Disruption of the D(2) dopamine receptor produces adrenergic and endothelin B receptor-dependent hypertension

Xiaoxil Li, Martin Bek, Laureano D. Asico, Zhiwei Yang, Marcelo Rubinstein, David Grandy, David S. Goldstein, Gilbert M. Eisner, Pedro A. Jose

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

OBJECTIVE: To assess whether D(2) receptors participate in the regulation of genetic hypertension. METHODS: Arterial pressure was measured in mice mutant for the D(2) dopamine receptors, and the interactions between D(2) dopamine receptors and other vasopressor systems were also studied. RESULTS: Both systolic blood pressure (BP) in D(2) mutant (D(2)-/-) and hybrid (D(2)+/-) mice (128 +/- 2 mm Hg, 129 +/- 4 mm Hg) and diastolic BP (107 +/- 2 mm Hg, 108 +/- 3 mm Hg) were higher than in wild-type (D(2)+/+) mice (104 +/- 2 mm Hg, 77 +/- 1 mm Hg). The BP after alpha-adrenergic blockade decreased to a greater extent in D(2)-/- than in D(2)+/+ mice. Epinephrine excretion was greater in D(2)-/- than in D(2)+/+ mice and adrenalectomy decreased blood pressure to a greater extent in D(2)-/- than in D(2)+/+ mice. The non specific endothelin B (ETB) blocker (BQ788) decreased BP in D(2)-/- but had not in D(2)+/+ mice. The ETB1 blocker RES 701 - 1 increased BP in D(2)-/- but not D(2)+/+ mice. ET-1 and the ETB agonist, sarafatoxin S6c increased BP to a greater extent in D(2)+/+ than in D(2)-/- mice. Circulating ET-like immunoreactive peptides were similar in D(2)-/- and D(2)+/+ mice but ETB receptor expression was greater in D(2)-/- than in D(2)+/+ mice. In contrast, blockade of ETA and V(1) vasopressin receptors had no effect on BP in either D(2)-/- and D(2)+/+ mice. The hypotensive effect of the AT(1) antagonist, losartan, was also similar in D(2)-/- and D(2)+/+ mice. The greater basal sodium excretion and lower renal Na(+)/K(+)ATPase activity in D(2)-/- than in D(2)+/+ mice indicate that sodium retention was not the cause of hypertension in these animals. CONCLUSION: Hypertension in the D(2) mutant mice may be caused by absent inhibitory effect of D(2) receptors on sympathetic outflow coupled with increased ETB2 activity.

Original languageEnglish (US)
Pages (from-to)703-707
Number of pages5
JournalZhonghua yi xue za zhi
Volume82
Issue number10
StatePublished - May 25 2002
Externally publishedYes

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Endothelin B Receptors
Dopamine Receptors
Adrenergic Agents
Hypertension
Blood Pressure
Sodium
Vasopressin Receptors
Losartan
Endothelins
Adrenalectomy
Endothelin-1

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Li, X., Bek, M., Asico, L. D., Yang, Z., Rubinstein, M., Grandy, D., ... Jose, P. A. (2002). Disruption of the D(2) dopamine receptor produces adrenergic and endothelin B receptor-dependent hypertension. Zhonghua yi xue za zhi, 82(10), 703-707.

Disruption of the D(2) dopamine receptor produces adrenergic and endothelin B receptor-dependent hypertension. / Li, Xiaoxil; Bek, Martin; Asico, Laureano D.; Yang, Zhiwei; Rubinstein, Marcelo; Grandy, David; Goldstein, David S.; Eisner, Gilbert M.; Jose, Pedro A.

In: Zhonghua yi xue za zhi, Vol. 82, No. 10, 25.05.2002, p. 703-707.

Research output: Contribution to journalArticle

Li, X, Bek, M, Asico, LD, Yang, Z, Rubinstein, M, Grandy, D, Goldstein, DS, Eisner, GM & Jose, PA 2002, 'Disruption of the D(2) dopamine receptor produces adrenergic and endothelin B receptor-dependent hypertension', Zhonghua yi xue za zhi, vol. 82, no. 10, pp. 703-707.
Li X, Bek M, Asico LD, Yang Z, Rubinstein M, Grandy D et al. Disruption of the D(2) dopamine receptor produces adrenergic and endothelin B receptor-dependent hypertension. Zhonghua yi xue za zhi. 2002 May 25;82(10):703-707.
Li, Xiaoxil ; Bek, Martin ; Asico, Laureano D. ; Yang, Zhiwei ; Rubinstein, Marcelo ; Grandy, David ; Goldstein, David S. ; Eisner, Gilbert M. ; Jose, Pedro A. / Disruption of the D(2) dopamine receptor produces adrenergic and endothelin B receptor-dependent hypertension. In: Zhonghua yi xue za zhi. 2002 ; Vol. 82, No. 10. pp. 703-707.
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T1 - Disruption of the D(2) dopamine receptor produces adrenergic and endothelin B receptor-dependent hypertension

AU - Li, Xiaoxil

AU - Bek, Martin

AU - Asico, Laureano D.

AU - Yang, Zhiwei

AU - Rubinstein, Marcelo

AU - Grandy, David

AU - Goldstein, David S.

AU - Eisner, Gilbert M.

AU - Jose, Pedro A.

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Y1 - 2002/5/25

N2 - OBJECTIVE: To assess whether D(2) receptors participate in the regulation of genetic hypertension. METHODS: Arterial pressure was measured in mice mutant for the D(2) dopamine receptors, and the interactions between D(2) dopamine receptors and other vasopressor systems were also studied. RESULTS: Both systolic blood pressure (BP) in D(2) mutant (D(2)-/-) and hybrid (D(2)+/-) mice (128 +/- 2 mm Hg, 129 +/- 4 mm Hg) and diastolic BP (107 +/- 2 mm Hg, 108 +/- 3 mm Hg) were higher than in wild-type (D(2)+/+) mice (104 +/- 2 mm Hg, 77 +/- 1 mm Hg). The BP after alpha-adrenergic blockade decreased to a greater extent in D(2)-/- than in D(2)+/+ mice. Epinephrine excretion was greater in D(2)-/- than in D(2)+/+ mice and adrenalectomy decreased blood pressure to a greater extent in D(2)-/- than in D(2)+/+ mice. The non specific endothelin B (ETB) blocker (BQ788) decreased BP in D(2)-/- but had not in D(2)+/+ mice. The ETB1 blocker RES 701 - 1 increased BP in D(2)-/- but not D(2)+/+ mice. ET-1 and the ETB agonist, sarafatoxin S6c increased BP to a greater extent in D(2)+/+ than in D(2)-/- mice. Circulating ET-like immunoreactive peptides were similar in D(2)-/- and D(2)+/+ mice but ETB receptor expression was greater in D(2)-/- than in D(2)+/+ mice. In contrast, blockade of ETA and V(1) vasopressin receptors had no effect on BP in either D(2)-/- and D(2)+/+ mice. The hypotensive effect of the AT(1) antagonist, losartan, was also similar in D(2)-/- and D(2)+/+ mice. The greater basal sodium excretion and lower renal Na(+)/K(+)ATPase activity in D(2)-/- than in D(2)+/+ mice indicate that sodium retention was not the cause of hypertension in these animals. CONCLUSION: Hypertension in the D(2) mutant mice may be caused by absent inhibitory effect of D(2) receptors on sympathetic outflow coupled with increased ETB2 activity.

AB - OBJECTIVE: To assess whether D(2) receptors participate in the regulation of genetic hypertension. METHODS: Arterial pressure was measured in mice mutant for the D(2) dopamine receptors, and the interactions between D(2) dopamine receptors and other vasopressor systems were also studied. RESULTS: Both systolic blood pressure (BP) in D(2) mutant (D(2)-/-) and hybrid (D(2)+/-) mice (128 +/- 2 mm Hg, 129 +/- 4 mm Hg) and diastolic BP (107 +/- 2 mm Hg, 108 +/- 3 mm Hg) were higher than in wild-type (D(2)+/+) mice (104 +/- 2 mm Hg, 77 +/- 1 mm Hg). The BP after alpha-adrenergic blockade decreased to a greater extent in D(2)-/- than in D(2)+/+ mice. Epinephrine excretion was greater in D(2)-/- than in D(2)+/+ mice and adrenalectomy decreased blood pressure to a greater extent in D(2)-/- than in D(2)+/+ mice. The non specific endothelin B (ETB) blocker (BQ788) decreased BP in D(2)-/- but had not in D(2)+/+ mice. The ETB1 blocker RES 701 - 1 increased BP in D(2)-/- but not D(2)+/+ mice. ET-1 and the ETB agonist, sarafatoxin S6c increased BP to a greater extent in D(2)+/+ than in D(2)-/- mice. Circulating ET-like immunoreactive peptides were similar in D(2)-/- and D(2)+/+ mice but ETB receptor expression was greater in D(2)-/- than in D(2)+/+ mice. In contrast, blockade of ETA and V(1) vasopressin receptors had no effect on BP in either D(2)-/- and D(2)+/+ mice. The hypotensive effect of the AT(1) antagonist, losartan, was also similar in D(2)-/- and D(2)+/+ mice. The greater basal sodium excretion and lower renal Na(+)/K(+)ATPase activity in D(2)-/- than in D(2)+/+ mice indicate that sodium retention was not the cause of hypertension in these animals. CONCLUSION: Hypertension in the D(2) mutant mice may be caused by absent inhibitory effect of D(2) receptors on sympathetic outflow coupled with increased ETB2 activity.

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