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Angiotensin II activates pressor and depressor sites of the pontomedulla that react to glutamate.
Clin Exp Pharmacol Physiol. 1996 May; 23(5):415-23.CE

Abstract

1. In cats anaesthetized with a mixture of alpha-chloralose (40 mg/kg) and urethane (400 mg/kg) and in rats anaesthetized with a mixture of alpha-chloralose (60 mg/kg) and urethane (800 mg/kg), changes in systemic arterial pressure (SAP), heart rate (HR) and sympathetic activities of vertebral (VNA) and renal (RNA) nerves were determined following the microinjection of angiotensin II (AngII; 0.16 mmol/L; 50 nL) into the pressor and depressor sites of the pontomedulla previously reacted to a microinjection of monosodium L-glutamate (Glu; 0.1 mol/L; 50 nL). Pressor sites included gigantocellular tegmental field (FTG) and dorsal medulla (DM) and rostral ventrolateral medulla (VLM). The depressor site was the caudal VLM (CVLM). The effects of losartan (1 mmol/L; 50 nL), a specific AT1 receptor non-peptide antagonist for AngII, on responses induced by AngII in the VLM, DM and CVLM were also determined. 2. In 30% of pressor sites in the FTG, 55% in the VLM and 67% in the DM and in 76% of depressor sites in the CVLM previously exposed to Glu, microinjection of AngII to the same site produced pressor or depressor responses similar to that of Glu, but smaller in magnitude, particularly in the pressor VLM. Changes in both VNA and RNA induced by AngII were also smaller than those induced by Glu, particularly RNA from DM activation. 3. In the dorsal motor nucleus of the vagus, AngII, as Glu, produced marked bradycardia, but again this was smaller in magnitude than the bradycardia produced by Glu. 4. In rats, in the DM near or around the nucleus of the solitary tract where Glu increased SAP, microinjection of AngII (0.8 mmol/L; 60 nL) produced a depressor response, while the microinjection of 1.6 mmol/L (60 nL) AngII produced a pressor response. 5. Losartan blocked the increase in SAP induced by AngII in the VLM and DM. Decreases in SAP induced by AngII in the CVLM, however, were only slightly decreased by losartan. 6. Our data suggest that a significant portion of pressor and depressor sites of the pontomedulla contain neurons responsive to both AngII and Glu. In neurons in the VLM and DM, AngII produced pressor responses that were primarily mediated through AT1 receptors, while the depressor actions of AngII in the CVLM were not mediated by AT1 receptors.

Authors+Show Affiliations

Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, ROC.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

8713681

Citation

Chai, C Y., et al. "Angiotensin II Activates Pressor and Depressor Sites of the Pontomedulla That React to Glutamate." Clinical and Experimental Pharmacology & Physiology, vol. 23, no. 5, 1996, pp. 415-23.
Chai CY, Chen SY, Lin AM, et al. Angiotensin II activates pressor and depressor sites of the pontomedulla that react to glutamate. Clin Exp Pharmacol Physiol. 1996;23(5):415-23.
Chai, C. Y., Chen, S. Y., Lin, A. M., & Tseng, C. J. (1996). Angiotensin II activates pressor and depressor sites of the pontomedulla that react to glutamate. Clinical and Experimental Pharmacology & Physiology, 23(5), 415-23.
Chai CY, et al. Angiotensin II Activates Pressor and Depressor Sites of the Pontomedulla That React to Glutamate. Clin Exp Pharmacol Physiol. 1996;23(5):415-23. PubMed PMID: 8713681.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Angiotensin II activates pressor and depressor sites of the pontomedulla that react to glutamate. AU - Chai,C Y, AU - Chen,S Y, AU - Lin,A M, AU - Tseng,C J, PY - 1996/5/1/pubmed PY - 1996/5/1/medline PY - 1996/5/1/entrez SP - 415 EP - 23 JF - Clinical and experimental pharmacology & physiology JO - Clin Exp Pharmacol Physiol VL - 23 IS - 5 N2 - 1. In cats anaesthetized with a mixture of alpha-chloralose (40 mg/kg) and urethane (400 mg/kg) and in rats anaesthetized with a mixture of alpha-chloralose (60 mg/kg) and urethane (800 mg/kg), changes in systemic arterial pressure (SAP), heart rate (HR) and sympathetic activities of vertebral (VNA) and renal (RNA) nerves were determined following the microinjection of angiotensin II (AngII; 0.16 mmol/L; 50 nL) into the pressor and depressor sites of the pontomedulla previously reacted to a microinjection of monosodium L-glutamate (Glu; 0.1 mol/L; 50 nL). Pressor sites included gigantocellular tegmental field (FTG) and dorsal medulla (DM) and rostral ventrolateral medulla (VLM). The depressor site was the caudal VLM (CVLM). The effects of losartan (1 mmol/L; 50 nL), a specific AT1 receptor non-peptide antagonist for AngII, on responses induced by AngII in the VLM, DM and CVLM were also determined. 2. In 30% of pressor sites in the FTG, 55% in the VLM and 67% in the DM and in 76% of depressor sites in the CVLM previously exposed to Glu, microinjection of AngII to the same site produced pressor or depressor responses similar to that of Glu, but smaller in magnitude, particularly in the pressor VLM. Changes in both VNA and RNA induced by AngII were also smaller than those induced by Glu, particularly RNA from DM activation. 3. In the dorsal motor nucleus of the vagus, AngII, as Glu, produced marked bradycardia, but again this was smaller in magnitude than the bradycardia produced by Glu. 4. In rats, in the DM near or around the nucleus of the solitary tract where Glu increased SAP, microinjection of AngII (0.8 mmol/L; 60 nL) produced a depressor response, while the microinjection of 1.6 mmol/L (60 nL) AngII produced a pressor response. 5. Losartan blocked the increase in SAP induced by AngII in the VLM and DM. Decreases in SAP induced by AngII in the CVLM, however, were only slightly decreased by losartan. 6. Our data suggest that a significant portion of pressor and depressor sites of the pontomedulla contain neurons responsive to both AngII and Glu. In neurons in the VLM and DM, AngII produced pressor responses that were primarily mediated through AT1 receptors, while the depressor actions of AngII in the CVLM were not mediated by AT1 receptors. SN - 0305-1870 UR - https://www.unboundmedicine.com/medline/citation/8713681/Angiotensin_II_activates_pressor_and_depressor_sites_of_the_pontomedulla_that_react_to_glutamate_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0305-1870&date=1996&volume=23&issue=5&spage=415 DB - PRIME DP - Unbound Medicine ER -