In conscious dogs, renovascular hypertension is driven initially by mechanical resistance and angiotensin II, and later maintained by cardiovascular hypertrophy.
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Does not support practice changes in renovascular hypertension; extends phased mechanism data from conscious dog models.
Evidence from experiments in conscious, instrumented dogs shows that hypertension from renal artery stenosis is due to: (i) the stimulus, the mechanical resistance of the stenosis; and (ii) the secondary responses to this, especially angiotensin II (initially) and cardiovascular hypertrophy. 2. The hydraulic resistance of the stenosis is responsible for about 20-25% of the rise in blood pressure. 3. Angiotensin II is initially the most important secondary response to the stenosis. Within days, however, other as yet undetermined factors become dominant in the maintenance of the hypertension. The most important of these factors is probably cardiovascular hypertrophy. 4. These secondary factors are homeostatic, in that they mitigate the effects of stenosis on renal function.
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Anderson et al. (1991) studied this question.
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