Abstract
Changes in carotid arterial wall properties were studied in rats following unilateral renal artery stenosis (RH) or deoxycorticosterone (DOCA) plus saline hypertension of 8 wk duration. Terminal systolic pressures were: RH, 146 .+-. 4 mm Hg; DOCA, 162 .+-. 5 mm Hg; and control, 127 .+-. 3 mm Hg. Transmural pressure and external diameter measurements were made under control conditions and with active (5 .mu.g/ml norepinephrine) and passive (2 mM EGTA [ethylene glycol bis[.beta.-aminoethylether]N,N''-tetraacetic acid]) smooth muscle. Only minor differences were found in values of passive mechanical properties between normal and hypertensive animals. Values of internal radius were smaller and wall thickness larger in the hypertensive arteries under passive conditions. There was a reduction in total connective tissue and the ratio of collagen to elastin contents, and an increase in water content of hypertensive arteries. Activation of smooth muscle produced larger responses in hypertensive carotid arteries. As a function of transmural pressure, values of elastic modulus were reduced to a greater degree and changes in values of characteristic impedance were greater. Maximum values of active stress development and active constriction responses to norepinephrine were larger. The changes in passive properties may be the result of changes in the architectural organization of connective tissue elements in the hypertensive arteries; the alterations in active properties may be due to a number of essentially unknown factors.

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