Lack of autonomic contributions to tonic nitric oxide-mediated vasodilatation in unanesthetized free-moving rats

Alberto Radaelli, Luca Mircoli, Stefano Perlini, Gianni Bolla, Ileana Mori, Giuseppe Mancia, Alberto U. Ferrari

Research output: Contribution to journalArticle

Abstract

Objective. To clarify the controversial issue of whether autonomic influences modulate vascular nitric oxide-mediated vasodilatation or even directly contribute to production of nitric oxide (NO) via nitroxidergic fibers. Methods. Chronic venous and arterial catheters were implanted in Wistar-Kyoto rats (n = 65) for continuous blood pressure measurement, drug administration and blood sampling. Tonic NO-dependent vasodilatation in the conscious free-moving animal was evaluated as the pressor response to inhibition of NO synthesis by intravenous L-monomethylarginine (a 100 mg/kg intravenous bolus plus 0.5 mg/kg per min infusion for 30 min). Experiments were performed under control conditions, chemical sympathectomy by 6-hydroxy-dopamine, ganglionic blockade by hexamethonium, and surgical denervation of sino-aortic baroreceptors. Results. Baseline mean arterial pressure was 100 ± 4 mmHg (mean ± SEM) in control rats and 73 ± 3, 62 ± 5, and 105 ± 10 mmHg in sympathectomized, ganglion-blocked, and denervated rats, respectively. The peak increase in mean arterial pressure after administration of L-monomethylarginine was 38 ± 3 mmHg in control rats and 51 ± 3, 50 ± 6, and 63 ± 10 mmHg in sympathectomized, ganglion-blocked, and denervated rats, respectively. Epinephrine and norepinephrine levels in rats of separate groups of unanesthetized control, sympathectomized and ganglion-blocked animals were measured by high-performance liquid chromatography from an arterial blood sample, the results indicating drastic reductions in levels of both catecholamines in the ganglion-blocked (but not in the sympathectomized) rats compared with those in the control rats. Conclusions. Tonic NO-dependent vasodilatation can normally be maintained in the unanesthetized unrestrained rat irrespective of autonomic or humoral adrenergic influences.

Original languageEnglish
Pages (from-to)55-61
Number of pages7
JournalJournal of Hypertension
Volume16
Issue number1
DOIs
Publication statusPublished - 1998

Fingerprint

Vasodilation
Nitric Oxide
Ganglia
omega-N-Methylarginine
Arterial Pressure
Chemical Sympathectomy
Hexamethonium
Pressoreceptors
Inbred WKY Rats
Denervation
Adrenergic Agents
Epinephrine
Catecholamines
Blood Vessels
Dopamine
Norepinephrine
Catheters
High Pressure Liquid Chromatography
Blood Pressure
Control Groups

Keywords

  • Blood pressure
  • Ganglionic blockade
  • L-nitromonomethyl-L-arginine
  • Nitric oxide
  • Sino-aortic denervation
  • Sympathectomy
  • Unanesthetized rat

ASJC Scopus subject areas

  • Endocrinology
  • Internal Medicine

Cite this

Lack of autonomic contributions to tonic nitric oxide-mediated vasodilatation in unanesthetized free-moving rats. / Radaelli, Alberto; Mircoli, Luca; Perlini, Stefano; Bolla, Gianni; Mori, Ileana; Mancia, Giuseppe; Ferrari, Alberto U.

In: Journal of Hypertension, Vol. 16, No. 1, 1998, p. 55-61.

Research output: Contribution to journalArticle

Radaelli, Alberto ; Mircoli, Luca ; Perlini, Stefano ; Bolla, Gianni ; Mori, Ileana ; Mancia, Giuseppe ; Ferrari, Alberto U. / Lack of autonomic contributions to tonic nitric oxide-mediated vasodilatation in unanesthetized free-moving rats. In: Journal of Hypertension. 1998 ; Vol. 16, No. 1. pp. 55-61.
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abstract = "Objective. To clarify the controversial issue of whether autonomic influences modulate vascular nitric oxide-mediated vasodilatation or even directly contribute to production of nitric oxide (NO) via nitroxidergic fibers. Methods. Chronic venous and arterial catheters were implanted in Wistar-Kyoto rats (n = 65) for continuous blood pressure measurement, drug administration and blood sampling. Tonic NO-dependent vasodilatation in the conscious free-moving animal was evaluated as the pressor response to inhibition of NO synthesis by intravenous L-monomethylarginine (a 100 mg/kg intravenous bolus plus 0.5 mg/kg per min infusion for 30 min). Experiments were performed under control conditions, chemical sympathectomy by 6-hydroxy-dopamine, ganglionic blockade by hexamethonium, and surgical denervation of sino-aortic baroreceptors. Results. Baseline mean arterial pressure was 100 ± 4 mmHg (mean ± SEM) in control rats and 73 ± 3, 62 ± 5, and 105 ± 10 mmHg in sympathectomized, ganglion-blocked, and denervated rats, respectively. The peak increase in mean arterial pressure after administration of L-monomethylarginine was 38 ± 3 mmHg in control rats and 51 ± 3, 50 ± 6, and 63 ± 10 mmHg in sympathectomized, ganglion-blocked, and denervated rats, respectively. Epinephrine and norepinephrine levels in rats of separate groups of unanesthetized control, sympathectomized and ganglion-blocked animals were measured by high-performance liquid chromatography from an arterial blood sample, the results indicating drastic reductions in levels of both catecholamines in the ganglion-blocked (but not in the sympathectomized) rats compared with those in the control rats. Conclusions. Tonic NO-dependent vasodilatation can normally be maintained in the unanesthetized unrestrained rat irrespective of autonomic or humoral adrenergic influences.",
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T1 - Lack of autonomic contributions to tonic nitric oxide-mediated vasodilatation in unanesthetized free-moving rats

AU - Radaelli, Alberto

AU - Mircoli, Luca

AU - Perlini, Stefano

AU - Bolla, Gianni

AU - Mori, Ileana

AU - Mancia, Giuseppe

AU - Ferrari, Alberto U.

PY - 1998

Y1 - 1998

N2 - Objective. To clarify the controversial issue of whether autonomic influences modulate vascular nitric oxide-mediated vasodilatation or even directly contribute to production of nitric oxide (NO) via nitroxidergic fibers. Methods. Chronic venous and arterial catheters were implanted in Wistar-Kyoto rats (n = 65) for continuous blood pressure measurement, drug administration and blood sampling. Tonic NO-dependent vasodilatation in the conscious free-moving animal was evaluated as the pressor response to inhibition of NO synthesis by intravenous L-monomethylarginine (a 100 mg/kg intravenous bolus plus 0.5 mg/kg per min infusion for 30 min). Experiments were performed under control conditions, chemical sympathectomy by 6-hydroxy-dopamine, ganglionic blockade by hexamethonium, and surgical denervation of sino-aortic baroreceptors. Results. Baseline mean arterial pressure was 100 ± 4 mmHg (mean ± SEM) in control rats and 73 ± 3, 62 ± 5, and 105 ± 10 mmHg in sympathectomized, ganglion-blocked, and denervated rats, respectively. The peak increase in mean arterial pressure after administration of L-monomethylarginine was 38 ± 3 mmHg in control rats and 51 ± 3, 50 ± 6, and 63 ± 10 mmHg in sympathectomized, ganglion-blocked, and denervated rats, respectively. Epinephrine and norepinephrine levels in rats of separate groups of unanesthetized control, sympathectomized and ganglion-blocked animals were measured by high-performance liquid chromatography from an arterial blood sample, the results indicating drastic reductions in levels of both catecholamines in the ganglion-blocked (but not in the sympathectomized) rats compared with those in the control rats. Conclusions. Tonic NO-dependent vasodilatation can normally be maintained in the unanesthetized unrestrained rat irrespective of autonomic or humoral adrenergic influences.

AB - Objective. To clarify the controversial issue of whether autonomic influences modulate vascular nitric oxide-mediated vasodilatation or even directly contribute to production of nitric oxide (NO) via nitroxidergic fibers. Methods. Chronic venous and arterial catheters were implanted in Wistar-Kyoto rats (n = 65) for continuous blood pressure measurement, drug administration and blood sampling. Tonic NO-dependent vasodilatation in the conscious free-moving animal was evaluated as the pressor response to inhibition of NO synthesis by intravenous L-monomethylarginine (a 100 mg/kg intravenous bolus plus 0.5 mg/kg per min infusion for 30 min). Experiments were performed under control conditions, chemical sympathectomy by 6-hydroxy-dopamine, ganglionic blockade by hexamethonium, and surgical denervation of sino-aortic baroreceptors. Results. Baseline mean arterial pressure was 100 ± 4 mmHg (mean ± SEM) in control rats and 73 ± 3, 62 ± 5, and 105 ± 10 mmHg in sympathectomized, ganglion-blocked, and denervated rats, respectively. The peak increase in mean arterial pressure after administration of L-monomethylarginine was 38 ± 3 mmHg in control rats and 51 ± 3, 50 ± 6, and 63 ± 10 mmHg in sympathectomized, ganglion-blocked, and denervated rats, respectively. Epinephrine and norepinephrine levels in rats of separate groups of unanesthetized control, sympathectomized and ganglion-blocked animals were measured by high-performance liquid chromatography from an arterial blood sample, the results indicating drastic reductions in levels of both catecholamines in the ganglion-blocked (but not in the sympathectomized) rats compared with those in the control rats. Conclusions. Tonic NO-dependent vasodilatation can normally be maintained in the unanesthetized unrestrained rat irrespective of autonomic or humoral adrenergic influences.

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KW - Sino-aortic denervation

KW - Sympathectomy

KW - Unanesthetized rat

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