• Webb, R Clinton (PI)

Project: Research project

Project Details


Current knowledge about hypertension suggests that an elevated peripheral
resistance maintains high levels of arterial pressure. This increase in
peripheral resistance may be caused by a vasoconstriction resulting from an
alteration in vascular smooth muscle which makes it more sensitive to
normal stimuli. There is evidence that this increased sensitivity reflects
a primary change in the membrane of vascular smooth muscle cells. The
long-term objective of this research is to develop a more complete
understanding of functional vascular changes in hypertension. Experiments
proposed in this research plan will test the following hypotheses: 1)
augmented vascular sensitivity in hypertensive animals is due to a
decreased ability of calcium ions to stabilize membrane properties; 2)
membrane bound calcium that serves as a source of activator calcium is
decreased in vascular smooth muscle of hypertensive animals; 3) sodium
intake will influence vascular reactivity in a genetically hypertensiverat
strain; and 4) altered vascular reactivity (reduced calcium stabilization,
electrogenic pump inhibition, norepinephrine-induced phasic contractions)
is genetically linked to elevated blood pressure. The proposed experiments
will be performed on isolated blood vessel segments (aorta, mesenteric
artery, tail artery) from hypertensive and normotensive rats. The
techniques used to evaluate vascular function include: 1) isometric
recording of contractile behavior; 2) biochemical assay procedures (calcium
binding in membrane fractions; calcium flux measurements in intact tissue);
and 3) analyses of vascular traits in a genetic experiment. It is
anticipated that this study will yield important information about
functional determinants of vascular reactivity in hypertension.
Effective start/end date4/1/823/31/91


  • National Institutes of Health


  • Medicine(all)


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