Abstract
Our first goal was to determine whether acute hyperglycemia alters endothelium-dependent reactivity of rat cerebral arterioles. Our second goal was to investigate a possible mechanism for impaired reactivity during acute hyperglycemia. Diameter of pial arterioles was measured during suffusion with ADP, acetylcholine, histamine, N-methyl-D-aspartate (NMDA), and nitroglycerin before and during application of a suffusate containing D-glucose (5, 10, 20, and 25 mM). ADP, acetylcholine, histamine, NMDA, and nitroglycerin produced dose-related vasodilatation before application of D-glucose. Vasodilatation in response to the agonists was not altered by 5 and 10 mM D-glucose. In contrast, vasodilatation in response to ADP, acetylcholine, histamine, and NMDA was impaired during application of 20 and 25 mM D-glucose. Dilatation in response to nitroglycerin was not altered. Application of the protein kinase C inhibitor calphostin C (1.0 nM) or chelerythrine (10 nM) restored endothelium-dependent vasodilatation during application of 25 mM D-glucose. Thus acute hyperglycemia impairs endothelium-dependent responses of cerebral arterioles via the activation of protein kinase C.
| Original language | English (US) |
|---|---|
| Journal | American Journal of Physiology - Heart and Circulatory Physiology |
| Volume | 269 |
| Issue number | 4 38-4 |
| State | Published - Jan 1 1995 |
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Keywords
- N-methyl-D- aspartate
- acetylcholine
- adenosine diphosphate
- brain
- calphostin C
- chelerythrine
- endothelium-dependent dilation
- histamine
- hyperglycemia
- nitroglycerin
- rats
ASJC Scopus subject areas
- Physiology
- Agricultural and Biological Sciences(all)
Cite this
Acute effects of glucose on reactivity of cerebral microcirculation : Role of activation of protein kinase C. / Mayhan, William; Patel, Kaushik P.
In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 269, No. 4 38-4, 01.01.1995.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Acute effects of glucose on reactivity of cerebral microcirculation
T2 - Role of activation of protein kinase C
AU - Mayhan, William
AU - Patel, Kaushik P
PY - 1995/1/1
Y1 - 1995/1/1
N2 - Our first goal was to determine whether acute hyperglycemia alters endothelium-dependent reactivity of rat cerebral arterioles. Our second goal was to investigate a possible mechanism for impaired reactivity during acute hyperglycemia. Diameter of pial arterioles was measured during suffusion with ADP, acetylcholine, histamine, N-methyl-D-aspartate (NMDA), and nitroglycerin before and during application of a suffusate containing D-glucose (5, 10, 20, and 25 mM). ADP, acetylcholine, histamine, NMDA, and nitroglycerin produced dose-related vasodilatation before application of D-glucose. Vasodilatation in response to the agonists was not altered by 5 and 10 mM D-glucose. In contrast, vasodilatation in response to ADP, acetylcholine, histamine, and NMDA was impaired during application of 20 and 25 mM D-glucose. Dilatation in response to nitroglycerin was not altered. Application of the protein kinase C inhibitor calphostin C (1.0 nM) or chelerythrine (10 nM) restored endothelium-dependent vasodilatation during application of 25 mM D-glucose. Thus acute hyperglycemia impairs endothelium-dependent responses of cerebral arterioles via the activation of protein kinase C.
AB - Our first goal was to determine whether acute hyperglycemia alters endothelium-dependent reactivity of rat cerebral arterioles. Our second goal was to investigate a possible mechanism for impaired reactivity during acute hyperglycemia. Diameter of pial arterioles was measured during suffusion with ADP, acetylcholine, histamine, N-methyl-D-aspartate (NMDA), and nitroglycerin before and during application of a suffusate containing D-glucose (5, 10, 20, and 25 mM). ADP, acetylcholine, histamine, NMDA, and nitroglycerin produced dose-related vasodilatation before application of D-glucose. Vasodilatation in response to the agonists was not altered by 5 and 10 mM D-glucose. In contrast, vasodilatation in response to ADP, acetylcholine, histamine, and NMDA was impaired during application of 20 and 25 mM D-glucose. Dilatation in response to nitroglycerin was not altered. Application of the protein kinase C inhibitor calphostin C (1.0 nM) or chelerythrine (10 nM) restored endothelium-dependent vasodilatation during application of 25 mM D-glucose. Thus acute hyperglycemia impairs endothelium-dependent responses of cerebral arterioles via the activation of protein kinase C.
KW - N-methyl-D- aspartate
KW - acetylcholine
KW - adenosine diphosphate
KW - brain
KW - calphostin C
KW - chelerythrine
KW - endothelium-dependent dilation
KW - histamine
KW - hyperglycemia
KW - nitroglycerin
KW - rats
UR - http://www.scopus.com/inward/record.url?scp=0028880793&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0028880793&partnerID=8YFLogxK
M3 - Article
VL - 269
JO - American Journal of Physiology - Renal Physiology
JF - American Journal of Physiology - Renal Physiology
SN - 0363-6127
IS - 4 38-4
ER -