Why the study?
Does infusion of angiotensin elicit different peripheral venous and arteriolar responses in hypertensive subjects compared to normotensive individuals?
Does infusion of angiotensin elicit different peripheral venous and arteriolar responses in hypertensive subjects compared to normotensive individuals?
Hypertensive patients exhibit altered peripheral venous responses to angiotensin compared to normotensive individuals, suggesting possible prior exposure to angiotensin-like substances.
Answers are grounded in this paper and cite their sources.
Hypertension may blunt angiotensin venoconstriction; hypothesis-generating for vascular adaptation and requires confirmation before any clinical consideration.
The distensibility of the peripheral veins of the hypertensive subject is normal, that is, there is no evidence of peripheral venoconstriction, despite the excessive arteriolar constriction. The forearm veins of hypertensive patients respond to pooling of blood in the upright position to a lesser degree than do veins of normotensive individuals, indicating a lesser degree of smypathetic nervous activity in response to this stimulus. The peripheral veins of hypertensive subjects constrict normally in response to an infusion of norepinephrine, indicating that failure of venoconstriction in any circumstance cannot be attributed to failure of the smooth muscle of the veins. Infusions of angiotensin produce constriction of the veins as well as the arterioles in normotensive individuals thus failing to mimic the naturally occurring state of essential hypertension. Infusions of angiotensin in hypertensive patients result in further arteriolar constriction and hypertension without concomitant venoconstriction. The results of these experiments suggest that peripheral venous responses of hypertensive subjects to angiotensin infusions may have been modified by previous exposure of these vessels to a material at least similar to angiotensin.
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J. Edwin Wood (1961) studied this question.
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