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Title: Studies on vascular intracellular pH in hypertension
Author: Izzard, Ashley S.
ISNI:       0000 0001 3587 7097
Awarding Body: University of Leicester
Current Institution: University of Leicester
Date of Award: 1990
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Changes in intracellular pH (pHi) in vascular smooth muscle cells influence growth and contraction. It has been proposed that both processes are critically dependent on cell alkalinisation due to increased Na+/H+ exchange; therefore pHi may be an important mediator of the vascular hypertrophy resulting in an increased peripheral resistance which characterises established hypertension. Resistance artery morphology followed by simultaneous recording of isometric contraction and pH were measured using a myograph in conjunction with a pH sensitive fluorescent probe and microscope capable of exciting the intracellular trapped dye at appropriate wavebands and recording the fluorescence. Mesenteric resistance arteries from the genetically hypertension prone spontaneously hypertensive rat were more alkaline than the normotensive Wistar Kyoto control. However secondary hypertension due to aortic coarctation did not result in mesenteric artery alkalinisation, although pHi regulation was altered. In contrast pHi and its regulation were unchanged in subcutaneous resistance arteries from the gluteal region from untreated hypertensive patients and first degree offspring of hypertensive patients compared to matched controls. Mesenteric arteries displayed anticipated pHi changes to manoeuvres which directly cause alkalinisation and acidification. On the other hand contraction induced intracellular acidification rather than alkalinisation as observed in cells grown in tissue culture conditions. These measurements of pHi carried out for the first time in human resistance arteries highlight the limitations of using animal models or surrogate cells when studying this potentially crippling vascular disorder.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available
Keywords: Physiology