Key result
Essential hypertension is linked to lower urinary prostaglandin E and kallikrein excretion vs normotensive controls.
Observational
Answers are grounded in this paper and cite their sources.
Reveals impaired renal kallikrein and prostaglandin E responses in essential hypertension, indicating compromised counter-regulation against the renin-angiotensin-aldosterone system.
The present study was done to investigate the interrelationships between renal kallikrein-kinin, renal prostaglandin E and renin-angiotensin-aldosterone systems in human and the possibility that renal kallikrein-kinin and renal prostaglandin E may participate in the pathogenesis of essential hypertension by means of measuring urinary excretion of kallikrein and prostaglandin E, plasma renin activity and plasma aldosterone concentration before and after stimulation or inhibition of the renin-angiotensin-aldosterone system and inhibition of renal prostaglandin E generation. Urinary kallikrein excretion was increased after the stimulation of the renin-angiotensin-aldosterone system by low Na diet or the administration of furosemide and upright posture, while it tended to decrease after the inhibition of the renin-angiotensin-aldosterone system by the administration of 1-sarcosine-8-isoleucine angiotensin II under sodium depletion or spironolactone. These data showed that the changes in urinary kallikrein excretion paralelled with those of the renin-angiotensin-aldosterone system following various stimuli, suggesting that renal kallikrein-kinin system may regulate blood pressure by opposing the action of the renin-angiotensin-aldosterone system. Urinary PGE excretion was decreased after sodium depletion and increased after the administration of furosemide in spite of the augmentation of the renin-angiotensin-aldosterone system. The changes in urinary PGE excretion was closely related to those in urinary Na output after various stimuli and a significant positive correlation was found between basal levels of urinary PGE and those of urinary Na, suggesting that renal prostaglandin E may be involved in the regulation of blood pressure by affecting renal sodium handing. The present data showed that basal level of urinary excretion of PGE and kallikrein was lower in essential hypertension than in normal subjects and that the release of renal kallikrein and PGE after furosemide administration was also suppressed in essential hypertension compared with that in normal subjects, suggesting that there exists an impaired defense mechanism against the renin-angiotensin-aldosterone system resulting in sodium retention.
No takes yet. Share an insight, caveat, or question.
Abe et al. (1979) conducted an observational in Essential hypertension. Stimulation or inhibition of the renin-angiotensin-aldosterone system (low Na diet, furosemide, upright posture, 1-sarcosine-8-isoleucine angiotensin II, spironolactone) vs. Normal subjects / baseline was evaluated on Urinary excretion of kallikrein and prostaglandin E (PGE), plasma renin activity, and plasma aldosterone concentration. Essential hypertension was associated with lower basal and furosemide-stimulated urinary excretion of prostaglandin E and kallikrein compared with normal subjects.
Synapse has enriched 10 related papers. Consider them for comparative context: