Key result
Indomethacin fails to inhibit saralasin-stimulated plasma renin activity in dogs despite reducing PGE2 excretion.
Why the study?
Does indomethacin inhibit saralasin-stimulated plasma renin activity in mildly sodium-depleted conscious dogs?
Does indomethacin inhibit saralasin-stimulated plasma renin activity in mildly sodium-depleted conscious dogs?
Renal prostaglandins do not appear to play an appreciable role in angiotensin II feedback control of renin release in conscious dogs.
Answers are grounded in this paper and cite their sources.
Challenges prostaglandin role in renin feedback in conscious dogs; leaves open relevance to human hypertension.
The hypothesis that prostaglandins play a role in the angiotensin II control mechanism for renin release was examined by interrupting the short-loop negative feedback of angiotensin II on the JG cells with the competitive angiotensin II antagonist saralasin. Mildly sodium-depleted conscious dogs received either indomethacin, or the vehicle alone followed by an intravenous infusion of saralasin. Saralasin produced equivalent increases in PRA in the vehicle- and indomethacin-treated groups with no detectable change in arterial pressure. Plasma renin activity increased in the indomethacin-treated group despite a 58% fall in the rate of excretion of PGE2. These results suggest that in the conscious dog renal prostaglandins do not play an appreciable role in angiotensin II feedback control of renin release.
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Dietz et al. (1981) studied Mild sodium depletion. Indomethacin followed by saralasin vs. Vehicle alone followed by saralasin was evaluated on Plasma renin activity (PRA). Indomethacin failed to inhibit saralasin-stimulated plasma renin activity in mildly sodium-depleted conscious dogs, despite a 58% reduction in PGE2 excretion.
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