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  • 1
    Online Resource
    Online Resource
    Leptin Mediates High-Fat Diet Sensitization of Angiotensin II–Elicited Hypertension by Upregulating the Brain Renin–Angiotensin System and Inflammation
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Hypertension Vol. 67, No. 5 ( 2016-05), p. 970-976
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 67, No. 5 ( 2016-05), p. 970-976
    Abstract: Obesity is characterized by increased circulating levels of the adipocyte-derived hormone leptin, which can increase sympathetic nerve activity and raise blood pressure. A previous study revealed that rats fed a high-fat diet (HFD) have an enhanced hypertensive response to subsequent angiotensin II administration that is mediated at least, in part, by increased activity of brain renin–angiotensin system and proinflammatory cytokines. This study tested whether leptin mediates this HFD-induced sensitization of angiotensin II–elicited hypertension by interacting with brain renin–angiotensin system and proinflammatory cytokine mechanisms. Rats fed an HFD for 3 weeks had significant increases in white adipose tissue mass, plasma leptin levels, and mRNA expression of leptin and its receptors in the lamina terminalis and hypothalamic paraventricular nucleus. Central infusion of a leptin receptor antagonist during HFD feeding abolished HFD sensitization of angiotensin II–elicited hypertension. Furthermore, central infusion of leptin mimicked the sensitizing action of HFD. Concomitant central infusions of the angiotensin II type 1 receptor antagonist irbesartan, the tumor necrosis factor-α synthesis inhibitor pentoxifylline, or the inhibitor of microglial activation minocycline prevented the sensitization produced by central infusion of leptin. RT-PCR analysis indicated that either HFD or leptin administration upregulated mRNA expression of several components of the renin–angiotensin system and proinflammatory cytokines in the lamina terminalis and paraventricular nucleus. The leptin antagonist and the inhibitors of angiotensin II type 1 receptor, tumor necrosis factor-α synthesis, and microglial activation all reversed the expression of these genes. The results suggest that HFD-induced sensitization of angiotensin II–elicited hypertension is mediated by leptin through upregulation of central renin–angiotensin system and proinflammatory cytokines.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.115.06736
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 2094210-2
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  • 2
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    Estrogen Receptor-β in the Paraventricular Nucleus and Rostroventrolateral Medulla Plays an Essential Protective Role in Aldosterone/Salt-Induced Hypertension in Female Rats
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Hypertension Vol. 61, No. 6 ( 2013-06), p. 1255-1262
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 61, No. 6 ( 2013-06), p. 1255-1262
    Abstract: The identification of the specific estrogen receptor (ER) subtypes that are involved in estrogen protection from hypertension and their specific locations in the central nervous system is critical to our understanding and design of effective estrogen replacement therapies in women. Using selective ER agonists and recombinant adeno-associated virus (AAV) carrying small interference (si) RNA to silence either ERα (AAV-siRNA-ERα) or ERβ (AAV-siRNA-ERβ), the present study investigated regional specificity of different ER subtypes in the protective actions of estrogen in aldosterone (Aldo)-induced hypertension. Intracerebroventricular infusions of either diarylpropionitrile, a selective ERβ agonist, or propyl-pyrazole-triol, a selective ERα agonist, attenuated Aldo/NaCl-induced hypertension in ovariectomized rats. In contrast, intracerebroventricular injections of siRNA-ERα or siRNA-ERβ augmented Aldo-induced hypertension in intact females. Site-specific paraventricular nucleus (PVN) or rostroventrolateral medulla (RVLM) injections of siRNA-ERβ augmented Aldo-induced hypertension. However, rats with PVN or RVLM injections of siRNA-ERα did not significantly increase blood pressure induced by Aldo. Real-time polymerase chain reaction analyses of the PVN and RVLM of siRNA-injected rat confirmed a marked reduction in the expression of ERα and ERβ. In cultured PVN neurons, silencing either ERα or ERβ by culturing PVN neurons with siRNA-ERα or siRNA-ERβ enhanced Aldo-induced reactive oxygen species production. Ganglionic blockade after Aldo infusion showed an increase in sympathetic activity in ERβ knockdown rats. These results indicate that both PVN and RVLM ERβ, but not ERα in these nuclei, contribute to the protective effects of estrogen against Aldo-induced hypertension. The brain regions responsible for the protective effects of estrogen interaction with ERα in Aldo-induced hypertension still need to be determined.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.111.00903
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
    detail.hit.zdb_id: 2094210-2
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  • 3
    Online Resource
    Online Resource
    Either sodium deprivation or sodium excess sensitizes angiotensin (ANG) II‐induced hypertension
    Wiley ; 2013
    In:  The FASEB Journal Vol. 27, No. S1 ( 2013-04)
    Details
    In: The FASEB Journal, Wiley, Vol. 27, No. S1 ( 2013-04)
    Type of Medium: Online Resource
    ISSN: 0892-6638 , 1530-6860
    URL: Issue
    URL: Article
    DOI: 10.1096/fsb2.v27.S1
    DOI: 10.1096/fasebj.27.1_supplement.695.12
    Language: English
    Publisher: Wiley
    Publication Date: 2013
    detail.hit.zdb_id: 1468876-1
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  • 4
    Online Resource
    Online Resource
    Sensitization of Rats with Low dose of Angiotensin II through Multiple Signaling Pathways in Lamina Terminalis
    Wiley ; 2012
    In:  The FASEB Journal Vol. 26, No. S1 ( 2012-04)
    Details
    In: The FASEB Journal, Wiley, Vol. 26, No. S1 ( 2012-04)
    Type of Medium: Online Resource
    ISSN: 0892-6638 , 1530-6860
    URL: Issue
    URL: Article
    DOI: 10.1096/fsb2.v26.S1
    DOI: 10.1096/fasebj.26.1_supplement.684.22
    Language: English
    Publisher: Wiley
    Publication Date: 2012
    detail.hit.zdb_id: 1468876-1
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  • 5
    Online Resource
    Online Resource
    Genetic knockdown of estrogen receptor-alpha in the subfornical organ augments ANG II-induced hypertension in female mice
    American Physiological Society ; 2015
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 308, No. 6 ( 2015-03-15), p. R507-R516
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 308, No. 6 ( 2015-03-15), p. R507-R516
    Abstract: The present study tested the hypotheses that 1) ERα in the brain plays a key role in the estrogen-protective effects against ANG II-induced hypertension, and 2) that the subfornical organ (SFO) is a key site where ERα mediates these protective actions. In this study, a “floxed” ERα transgenic mouse line (ERα flox ) was used to create models in which ERα was knocked down in the brain or just in the SFO. Female mice with ERα ablated in the nervous system (Nestin-ERα − mice) showed greater increases in blood pressure (BP) in response to ANG II. Furthermore, females with ERα knockdown specifically in the SFO [SFO adenovirus-Cre (Ad-Cre) injected ERα flox mice] also showed an enhanced pressor response to ANG II. Immunohistochemical (IHC), RT-PCR, and Western blot analyses revealed a marked reduction in the expression of ERα in nervous tissues and, in particular, in the SFO. These changes were not present in peripheral tissues in Nestin-ERα − mice or Ad-Cre-injected ERα flox mice. mRNA expression of components of the renin-angiotensin system in the lamina terminalis were upregulated in Nestin-ERα − mice. Moreover, ganglionic blockade on day 7 after ANG II infusions resulted in a greater reduction of BP in Nestin-ERα − mice or SFO Ad-Cre-injected mice, suggesting that knockdown of ERα in the nervous system or the SFO alone augments central ANG II-induced increase in sympathetic tone. The results indicate that interfering with the action of estrogen on SFO ERα is sufficient to abolish the protective effects of estrogen against ANG II-induced hypertension.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.00406.2014
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2015
    detail.hit.zdb_id: 1477297-8
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  • 6
    Online Resource
    Online Resource
    Estrogen regulation of the brain renin-angiotensin system in protection against angiotensin II-induced sensitization of hypertension
    American Physiological Society ; 2014
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 307, No. 2 ( 2014-07-15), p. H191-H198
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 307, No. 2 ( 2014-07-15), p. H191-H198
    Abstract: This study investigated sex differences in the sensitization of angiotensin (ANG) II-induced hypertension and the role of central estrogen and ANG-(1–7) in this process. Male and female rats were implanted for telemetered blood pressure (BP) recording. A subcutaneous subpressor dose of ANG II was given alone or concurrently with intracerebroventricular estrogen, ANG-(1–7), an ANG-(1–7) receptor antagonist A-779 or vehicle for 1 wk (induction). After a 1-wk rest (delay), a pressor dose of ANG II was given for 2 wk (expression). In males and ovariectomized females, subpressor ANG II had no sustained effect on BP during induction, but produced an enhanced hypertensive response to the subsequent pressor dose of ANG II during expression. Central administration of estrogen or ANG-(1–7) during induction blocked ANG II-induced sensitization. In intact females, subpressor ANG II treatment produced a decrease in BP during induction and delay, and subsequent pressor ANG II treatment given during expression produced only a slight but significant increase in BP. However, central blockade of ANG-(1–7) by intracerebroventricular infusion of A-779 during induction restored the decreased BP observed in females during induction and enhanced the pressor response to the ANG II treatment during expression. RT-PCR analyses indicated that estrogen given during induction upregulated mRNA expression of the renin-angiotensin system (RAS) antihypertensive components, whereas both central estrogen and ANG-(1–7) downregulated mRNA expression of RAS hypertensive components in the lamina terminalis. The results indicate that females are protected from ANG II-induced sensitization through central estrogen and its regulation of brain RAS.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.01012.2013
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2014
    detail.hit.zdb_id: 1477308-9
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  • 7
    Online Resource
    Online Resource
    Central endogenous angiotensin-(1–7) protects against aldosterone/NaCl-induced hypertension in female rats
    American Physiological Society ; 2013
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 305, No. 5 ( 2013-09-01), p. H699-H705
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 305, No. 5 ( 2013-09-01), p. H699-H705
    Abstract: In comparison to male rodents, females are protected against angiotensin (ANG) II- and aldosterone (Aldo)-induced hypertension. However, the mechanisms underlying this protective effect are not well understood. ANG-(1–7) is formed from ANG II by angiotensin-converting enzyme 2 (ACE2) and has an antihypertensive effect in the central nervous system (CNS). The present study tested the hypothesis that central ANG-(1–7) plays an important protective role in attenuating the development of Aldo/NaCl-hypertension in female rats. Systemic infusion of Aldo into intact female rats with 1% NaCl as their sole drinking fluid resulted in a slight increase in blood pressure (BP). Intracerebroventricular (icv) infusion of A-779, an ANG-(1–7) receptor (Mas-R) antagonist, significantly augmented the pressor effects of Aldo/NaCl. In contrast, systemic Aldo/NaCl induced a significant increase in BP in ovariectomized (OVX) female rats, and central infusion of ANG-(1–7) significantly attenuated this Aldo/NaCl pressor effect. The inhibitory effect of ANG-(1–7) on the Aldo/NaCl pressor effect was abolished by concurrent infusion of A-779. RT-PCR analyses showed that there was a corresponding change in mRNA expression of several renin-angiotensin system components, estrogen receptors and an NADPH oxidase subunit in the lamina terminalis. Taken together these results suggest that female sex hormones regulate an antihypertensive axis of the brain renin-angiotensin system involving ACE2/ANG-(1–7)/Mas-R that plays an important counterregulatory role in protecting against the development of Aldo/NaCl-induced hypertension.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00193.2013
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2013
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    Sex difference in low dose of angiotensin (ANG) II sensitizing effect on pressor effect of subsequent high dose of ANG II
    Wiley ; 2013
    In:  The FASEB Journal Vol. 27, No. S1 ( 2013-04)
    Details
    In: The FASEB Journal, Wiley, Vol. 27, No. S1 ( 2013-04)
    Type of Medium: Online Resource
    ISSN: 0892-6638 , 1530-6860
    URL: Issue
    URL: Article
    DOI: 10.1096/fsb2.v27.S1
    DOI: 10.1096/fasebj.27.1_supplement.904.6
    Language: English
    Publisher: Wiley
    Publication Date: 2013
    detail.hit.zdb_id: 1468876-1
    SSG: 12
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  • 9
    Online Resource
    Online Resource
    Aldosterone Acting Through the Central Nervous System Sensitizes Angiotensin II-Induced Hypertension
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Hypertension Vol. 60, No. 4 ( 2012-10), p. 1023-1030
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 60, No. 4 ( 2012-10), p. 1023-1030
    Abstract: Previous studies have shown that preconditioning rats with a nonpressor dose of angiotensin II (Ang II) sensitizes the pressor response produced by later treatment with a higher dose of Ang II and that Ang II and aldosterone (Aldo) can modulate each other’s pressor effects through actions involving the central nervous system. The current studies tested whether Aldo can cross-sensitize the pressor actions of Ang II to enhance hypertension by employing an induction–delay–expression experimental design. Male rats were implanted for telemetered blood pressure recording. During induction, subpressor doses of either subcutaneous or intracerebroventricular Aldo were delivered for 1 week. Rats were then rested for 1 week (delay) to assure that any exogenous Aldo was metabolized. After this, Ang II was given subcutaneously for 2 weeks (expression). During induction and delay, Aldo had no sustained effect on blood pressure. However, during expression, Ang II-induced hypertension was greater in the groups receiving subcutaneous or intracerebroventricular Aldo during induction in comparison with those groups receiving vehicle. Central administration of mineralocorticoid receptor antagonist blocked sensitization. Brain tissue collected at the end of delay and expression showed increased mRNA expression of several renin–angiotensin–aldosterone system components in cardiovascular-related forebrain regions of cross-sensitized rats. Cultured subfornical organ neurons preincubated with Aldo displayed greater increases in [Ca 2+ ] i after Ang II treatment, and there was a greater Fra-like immunoreactivity present at the end of expression in cardiovascular-related forebrain structures. Taken together, these results indicate that Aldo pretreatment cross-sensitizes the development of Ang II-induced hypertension probably by mechanisms that involve the central nervous system.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.112.196576
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 2094210-2
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  • 10
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    Online Resource
    Abstract 441: Central Infusion of Angiotensin(1-7) Attenuates Aldosterone/Salt-Induced Increases in Blood Pressure in Ovariectomized Female Rats
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Hypertension Vol. 60, No. suppl_1 ( 2012-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 60, No. suppl_1 ( 2012-09)
    Abstract: In comparison to male rodents, females are protected against angiotensin II (ANG II)- and aldosterone (Aldo)-induced hypertension. However, the mechanism underlying this protective effect is not well understood. ANG(1-7) is formed from ANG II by angiotensin converting enzyme 2 (ACE2) and plays an anti-hypertensive effect in the CNS. Recent studies from our laboratory demonstrate that central blockade ANG(1-7) augments Aldo-induced hypertension in intact female rats. The present study further determined whether central infusion of ANG(1-7) will attenuate Aldo/salt-induced increase in blood pressure (BP) in ovariectomized (OVX) female rats. Systemic infusion of Aldo (0.75 μg/h, 4 weeks) into OVX female rats with 1% salt as their sole drinking fluid resulted in a significant increase in BP (Δ26.9±2.9 mmHg). Central infusion of ANG(1-7) significantly attenuated this Aldo/salt pressor effect (Δ11.9±2.8 mmHg). RT-PCR analysis revealed that mRNA expression of renin (from 3.6 to1.1-fold) and ACE1 (from 2.6 to 0.9-fold) were significantly reduced in Aldo/salt treated rats with central infusion of ANG(1-7) when compared with central vehicle infusion. In contrast, mRNA expression of ACE2 (from 1.0 to 1.4-fold), AT 2 R (from 0.4 to 1.2-fold) and estrogen receptor alpha (ERα, from 0.9 to 1.7-fold) were significantly increased in the lamina terminalis. Taken together these results suggest that a central antihypertensive arm of the brain renin-angiotensin system (ACE2/ANG(1-7)/Mas) may play an important compensatory role in the development of Aldo/salt induced hypertension in females. (HL-14388, HL-98207, DK-66086, and MH-80241)
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.60.suppl_1.A441
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 2094210-2
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