Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The renal prostaglandins PGS2 and PGE2 possess potent antihypertensive and vasodepressor activity. The mechanism of blood pressure lowering effect is through peripheral arteriolar dilation with a fall in total peripheral resistance. PGA unlike PGE escape degradation by the lung and thus could circulate as antihypertensive hormones. Since plasma PGA levels rise in humans on a low sodium intake, it has been postulated that the beneficial effects of a low sodium diet in some hypertensives may be the result of an increase in peripheral vasodilating PGA. Support that plasma PGA may be a regulator of systemic blood pressure is also derived from the fact a PGA-secreting renal tumor was associated with a fall in blood pressure and a rise in plasma PGA in a previously hypertensive woman. The removal of the tumor resulted in a return of blood pressure to elevated levels and a concomitant fall in PGA. Recently, a number of human patients with essential hypertension have been infused with PGA1 and PGA2. It was observed that there was an initial increase in renal blood flow, sodium and water excretion which was associated with no change in the elevated blood pressure. When blood pressure ultimately fell, there was a return of renal blood flow, sodium and water excretion to preinfusion levels. It would appear that PGA compounds act as 'ideal' antihypertensive agents since they favorably effect renal resistance, sodium and water homeostasis, plasma volume, total peripheral resistance, blood pressure and indirectly cardiac output through baroreceptor stimulation, all factors known to be important in etiology in human hypertension.
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PMID:Renal prostaglandins. 110 Oct 92

Substantial evidence has accumulated that the prostaglandins A (PGA) compounds, potent naturally occurring renal antihypertensive agents, may function as circulating renal vasodilators and may be responsible at least in part for the antihypertensive function of the kidney. The concept that essential hypertension is not solely the result of increased renal pressure mechanisms but may be a deficiency disorder of renal vasodepressor agents has been reinforced with isolation from the kidney of the naturally occurring peripheral vasodilator, PGA2. Along with its possible role in essential hypertension, PGA2 might function as a natriuretic "hormone." All available data indicate that the renal response to prostaglandin infusion in animals and humans with essential hypertension is characterized by an increase in cortical blood flow, glomerular filtration rate, sodium and potassium excretion, urine flow, and free-water clearance. Of all the prostaglandins investigated thus far, the most promising compounds from a cardiovascular-renal perspective are the PGA class. From their highly desirable mechanism of antihypertension and natriuretic action, the greatest immediate potential for PGA1 and PGA2 is for pharmacological use in the treatment of such disorders as hypertension and edema.
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PMID:Hypertension, natriuresis, and the renal prostaglandins. 576 18