The aim of this proposal is to study the characteristics of resistance arteries, and their adrenergic innervation. Relatively little is known from direct in vitro experimentation of this important class of vessels. They will be obtained from the vasculature of the ear of the rabbit and compared with the central ear artery which has been extremely well characterized. Utilizing a resistance vessel myograph that allows study of arteries as small as 50 Mu O.D. and structural and biochemical measurements, functional features of their innervation, smooth muscle, and endothelium will be documented. These will be related to vessel diameter and the in vivo intramural pressure they experience. The objectives of research include an assessment of the asymmetry of the response of the artery wall to agonists entering through its outer and inner surface which is dependent upon cellular uptake systems and possibly long-term neurotropism, differences in Alpha- and Beta-adrenoceptorlocation, intimal dependent dilation, myogenic tone, functional consequences dependent upon differences in synaptic cleft width and agonist sensitivity in relation to resting length. The overall objective is to understand changes that occur in vessel characteristics with change in their diameter. Although resistance arteries play a pivotal role in circulatory function and appear to be altered in hypertension, only recently have direct studies of these vessels been undertaken in vitro.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Method to Extend Research in Time (MERIT) Award (R37)
Project #
5R37HL032985-10
Application #
3486056
Study Section
Special Emphasis Panel (NSS)
Project Start
1984-03-01
Project End
1997-02-28
Budget Start
1993-03-01
Budget End
1994-02-28
Support Year
10
Fiscal Year
1993
Total Cost
Indirect Cost
Name
University of Vermont & St Agric College
Department
Type
Schools of Medicine
DUNS #
066811191
City
Burlington
State
VT
Country
United States
Zip Code
05405
Gokina, N I; Bevan, J A (2000) Histamine-induced depolarization: ionic mechanisms and role in sustained contraction of rabbit cerebral arteries. Am J Physiol Heart Circ Physiol 278:H2094-104
Gokina, N I; Bevan, J A (2000) Role of intracellular Ca(2+) release in histamine-induced depolarization in rabbit middle cerebral artery. Am J Physiol Heart Circ Physiol 278:H2105-14
Thorin-Trescases, N; Bevan, J A (1998) High levels of myogenic tone antagonize the dilator response to flow of small rabbit cerebral arteries. Stroke 29:1194-200;discussion 1200-1
Xie, H; Bevan, J A (1998) Barium and 4-aminopyridine inhibit flow-initiated endothelium-independent relaxation. J Vasc Res 35:428-36
Xie, H; Bartolotta, T; Bevan, J A (1997) Flow relaxation is not ATP-mediated in the rabbit ear artery. Endothelium 5:333-8
Thorin-Trescases, N; Bartolotta, T; Hyman, N et al. (1997) Diameter dependence of myogenic tone of human pial arteries. Possible relation to distensibility. Stroke 28:2486-92
Xie, H; Laher, I; Bevan, J A (1996) Protein kinase C modulates flow-initiated contraction. J Pharmacol Exp Ther 279:668-74
Xie, H; Laher, I; Bevan, J A (1995) Intracellular Ca2+ release in flow-induced contraction of venous smooth muscle. Hypertension 26:1051-5
Dunn, W R; Wellman, G C; Bevan, J A (1994) Enhanced resistance artery sensitivity to agonists under isobaric compared with isometric conditions. Am J Physiol 266:H147-55
Bevan, J A; Joyce, E H (1993) Calcium dependence of flow-induced dilation. Cooperative interaction with sodium. Hypertension 21:16-21

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