Why the study?
Does chronic infusion of angiotensin II into vertebral arteries increase arterial pressure in unanaesthetized dogs?
Does chronic infusion of angiotensin II into vertebral arteries increase arterial pressure in unanaesthetized dogs?
Chronic infusion of angiotensin II into the vertebral circulation of dogs causes a sustained increase in arterial pressure, suggesting a central nervous system mechanism for angiotensin-mediated hypertension.
Answers are grounded in this paper and cite their sources.
May support central angiotensin effects on BP in dogs; leaves open translation to human hypertension.
Synthetic angiotensin II was infused chronically through catheters implanted into a vertebral artery and an external jugular vein of unanaesthetized dogs. Arterial pressure was recorded daily from an indwelling catheter in the abdominal aorta before, during and after the infusions. 2. Infusion of angiotensin 1 μg kg−1 day−1 into a vertebral artery caused mean arterial pressure to increase by an average of 12 mmHg in five dogs, and the rise was sustained throughout the infusion period of 7 days in all dogs. 3. When the infusion rate of angiotensin was increased to 10 μg kg−1 day−1, arterial pressure during vertebral artery infusion rose initially to a slightly greater extent but decreased at the end of the infusion, indicating tachyphylaxis. 4. During infusion of angiotensin into the vertebral circulation, arterial pressure rose rather than fell during sleep; awakening was accompanied by sharp fall in pressure. 5. It is concluded that there is an area in the central nervous system responsive to angiotensin that can cause a sustained rise in arterial pressure.
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Fukiyama et al. (1971) studied this question.
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