Key result
Intraventricular injection of saralasin acutely reversed experimental pregnancy-induced hypertension (which had risen to 160/100 mm Hg), whereas intravenous saralasin elicited no response.
Why the study?
Does intraventricular saralasin reverse experimental pregnancy-induced hypertension in Sprague-Dawley rats?
Does intraventricular saralasin reverse experimental pregnancy-induced hypertension in Sprague-Dawley rats?
Experimental pre-eclampsia in rats appears to depend on a central nervous system angiotensin II mechanism rather than enhanced sympathetic nervous system activation.
Answers are grounded in this paper and cite their sources.
Central angiotensin II may mediate experimental pregnancy hypertension; leaves open whether brain RAS blockade merits human study.
The Sprague-Dawley laboratory rat served as an experimental model for pregnancy-induced hypertension. Generation of systemic hypertension depended upon a surgical reduction of blood pressure by 30–35% to the uteroplacental unit. Blood pressures during the final trimester of rat pregnancy typically rose from a normal of 125/80 mm Hg to 160/100 mm Hg within 4 days of surgery; they fell to normal by 5 days post partum. A 7.5-fold rise in proteinuria accompanied development of the hypertension. Hypertension was reversed acutely by injection of the angiotensin II antagonist, saralasin, into the brain ventricular system; intravenous saralasin injection elicited no observable response. Intraventricular injection of the alpha-2 adrenergic agonist, clonidine, did not lower blood pressure in experimental rats. We conclude that the experimental pre-eclampsia observed in these rats depends upon a central nervous system angiotensin II mechanism and not upon enhanced activation of the sympathetic nervous system.
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Eder et al. (1987) studied Pregnancy-induced hypertension. Intraventricular saralasin vs. Intravenous saralasin and intraventricular clonidine was evaluated on Blood pressure. Intraventricular injection of saralasin acutely reversed experimental pregnancy-induced hypertension (which had risen to 160/100 mm Hg), whereas intravenous saralasin elicited no response.
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