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dc.contributor.author
Li, Xiao Xi
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Bek, Martin
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Asico, Laureano D.
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Yang, Zhiwei
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Grandy, David K.
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dc.contributor.author
Goldstein, David S.
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Rubinstein, Marcelo
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Eisner, Gilbert M.
dc.contributor.author
Jose, Pedro A.
dc.date.available
2019-07-10T19:42:04Z
dc.date.issued
2001-09
dc.identifier.citation
Li, Xiao Xi; Bek, Martin; Asico, Laureano D.; Yang, Zhiwei; Grandy, David K.; et al.; Adrenergic and Endothelin B Receptor-Dependent Hypertension in Dopamine Receptor Type-2 Knockout Mice; Lippincott Williams; Hypertension; 38; 3; 9-2001; 303-308
dc.identifier.issn
0263-6352
dc.identifier.uri
http://hdl.handle.net/11336/79320
dc.description.abstract
Polymorphism of the dopamine receptor type-2 (D2) gene is associated with essential hypertension. To assess whether D2 receptors participate in regulation of blood pressure (BP), we studied mice in which the D2 receptor was disrupted. In anesthetized mice, systolic and diastolic BPs (in millimeters of mercury) were higher in D2 homozygous and heterozygous mutant mice than in D2+/+ littermates. BP after α-adrenergic blockade decreased to a greater extent in D2−/− mice than in D2+/+ mice. Epinephrine excretion was greater in D2−/− mice than in D2+/+ mice, and acute adrenalectomy decreased BP to a similar level in D2−/− and D2+/+ mice. An endothelin B (ET[B]) receptor blocker for both ET(B1) and ET(B2) receptors decreased, whereas a selective ET(B1) blocker increased, BP in D2−/− mice but not D2+/+ mice. ET(B) receptor expression was greater in D2−/− mice than in D2+/+ mice. In contrast, blockade of ET(A) and V1 vasopressin receptors had no effect on BP in either D2−/− or D2+/+ mice. The hypotensive effect of an AT1 antagonist was also similar in D2−/− and D2+/+ mice. Basal Na+,K+-ATPase activities in renal cortex and medulla were higher in D2+/+ mice than in D2−/− mice. Urine flow and sodium excretion were higher in D2−/− mice than in D2+/+ mice before and after acute saline loading. Thus, complete loss of the D2 receptor results in hypertension that is not due to impairment of sodium excretion. Instead, enhanced vascular reactivity in the D2 mutant mice may be caused by increased sympathetic and ET(B) receptor activities.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Lippincott Williams
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Dopamina
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Hipertensión
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Fisiología
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Medicina Básica
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CIENCIAS MÉDICAS Y DE LA SALUD
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dc.title
Adrenergic and Endothelin B Receptor-Dependent Hypertension in Dopamine Receptor Type-2 Knockout Mice
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2019-07-05T17:31:52Z
dc.identifier.eissn
0194-911X
dc.journal.volume
38
dc.journal.number
3
dc.journal.pagination
303-308
dc.journal.pais
Estados Unidos
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dc.journal.ciudad
Philadelphia
dc.description.fil
Fil: Li, Xiao Xi. Georgetown University Medical Center; Estados Unidos
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Fil: Bek, Martin. Georgetown University Medical Center; Estados Unidos
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Fil: Asico, Laureano D.. Georgetown University Medical Center; Estados Unidos
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Fil: Yang, Zhiwei. Georgetown University Medical Center; Estados Unidos
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Fil: Grandy, David K.. Oregon Health Sciences University; Estados Unidos
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Fil: Goldstein, David S.. Oregon Health Sciences University; Estados Unidos
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Fil: Rubinstein, Marcelo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina
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Fil: Eisner, Gilbert M.. Georgetown University Medical Center; Estados Unidos
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Fil: Jose, Pedro A.. Georgetown University Medical Center; Estados Unidos
dc.journal.title
Hypertension
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/https://doi.org/10.1161/01.HYP.38.3.303
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.ahajournals.org/doi/10.1161/01.HYP.38.3.303
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