory function in very elderly hypertensive patients

Neural Mechanisms Subserving Central Angiotensinergic Influences on Plasma Renin in Sheep

Angiotensin II-induced depolarizations in hamster submandibular ganglion neurons.

Contact Info

Product

Resources

About