New insights into the electrophysiology of brainstem circuits controlling blood pressure

Mifflin, Steve

doi:10.1007/s11906-007-0042-2

Cited by 5 publications

(2 citation statements)

References 41 publications

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“…The effect of TRIM suggests that nNOS contributes to ACh-induced cardiovascular responses. Similar effects of L-NAME and TRIM on glutamatergic transmission were previously observed in modulation of NTS neurons discharge (10,24). A study by Scislo et al (33) reported that L-NAME and TRIM are equipotent in inhibiting cardiovascular responses elicited by the stimulation of adenosine A2a receptors in the NTS.…”

Section: Discussionsupporting

confidence: 62%

Nitric oxide modulates the cardiovascular effects elicited by acetylcholine in the NTS of awake rats

Silva

Dias²,

Furlan³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Microinjection of acetylcholine chloride (ACh) in the nucleus of the solitary tract (NTS) of awake rats caused a transient and dose-dependent hypotension and bradycardia. Because it is known that cardiovascular reflexes are affected by nitric oxide (NO) produced in the NTS, we investigated whether these ACh-induced responses depend on NO in the NTS. Responses to ACh (500 pmol in 100 nl) were strongly reduced by ipsilateral microinjection of the NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 10 nmol in 100 nl) in the NTS: mean arterial pressure (MAP) fell by 50 +/- 5 mmHg before L-NAME to 9 +/- 4 mmHg, 10 min after L-NAME, and HR fell by 100 +/- 26 bpm before L-NAME to 20 +/- 10 bpm, 10 min after L-NAME (both P < 0.05). Microinjection of the selective inhibitor of neuronal nitric oxide synthase (nNOS), 1-(2-trifluoromethylphenyl) imidazole (TRIM; 13.3 nmol in 100 nl), in the NTS also reduced responses to ACh: MAP fell from 42 +/- 3 mmHg before TRIM to 27 +/- 6 mmHg, 10 min after TRIM (P < 0.05). TRIM also tended to reduce ACh-induced bradycardia, but this effect was not statistically significant. ACh-induced hypotension and bradycardia returned to control levels 30-45 min after NOS inhibition. Control injections with D-NAME and saline did not affect resting values or the response to ACh. In conclusion, injection of ACh into the NTS of conscious rats induces hypotension and bradycardia, and these effects may be mediated at least partly by NO produced in NTS neurons.

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Section: Discussionsupporting

confidence: 62%

Nitric oxide modulates the cardiovascular effects elicited by acetylcholine in the NTS of awake rats

Silva

Dias²,

Furlan³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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show abstract

“…20 Alternatively, the lowering of the arterial pressure could depend on central effects of the hypoxia on the center of the arterial pressure regulation. 21 However, the effects of hypoxia on blood pressure are believed to result in sympathetic activity increase, leading to upregulation of blood pressure and heart rate. 22 Our results also show that hypoxia did not affect cardiac output but decreased TPR and subsequently blood pressure levels.…”

Section: Discussionmentioning

confidence: 99%

Chronic Hypoxia–Induced Angiogenesis Normalizes Blood Pressure in Spontaneously Hypertensive Rats

Vilar

Waeckel

Bonnin

et al. 2008

Circulation Research

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Abstract-We hypothesized that activation of angiogenesis by chronic hypoxia may affect vascular resistance and, subsequently, blood pressure levels in spontaneously hypertensive rats (SHRs). Five-week-old prehypertensive SHRs and age-matched normotensive Wistar-Kyoto (WKY) rats (nϭ8 per group) were maintained under normobaric normoxic or hypoxic (10% O 2 ) conditions for 8 weeks. Three weeks later, the systolic blood pressure was lower by 26% in hypoxic SHRs compared to normoxic SHRs (PϽ0.05) and remained at the normoxic WKY level. Total peripheral vascular resistance, calculated as the mean arterial pressure/cardiac output (assessed by ultrasound imaging and Doppler), was 30% lower in hypoxic than in normoxic SHRs (PϽ0.001) and returned to WKY levels. Interestingly, chronic hypoxia also significantly reduced systolic blood pressure in adult 12-week-old SHRs with established hypertension; blood pressure was normalized (versus normoxic WKY rats) after 4 weeks of hypoxia. Changes in hemodynamic parameters were associated with activation of proangiogenic pathways. Protein levels of vascular endothelial growth factor (VEGF)-A in the skeletal muscles were increased by 2.2-fold in hypoxic compared to normoxic SHRs (PϽ0.001). At the end of the hypoxic period, capillary density in the quadriceps muscle was 1.2-fold higher in hypoxic than in normoxic SHRs (PϽ0.001). Myocardial capillary density and VEGF-A protein contents were also 1.2-and 2.1-fold higher in hypoxic compared to normoxic SHRs (PϽ0.001 and PϽ0.05, respectively). Moreover, treatment with neutralizing VEGF-A antibody abrogated the hypoxia-induced angiogenesis and subsequently worsened arterial hypertension. Therefore, our results suggest that chronic normobaric hypoxia (1) activates VEGF-A-induced angiogenesis and thereafter (2)

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Hypoxia, Arterial Blood Pressure, and Microcirculation

Mourad

Silvestre

Lévy

2014

Blood Pressure and Arterial Wall Mechanics in Cardiovascular Diseases

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New insights into the electrophysiology of brainstem circuits controlling blood pressure

Cited by 5 publications

References 41 publications

Nitric oxide modulates the cardiovascular effects elicited by acetylcholine in the NTS of awake rats

Nitric oxide modulates the cardiovascular effects elicited by acetylcholine in the NTS of awake rats

Chronic Hypoxia–Induced Angiogenesis Normalizes Blood Pressure in Spontaneously Hypertensive Rats

Hypoxia, Arterial Blood Pressure, and Microcirculation

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