Depressor effect of microinjection of angiotensin II in the brainstem nuclei of renal hypertensive rats

Tseng, Chuen-Den; Tung, Che‐Se; Kuan, Chia-Jen; Mosqueda‐Garcia, Rogelio

doi:10.1016/0014-2999(90)92429-m

Cited by 4 publications

(4 citation statements)

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“…Evidence has accumulated that the increase in blood pressure caused by central AT 1 activation is mediated with [37][38][39][40] or without [41][42][43][44] activation of the sympathetic nervous system. In the present study, ␣-adrenergic blockade with phentolamine decreased blood pressure to a similar extent in D 4 Ϫ/Ϫ and D 4 ϩ/ϩ mice.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin-II Type 1 Receptor–Mediated Hypertension in D ₄ Dopamine Receptor–Deficient Mice

et al. 2006

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Key Words: dopamine Ⅲ receptors, angiotensin II Ⅲ mice Ⅲ hypertension Ⅲ angiotensin II Ⅲ endothelin Ⅲ vasopressins E ssential hypertension is a major risk factor for the development of cardiovascular disease. 1 It is a heterogeneous disease in which both genetics and environment influence blood pressure. 2 Dopamine affects cardiovascular regulatory mechanisms by its actions on renal hemodynamics and ion and water transport and by its regulation of hormones and humoral agents, such as aldosterone, catecholamines, endothelin, prolactin, proopiomelanocortin, renin, and vasopressin. In addition, dopamine can control blood pressure by acting on neuronal cardiovascular centers, heart, and arterial and venous vessels. Methods Generation of D 4 Dopamine-Receptor Mutant MiceThe original F 2 hybrid strain (129/SvϫC57BL/6) carrying a mutant form of the D 4 dopamine receptor was initially generated and backcrossed to C57BL/6 mice. Heterozygous (D 4 ϩ/Ϫ ) mice were mated to obtain D 4 Ϫ/Ϫ and D 4 ϩ/ϩ littermates, and the D 4 Ϫ/Ϫ mice were backcrossed with C57BL/6 mice to obtain sixth-and tenthgeneration mice in the Department of Physiology and Pharmacology, Oregon Health and Science University. 21 We used sixth-generation mice for acute studies and tenth-generation mice for chronic and immunoblotting studies. All of the animals were genotyped 21 and treated in accordance with National Institutes of Health guidelines for ethical treatment and handling of animals in research.

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Section: Discussionmentioning

confidence: 99%

Angiotensin-II Type 1 Receptor–Mediated Hypertension in D ₄ Dopamine Receptor–Deficient Mice

et al. 2006

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“…The preparation of animals for intra-NTS microinjection and the methods used in the localization of NTS have been described previously. 17,18 The changes of arterial pressure and heart rate were measured intra-arterially in anesthetized rats through unilateral microinjection of hematin (0.33 nmol/60 nL) before and 10 minutes after intra-NTS administration with HO inhibitor (ZnDPBG; 1 nmol/60 nL) or vehicle alone (50 mmol/L Na 2 CO 3 , 60 nL). Baroreflex responses were elicited by increasing doses of phenylephrine (10 to 30 g/kg IV) before and after intra-NTS administration of different doses of ZnDPBG (0.1 to 3.3 nmol) or vehicle to test the induced baroreflex responses of phenylephrine (10 to 30 g/kg IV).…”

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confidence: 99%

Modulatory Effects of Carbon Monoxide on Baroreflex Activation in Nucleus Tractus Solitarii of Rats

Jan

Chiang

et al. 2000

Hypertension

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Abstract-Recent studies suggest that carbon monoxide (CO), which is produced in significant quantities in many brain regions, may function as a neurotransmitter. Heme oxygenase catalyzes the metabolism of heme to CO and biliverdin; however, the physiological role of CO in central cardiovascular regulation was not well understood. In the present study, we evaluated the baroreflex response of CO in the nucleus tractus solitarii (NTS) of rats. Male Sprague-Dawley rats were anesthetized with urethane, and blood pressure and heart rate were monitored intra-arterially. Unilateral microinjection (60 nL) of hematin, a heme molecule cleaved by heme oxygenase to yield CO, into the NTS produced prominent dose-related depressor and bradycardic effects. Baroreflex responses were elicited by increasing doses of phenylephrine (10 to 30 g/kg IV) before and after intra-NTS administration of zinc deuteroporphyrin 2,4-bis-glycol (ZnDPBG) (1 nmol), an inhibitor of heme oxygenase activity, or vehicle alone. The reflex bradycardia elicited by phenylephrine was significantly inhibited by pretreatment with ZnDPBG. Furthermore, the inhibitory effect of ZnDPBG on baroreflex activation was dose dependent. These results suggest CO formed by brain heme oxygenase plays a significant role in central cardiovascular regulation and that inhibition of heme oxygenase attenuated baroreflex activation. (Hypertension. 2000;35:1253-1257.)Key Words: bradycardia Ⅲ brain Ⅲ baroreflex C arbon monoxide (CO), previously thought to be a toxic gas and biological waste product, is now being considered a likely candidate in the new class of gaseous neural messengers. 1 In animals, the predominant source of CO generation is heme degradation. Heme oxygenase (HO) is the rate-limiting enzyme responsible for the catabolism of heme and subsequent production of CO and bilirubin. Two forms of HO have been identified. HO-1 is enriched in spleen and liver and is induced by heme and numerous oxidative stressors. In contrast, HO-2 is a constitutive enzyme and is present abundantly in the brain and testis. 2 Recent studies have suggested that CO stimulates soluble guanylate cyclase activity and promotes elevation of cGMP in neural and cardiovascular tissues. [3][4][5][6][7][8] These results have implicated the HO-CO system as a potential regulator of various neural 5,6 and cardiovascular functions. 4,7,8 HO is widely expressed in the brain and is responsible for the impressive CO-generating ability of the brain, including brain stem. 3,6 Zinc deuteroprophyrin 2,4-bis-glycol (ZnDPBG) is an inhibitor of HO activity. 5,9,10 ZnDPBG has been shown to inhibit endogenous CO production in rats 11 and thus has been applied in in vivo studies of the physiological actions of HO.In the central nervous system, the nucleus of the solitary tract (NTS) is the site where afferent fibers arising from arterial baroreceptor, chemoreceptors, cardiopulmonary receptors, and other visceral receptors make the first central synapses 12 and thus play an important role in the integration of autonomic ...

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“…It is notable that in most instances, Ang III agonistic effects in the brain are similar to Ang II. Both peptides have been shown to induce similar central-mediated increases in blood pressure or mean arterial pressure [30, 31] and equivalent central effects on thirst and sodium appetite [32]. Centrally administered Ang III was as potent as Ang II in causing pressor and renal effects in rats on normal and high sodium diets [33].…”

Section: Discussionmentioning

confidence: 99%

Distinct Molecular Effects of Angiotensin II and Angiotensin III in Rat Astrocytes

Clark

Nguyen²,

Tran³

2013

International Journal of Hypertension

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It is postulated that central effects of angiotensin (Ang) II may be indirect due to rapid conversion to Ang III by aminopeptidase A (APA). Previously, we showed that Ang II and Ang III induced mitogen-activated protein (MAP) kinases ERK1/2 and stress-activated protein kinase/Jun-terminal kinases (SAPK/JNK) phosphorylation in cultured rat astrocytes. Most importantly, both peptides were equipotent in causing phosphorylation of these MAP kinases. In these studies, we used brainstem and cerebellum astrocytes to determine whether Ang II's phosphorylation of these MAP kinases is due to the conversion of the peptide to Ang III. We pretreated astrocytes with 10 μM amastatin A or 100 μM glutamate phosphonate, selective APA inhibitors, prior to stimulating with either Ang II or Ang III. Both peptides were equipotent in stimulating ERK1/2 and SAPK/JNK phosphorylation. The APA inhibitors failed to prevent Ang II- and Ang III-mediated phosphorylation of the MAP kinases. Further, pretreatment of astrocytes with the APA inhibitors did not affect Ang II- or Ang III-induced astrocyte growth. These findings suggest that both peptides directly induce phosphorylation of these MAP kinases as well as induce astrocyte growth. These studies establish both peptides as biologically active with similar intracellular and physiological effects.

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Depressor effect of microinjection of angiotensin II in the brainstem nuclei of renal hypertensive rats

Cited by 4 publications

References 1 publication

Angiotensin-II Type 1 Receptor–Mediated Hypertension in D ₄ Dopamine Receptor–Deficient Mice

Angiotensin-II Type 1 Receptor–Mediated Hypertension in D ₄ Dopamine Receptor–Deficient Mice

Modulatory Effects of Carbon Monoxide on Baroreflex Activation in Nucleus Tractus Solitarii of Rats

Distinct Molecular Effects of Angiotensin II and Angiotensin III in Rat Astrocytes

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Depressor effect of microinjection of angiotensin II in the brainstem nuclei of renal hypertensive rats

Cited by 4 publications

References 1 publication

Angiotensin-II Type 1 Receptor–Mediated Hypertension in D 4 Dopamine Receptor–Deficient Mice

Angiotensin-II Type 1 Receptor–Mediated Hypertension in D 4 Dopamine Receptor–Deficient Mice

Modulatory Effects of Carbon Monoxide on Baroreflex Activation in Nucleus Tractus Solitarii of Rats

Distinct Molecular Effects of Angiotensin II and Angiotensin III in Rat Astrocytes

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Angiotensin-II Type 1 Receptor–Mediated Hypertension in D ₄ Dopamine Receptor–Deficient Mice

Angiotensin-II Type 1 Receptor–Mediated Hypertension in D ₄ Dopamine Receptor–Deficient Mice