American journal of physiology. Regulatory, integrative and comparative physiology
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Am. J. Physiol. Regul. Integr. Comp. Physiol. · May 2007
Investigation of the mechanisms by which chronic infusion of an acutely subpressor dose of angiotensin II induces hypertension.
The mechanisms by which chronic infusion of an initially subpressor low dose of angiotensin II (ANG II) causes a progressive and sustained hypertension remain unclear. In conscious sheep (n = 6), intravenous infusion of ANG II (2 microg/h) gradually increased mean arterial pressure (MAP) from 82 +/- 3 to 96 +/- 5 mmHg over 7 days (P < 0.001). This was accompanied by peripheral vasoconstriction; total peripheral conductance decreased from 44.6 +/- 6.4 to 38.2 +/- 6.7 ml.min(-1).mmHg(-1) (P < 0.001). ⋯ In summary, hypertension due to infusion of a low dose of ANG II was accompanied by generalized peripheral vasoconstriction. Indirect evidence suggested that the hypertension was not neurogenic, but measurement of sympathetic nerve activity is required to confirm this conclusion. There was no evidence for a role for central angiotensinergic mechanisms, increased pressor responsiveness to ANG II, or sodium and fluid retention.