Effects of N(G)-nitro-L-arginine and L-arginine on regional cerebral blood flow in the cat

A. G B Kovach, Csaba Szabo, Z. Benyo, C. Csaki, J. H. Greenberg, R. Reivich

Research output: Contribution to journalArticle

116 Citations (Scopus)

Abstract

1. We studied the effects of N(G)-nitro-L-arginine (NOLA), a potent inhibitor of the L-arginine-nitric oxide pathway, and L-arginine, the precursor of nitric oxide, on regional cerebral blood flow, electrocortical activity and ex vivo cerebrovascular reactivity in the cat. Flow was measured via radiolabelled microspheres, and vascular responses were studied by measuring isometric tension of isolated middle cerebral arterial rings. 2. NOLA (30 mg kg-1 bolus followed by 1 mg kg-1 min-1 infusion) caused an approximately 40 mmHg elevation in the mean arterial blood pressure, a regionally heterogenous increase of the regional cerebrovascular resistance and a decrease in the regional cerebral blood flow 15 and 40 min after the start of its administration. In contrast L-arginine (30 mg kg-1 bolus followed by 10 mg kg-1 min-1 infusion) did not alter blood pressure, cerebrovascular resistance nor regional cerebral blood flow 15 min after the start of its administration. The NOLA-induced changes in tissue flow were the most pronounced in the cerebellum, pituitary and medulla oblongata, whereas there was no decrease in the flow of the cortex and white matter. 3. NOLA caused characteristic changes in total fronto-occipital EEG power and in power spectra which were unlikely to have been due to cerebral ischaemia. In addition, the ex vivo reactivity of the middle cerebral arteries showed signs of impaired endothelial nitric oxide synthesis: there were enhanced noradrenaline induced contractions and N-ethoxycarbonyl-3-morpholino-sydnonimine (SIN-1)-induced relaxations and markedly attenuated acetylcholine- and ATP-induced relaxations after NOLA treatment. 4. The present data indicate that resting cerebral blood flow and cerebrovascular resistance are regulated by nitric oxide derived from L-arginine in a regionally heterogenous way and that exogenous L-arginine availability is not a limiting factor in this nitric oxide generation. Possibly, both the vascular endothelium and the neurons contribute to this basal nitric oxide release.

Original languageEnglish (US)
Pages (from-to)183-196
Number of pages14
JournalJournal of Physiology
Volume449
StatePublished - 1992
Externally publishedYes

Fingerprint

Cerebrovascular Circulation
Regional Blood Flow
Arginine
Cats
Nitric Oxide
Arterial Pressure
Medulla Oblongata
Vascular Endothelium
Middle Cerebral Artery
Brain Ischemia
Microspheres
Cerebellum
Acetylcholine
Blood Vessels
Electroencephalography

ASJC Scopus subject areas

  • Physiology

Cite this

Kovach, A. G. B., Szabo, C., Benyo, Z., Csaki, C., Greenberg, J. H., & Reivich, R. (1992). Effects of N(G)-nitro-L-arginine and L-arginine on regional cerebral blood flow in the cat. Journal of Physiology, 449, 183-196.

Effects of N(G)-nitro-L-arginine and L-arginine on regional cerebral blood flow in the cat. / Kovach, A. G B; Szabo, Csaba; Benyo, Z.; Csaki, C.; Greenberg, J. H.; Reivich, R.

In: Journal of Physiology, Vol. 449, 1992, p. 183-196.

Research output: Contribution to journalArticle

Kovach, AGB, Szabo, C, Benyo, Z, Csaki, C, Greenberg, JH & Reivich, R 1992, 'Effects of N(G)-nitro-L-arginine and L-arginine on regional cerebral blood flow in the cat', Journal of Physiology, vol. 449, pp. 183-196.
Kovach, A. G B ; Szabo, Csaba ; Benyo, Z. ; Csaki, C. ; Greenberg, J. H. ; Reivich, R. / Effects of N(G)-nitro-L-arginine and L-arginine on regional cerebral blood flow in the cat. In: Journal of Physiology. 1992 ; Vol. 449. pp. 183-196.
@article{458e556782dc46cc92b55fed7b18281b,
title = "Effects of N(G)-nitro-L-arginine and L-arginine on regional cerebral blood flow in the cat",
abstract = "1. We studied the effects of N(G)-nitro-L-arginine (NOLA), a potent inhibitor of the L-arginine-nitric oxide pathway, and L-arginine, the precursor of nitric oxide, on regional cerebral blood flow, electrocortical activity and ex vivo cerebrovascular reactivity in the cat. Flow was measured via radiolabelled microspheres, and vascular responses were studied by measuring isometric tension of isolated middle cerebral arterial rings. 2. NOLA (30 mg kg-1 bolus followed by 1 mg kg-1 min-1 infusion) caused an approximately 40 mmHg elevation in the mean arterial blood pressure, a regionally heterogenous increase of the regional cerebrovascular resistance and a decrease in the regional cerebral blood flow 15 and 40 min after the start of its administration. In contrast L-arginine (30 mg kg-1 bolus followed by 10 mg kg-1 min-1 infusion) did not alter blood pressure, cerebrovascular resistance nor regional cerebral blood flow 15 min after the start of its administration. The NOLA-induced changes in tissue flow were the most pronounced in the cerebellum, pituitary and medulla oblongata, whereas there was no decrease in the flow of the cortex and white matter. 3. NOLA caused characteristic changes in total fronto-occipital EEG power and in power spectra which were unlikely to have been due to cerebral ischaemia. In addition, the ex vivo reactivity of the middle cerebral arteries showed signs of impaired endothelial nitric oxide synthesis: there were enhanced noradrenaline induced contractions and N-ethoxycarbonyl-3-morpholino-sydnonimine (SIN-1)-induced relaxations and markedly attenuated acetylcholine- and ATP-induced relaxations after NOLA treatment. 4. The present data indicate that resting cerebral blood flow and cerebrovascular resistance are regulated by nitric oxide derived from L-arginine in a regionally heterogenous way and that exogenous L-arginine availability is not a limiting factor in this nitric oxide generation. Possibly, both the vascular endothelium and the neurons contribute to this basal nitric oxide release.",
author = "Kovach, {A. G B} and Csaba Szabo and Z. Benyo and C. Csaki and Greenberg, {J. H.} and R. Reivich",
year = "1992",
language = "English (US)",
volume = "449",
pages = "183--196",
journal = "Journal of Physiology",
issn = "0022-3751",
publisher = "Wiley-Blackwell",

}

TY - JOUR

T1 - Effects of N(G)-nitro-L-arginine and L-arginine on regional cerebral blood flow in the cat

AU - Kovach, A. G B

AU - Szabo, Csaba

AU - Benyo, Z.

AU - Csaki, C.

AU - Greenberg, J. H.

AU - Reivich, R.

PY - 1992

Y1 - 1992

N2 - 1. We studied the effects of N(G)-nitro-L-arginine (NOLA), a potent inhibitor of the L-arginine-nitric oxide pathway, and L-arginine, the precursor of nitric oxide, on regional cerebral blood flow, electrocortical activity and ex vivo cerebrovascular reactivity in the cat. Flow was measured via radiolabelled microspheres, and vascular responses were studied by measuring isometric tension of isolated middle cerebral arterial rings. 2. NOLA (30 mg kg-1 bolus followed by 1 mg kg-1 min-1 infusion) caused an approximately 40 mmHg elevation in the mean arterial blood pressure, a regionally heterogenous increase of the regional cerebrovascular resistance and a decrease in the regional cerebral blood flow 15 and 40 min after the start of its administration. In contrast L-arginine (30 mg kg-1 bolus followed by 10 mg kg-1 min-1 infusion) did not alter blood pressure, cerebrovascular resistance nor regional cerebral blood flow 15 min after the start of its administration. The NOLA-induced changes in tissue flow were the most pronounced in the cerebellum, pituitary and medulla oblongata, whereas there was no decrease in the flow of the cortex and white matter. 3. NOLA caused characteristic changes in total fronto-occipital EEG power and in power spectra which were unlikely to have been due to cerebral ischaemia. In addition, the ex vivo reactivity of the middle cerebral arteries showed signs of impaired endothelial nitric oxide synthesis: there were enhanced noradrenaline induced contractions and N-ethoxycarbonyl-3-morpholino-sydnonimine (SIN-1)-induced relaxations and markedly attenuated acetylcholine- and ATP-induced relaxations after NOLA treatment. 4. The present data indicate that resting cerebral blood flow and cerebrovascular resistance are regulated by nitric oxide derived from L-arginine in a regionally heterogenous way and that exogenous L-arginine availability is not a limiting factor in this nitric oxide generation. Possibly, both the vascular endothelium and the neurons contribute to this basal nitric oxide release.

AB - 1. We studied the effects of N(G)-nitro-L-arginine (NOLA), a potent inhibitor of the L-arginine-nitric oxide pathway, and L-arginine, the precursor of nitric oxide, on regional cerebral blood flow, electrocortical activity and ex vivo cerebrovascular reactivity in the cat. Flow was measured via radiolabelled microspheres, and vascular responses were studied by measuring isometric tension of isolated middle cerebral arterial rings. 2. NOLA (30 mg kg-1 bolus followed by 1 mg kg-1 min-1 infusion) caused an approximately 40 mmHg elevation in the mean arterial blood pressure, a regionally heterogenous increase of the regional cerebrovascular resistance and a decrease in the regional cerebral blood flow 15 and 40 min after the start of its administration. In contrast L-arginine (30 mg kg-1 bolus followed by 10 mg kg-1 min-1 infusion) did not alter blood pressure, cerebrovascular resistance nor regional cerebral blood flow 15 min after the start of its administration. The NOLA-induced changes in tissue flow were the most pronounced in the cerebellum, pituitary and medulla oblongata, whereas there was no decrease in the flow of the cortex and white matter. 3. NOLA caused characteristic changes in total fronto-occipital EEG power and in power spectra which were unlikely to have been due to cerebral ischaemia. In addition, the ex vivo reactivity of the middle cerebral arteries showed signs of impaired endothelial nitric oxide synthesis: there were enhanced noradrenaline induced contractions and N-ethoxycarbonyl-3-morpholino-sydnonimine (SIN-1)-induced relaxations and markedly attenuated acetylcholine- and ATP-induced relaxations after NOLA treatment. 4. The present data indicate that resting cerebral blood flow and cerebrovascular resistance are regulated by nitric oxide derived from L-arginine in a regionally heterogenous way and that exogenous L-arginine availability is not a limiting factor in this nitric oxide generation. Possibly, both the vascular endothelium and the neurons contribute to this basal nitric oxide release.

UR - http://www.scopus.com/inward/record.url?scp=0026612638&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026612638&partnerID=8YFLogxK

M3 - Article

VL - 449

SP - 183

EP - 196

JO - Journal of Physiology

JF - Journal of Physiology

SN - 0022-3751

ER -