Adaptive changes in control of blood vessel tone

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Chronic high systemic intravascular pressure is a major cause of morbidity and mortality. High systemic pressure is defined as systolic/diastolic pressure >140/ >90 mmHg. The systolic pressure is the pressure in the vessels when the heart contracts and the diastolic pressure is the pressure when the heart relaxes. Blood vessel diameter, a major influence on systemic intravascular pressure, is determined by changes in the size of the smooth muscle cells, the main component of the vessel wall. For example, when smooth muscle shortens, or contracts, the diameter of the blood vessel becomes smaller. By the same token, when smooth muscle relaxes and lengthens, the blood vessels dilate (i.e. the diameter of the blood vessels increases). An increase in the diameter of blood vessels reduces resistance to blood flow which leads to lowering of systemic intravascular pressure. On the other hand, a reduction in the diameter of blood vessels leads to an increase in vascular resistance. This increase in resistance to flow can lead to a lower blood flow and reduced delivery of nutrients and oxygen and the removal of waste products from organs and thus reduce optimal function of the tissue, at times causing cell death. In our laboratory we are interested in the function of vascular smooth muscle and endothelial cells, and control of systemic vascular pressure. Our goals are to study the processes that are involved in the control of smooth muscle function, blood vessel lumen diameter, regional blood flow, vascular conductance and vascular stiffness. My plan is to examine the effect of elevation in systemic arterial blood pressure on haemodynamics, blood flow, vascular conductance and stiffness in order to determine how chronic increase in intravascular pressure manifests its detrimental effects on blood vessel response and function. Findings from our studies should provide insight into the effects of high systemic pressure on blood vessel biology and behavior. The information obtained from our studies will greatly advance our understanding of how vessels adapt, or are negatively impacted, under abnormal and stressful conditions. The outcome from our work will lead to improved quality of life in mammalians.