Why the study?
Does local beta-adrenoceptor stimulation or adenosine infusion affect the release of renin and angiotensin II in the vascular beds of hypertensive patients?
Does local beta-adrenoceptor stimulation or adenosine infusion affect the release of renin and angiotensin II in the vascular beds of hypertensive patients?
The study provides direct evidence for a functional vascular tissue renin-angiotensin system in essential hypertensives that interacts with sympathetic neurotransmission.
Suggests local vascular RAS involvement in hypertension; leaves open its role in sympathetic modulation pending confirmatory studies.
AIM: To obtain direct evidence for and evaluate functional aspects of the vascular tissue renin-angiotensin system. METHODS: The local release of renin and angiotensin II was studied in forearm and coronary vascular beds of hypertensive hospitalized patients. The interaction between the vascular tissue renin-angiotensin system and sympathetic neurotransmission was also evaluated. RESULTS: Local beta-adrenoceptor stimulation released active and inactive renin and angiotensin II from forearm vessels, indicating the presence of a vascular tissue renin-angiotensin system in essential hypertensives. Local production of active renin and angiotensin II was closely correlated with circulating renin levels, suggesting that this vascular tissue renin-angiotensin system is at least partly dependent on uptake of renin from the circulating renin-angiotensin system. The local active renin and angiotensin II production was rapidly exhausted; this might represent a short-term control mechanism. Locally generated angiotensin II increased sympathetic vasoconstriction through the presynaptic release of noradrenaline and this effect was mediated by beta-adrenoceptor stimulation. Infusions of adenosine promoted the release of active renin and angiotensin II from the forearm and the coronary vessels.
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Taddei et al. (1992) studied this question.
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