Roles of nitric oxide and angiotensin II in the impaired baroreflex gain of pregnancy

Daisy L. Daubert, Dongmei Liu, Irving H. Zucker, Virginia Brooks

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

The present study tested the hypothesis that nitric oxide (NO) contributes to impaired baroreflex gain of pregnancy and that this action is enhanced by angiotensin II. To test these hypotheses, we quantified baroreflex control of heart rate in nonpregnant and pregnant conscious rabbits before and after: 1) blockade of NO synthase (NOS) with Nω-nitro-L-arginine (20 mg/kg iv); 2) blockade of the angiotensin II AT1 receptor with L-158,809 (5 μg·kg-1·min-1 iv); 3) infusion of angiotensin II (1 ng·kg-1·min-1 nonpregnant, 1.6-4 ng·kg-1·min-1 pregnant iv); 4) combined blockade of angiotensin II AT1 receptors and NOS; and 5) combined infusion of angiotensin II and blockade of NOS. To determine the potential role of brain neuronal NOS (nNOS), mRNA and protein levels were measured in the paraventricular nucleus, nucleus of the solitary tract, caudal ventrolateral medulla, and rostral ventrolateral medulla in pregnant and nonpregnant rabbits. The decrease in baroreflex gain observed in pregnant rabbits (from 23.3 ± 3.6 to 7.1 ± 0.9 beats·min -1·mmHg-1, P <0.05) was not reversed by NOS blockade (to 8.3 ± 2.5 beats·min-1·mmHg -1), angiotensin II blockade (to 5.0 ± 1.1 beats·min-1·mmHg-1), or combined blockade (to 12.3 ± 4.8 beats·min-1·mmHg-1). Angiotensin II infusion with (to 5.7 ± 1.0 beats·min -1·mmHg-1) or without (to 8.4 ± 2.4 beats·min-1·mmHg-1) NOS blockade also failed to improve baroreflex gain in pregnant or nonpregnant rabbits. In addition, nNOS mRNA and protein levels in cardiovascular brain regions were not different between nonpregnant and pregnant rabbits. Therefore, we conclude that NO, either alone or via an interaction with angiotensin II, is not responsible for decrease in baroreflex gain during pregnancy.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume292
Issue number6
DOIs
StatePublished - Jun 2007

Fingerprint

Baroreflex
Angiotensin II
Nitric Oxide
Nitric Oxide Synthase
Pregnancy
Rabbits
Angiotensin Type 1 Receptor
Angiotensin Receptors
Messenger RNA
Solitary Nucleus
Paraventricular Hypothalamic Nucleus
Brain
Arginine
Proteins
Heart Rate

Keywords

  • AT-receptor blockade
  • Conscious rabbits
  • L-158,809
  • N -nitro-L-arginine
  • Neuronal nitric oxide synthase

ASJC Scopus subject areas

  • Physiology

Cite this

Roles of nitric oxide and angiotensin II in the impaired baroreflex gain of pregnancy. / Daubert, Daisy L.; Liu, Dongmei; Zucker, Irving H.; Brooks, Virginia.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 292, No. 6, 06.2007.

Research output: Contribution to journalArticle

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N2 - The present study tested the hypothesis that nitric oxide (NO) contributes to impaired baroreflex gain of pregnancy and that this action is enhanced by angiotensin II. To test these hypotheses, we quantified baroreflex control of heart rate in nonpregnant and pregnant conscious rabbits before and after: 1) blockade of NO synthase (NOS) with Nω-nitro-L-arginine (20 mg/kg iv); 2) blockade of the angiotensin II AT1 receptor with L-158,809 (5 μg·kg-1·min-1 iv); 3) infusion of angiotensin II (1 ng·kg-1·min-1 nonpregnant, 1.6-4 ng·kg-1·min-1 pregnant iv); 4) combined blockade of angiotensin II AT1 receptors and NOS; and 5) combined infusion of angiotensin II and blockade of NOS. To determine the potential role of brain neuronal NOS (nNOS), mRNA and protein levels were measured in the paraventricular nucleus, nucleus of the solitary tract, caudal ventrolateral medulla, and rostral ventrolateral medulla in pregnant and nonpregnant rabbits. The decrease in baroreflex gain observed in pregnant rabbits (from 23.3 ± 3.6 to 7.1 ± 0.9 beats·min -1·mmHg-1, P <0.05) was not reversed by NOS blockade (to 8.3 ± 2.5 beats·min-1·mmHg -1), angiotensin II blockade (to 5.0 ± 1.1 beats·min-1·mmHg-1), or combined blockade (to 12.3 ± 4.8 beats·min-1·mmHg-1). Angiotensin II infusion with (to 5.7 ± 1.0 beats·min -1·mmHg-1) or without (to 8.4 ± 2.4 beats·min-1·mmHg-1) NOS blockade also failed to improve baroreflex gain in pregnant or nonpregnant rabbits. In addition, nNOS mRNA and protein levels in cardiovascular brain regions were not different between nonpregnant and pregnant rabbits. Therefore, we conclude that NO, either alone or via an interaction with angiotensin II, is not responsible for decrease in baroreflex gain during pregnancy.

AB - The present study tested the hypothesis that nitric oxide (NO) contributes to impaired baroreflex gain of pregnancy and that this action is enhanced by angiotensin II. To test these hypotheses, we quantified baroreflex control of heart rate in nonpregnant and pregnant conscious rabbits before and after: 1) blockade of NO synthase (NOS) with Nω-nitro-L-arginine (20 mg/kg iv); 2) blockade of the angiotensin II AT1 receptor with L-158,809 (5 μg·kg-1·min-1 iv); 3) infusion of angiotensin II (1 ng·kg-1·min-1 nonpregnant, 1.6-4 ng·kg-1·min-1 pregnant iv); 4) combined blockade of angiotensin II AT1 receptors and NOS; and 5) combined infusion of angiotensin II and blockade of NOS. To determine the potential role of brain neuronal NOS (nNOS), mRNA and protein levels were measured in the paraventricular nucleus, nucleus of the solitary tract, caudal ventrolateral medulla, and rostral ventrolateral medulla in pregnant and nonpregnant rabbits. The decrease in baroreflex gain observed in pregnant rabbits (from 23.3 ± 3.6 to 7.1 ± 0.9 beats·min -1·mmHg-1, P <0.05) was not reversed by NOS blockade (to 8.3 ± 2.5 beats·min-1·mmHg -1), angiotensin II blockade (to 5.0 ± 1.1 beats·min-1·mmHg-1), or combined blockade (to 12.3 ± 4.8 beats·min-1·mmHg-1). Angiotensin II infusion with (to 5.7 ± 1.0 beats·min -1·mmHg-1) or without (to 8.4 ± 2.4 beats·min-1·mmHg-1) NOS blockade also failed to improve baroreflex gain in pregnant or nonpregnant rabbits. In addition, nNOS mRNA and protein levels in cardiovascular brain regions were not different between nonpregnant and pregnant rabbits. Therefore, we conclude that NO, either alone or via an interaction with angiotensin II, is not responsible for decrease in baroreflex gain during pregnancy.

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