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Biomedical subjects

P Sweet

Publications and source records attributed to P Sweet.

23 records · Page 2Linked to original sources
PubMed1979

Influence of angiotensins (I, II, & III), bradykinin and arachidonic acid on renomedullary PGE production in vitro.

Renomedullary tissue from rabbit or rat was incubated with angiotensin I, II, III, arachidonic acid, bradykinin, indomethacin and meclofenamate to study their effect on PGE2 production. Arachidonic acid and bradykinin enhanced PGE2 production significantly. Indomethacin and meclofenamate inhibited PGE2 production by more than 70%. Angiotensin I, II and III did not influence PGE2 production. These results suggest that bradykinin and arachidonic acid stimulate PGE2 production by a direct cellular action whereas the angiotensins do not.

Angiotensin I↗
PubMed1979

Inhibition of mitogen induced blast transformation by a multiple sclerosis serum factor.

A factor in the sera of multiple sclerosis patients inhibits RNA, protein and DNA synthesis in actively metabolizing mitogen stimulated lymphocytes. Inhibition of macromolecular synthesis precedes cell death by 24 to 36 hours. The factor is effective on cells which are already committed to transformation by previous exposure to mitogen and cells which are simultaneously exposed to the factor and mitogen. Previous exposure of unstimulated cells to the factor does not alter their subsequent response to mitogen. The factor does not inhibit RNA synthesis of unstimulated lymphocytes isolated on a Ficoll-Hypaque gradient, nor is it toxic to these cells.

Biological Products↗
PubMed1978

Impaired renal production of prostaglandin E2: a newly identified lesion in human essential hypertension.

To test the hypothesis that impaired renal prostaglandin production may accompany the hypertensive state, we have measured urinary PGE2 by radioimmunoassay in 52 normotensive and 50 hypertensive subjects. PGE2 levels were lower in females, and were not affected by Na+ intake or age. Patients with essential hypertension had significantly lower PGE2, particularly those with low-renin hypertension. Forty percent of the hypertensives excreted less than 70 ng/24 hr, values never observed in normotensives except after receiving indomethacin, a well-known prostaglandin synthetase inhibitor. It appears that impaired renal prostaglandin production is commonly encountered in patients with essential hypertension, perhaps contributing to their increased renal resistance. The data further suggest a role for renal prostaglandins in the pathogenesis of low-renin hypertension.

Female↗