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Biomedical subjects

P Ramwell

Publications and source records attributed to P Ramwell.

31 records · Page 2Linked to original sources
PubMed1979

Bradykinin-induced renal hemodynamic alterations: renin and prostaglandin relationships.

The present studies examined the role of the renin-angiotensin system as a modifier of the renal vasomotor response to bradykinin. Renal arterial bradykinin infusion (80 ng.kg-1.min-1) initially resulted in increased renal blood flow (RBF). The secretory rates of renin and prostaglandins increased after 60 min. With continued bradykinin administration (120 min) RBF and prostaglandin secretory rates returned toward control values, although renin secretory rate remained elevated (P less than 0.02). After prostaglandin synthetase inhibition, RBF decreased and bradykinin administration returned RBF to control values. Prostaglandin secretory rates decreased after meclofenamate (P less than 0.005). Continued bradykinin infusion resulted in a return of the renin secretory rate to control values. The administration of bradykinin after competitive inhibition of angiotensin II resulted in a sustained increase in renal blood flow. These results suggest that the initial bradykinin-induced renal hyperemia is only partially dependent on enhanced prostaglandin release, the increase in renin secretion by bradykinin infusion after prostaglandin synthetase inhibition is consistent with a bradykinin and renin interaction, and the lack of a sustained hyperemia after bradykinin is related to increased renin-angiotensin system activity.

Angiotensin II↗
PubMed1979

Interrelationship between acetylcholine and prostaglandins in the control of sodium excretion and renin secretion in anesthetized dogs. I.

The interrelationships between acetylcholine (ACH) and prostaglandins in the control of sodium excretion (UNaV) and of renin secretion (RS) were examined in unilaterally-nephrectomized, anesthetized dogs with or without treatment with indomethacin, an inhibitor of prostaglandin synthetase. Inrarenal infusion of ACH (40 microgram/min) in control animals produced diuresis and natriuresis. UNaV was 9.2 +/- 3.1 muEq/min during control periods and was 74.7 +/- 31.6 muEq/min after 40 min of infusion of ACH (p less than 0.05). UNaV was still 48.0 +/- 16.8 muEq/min after 100 min of infusion of ACH (p less than 0.05). RS rate was 930.6 +/- 188.5 U/min during control periods, and was 737.4 +/- 220.3 U/min after 100 min of infusion of ACH (p greater than 0.1). In the dogs treated with indomethacin, the natriuresis produced by ACH could not be sustained. UNaV was 46.6 +/- 12.1 muEq/min before and was 34.7 +/- 12.8 muEq/min 100 min following the infusion of ACH (p greater than 0.1). Arterial plasma renin activity was 3.29 +/- 0.83 ng/ml/h before and was 20.97 +/- 7.78 ng/ml/h after 100 min of infusion of ACH (p less than 0.025). The data suggest that prostaglandins are involved in the sodium excretion and the renin secretion produced by acetylcholine.

Acetylcholine↗
PubMed1978

Possible role for impaired renal prostaglandin production in pathogenesis of hyporeninaemic hypoaldosteronism.

A 57-year-old woman with hypertension and moderate renal insufficiency had chronic unexplained hyperkalaemia. Metabolic balance studies confirmed a diagnosis of hyporeninaemic hypoaldosteronism. Two observations suggested that impaired renal prostaglandin production contributed to the pathogenesis of the patient's disorder. Baseline renal-prostaglandin synthesis (as determined by urinary excretion of P.G.E and P.G.F) was was substantially depressed when compared with that in nine normal females. Infusion of low doses of P.G.A1 produced a significant increase in serum-aldosterone and urinary potassium excretion; it also led to a dramatic fall in blood-pressure and serum-potassium. It appears from these studies that a defect in renal prostaglandin synthesis has an important role in the pathogenesis of hyporeninaemic hypoaldosteronism.

Adrenal Insufficiency↗
PubMed1978

The effect of prostacyclin on the human umbilical artery.

Prostacyclin was tested on human umbilical artery obtained after spontaneous delivery or by Cesarean section. Isometric and isotonic responses were measured on spiral preparations in Krebs-bicarbonate buffer at 37 degrees C equilibrated with 95% O2 and 5% CO2. Spiral artery strips, whether superfused or mounted in organ baths isometrically or isotonically, responded in a dose-dependent manner to both prostacyclin and serotonin; the PGI2 response was biphasic in that low doses (2.5 x 10(-8) M -1.0 x 10(-6) M) elicited a dose-dependent relaxation which changed with higher concentrations (1.0 x 10(-6) M -2.53 X 10(-5) M) to a contractile response. The maximum tension exerted was 50% less than that elicited by serotonin. The data indicate that the human umbilical artery is responsive to prostacyclin and may be involved in the regulation of fetal placenta blood flow.

Buffers↗
PubMed1976

Prostaglandins and aspirin therapy in Bartter's syndrome.

A young patient with Bartter's syndrome was treated for three months with 100 mg/kg/day of aspirin to inhibit prostaglandin synthesis. Clinical symptoms resolved and serum-potassium increased from 2-9 to 3-5 mmol/l. Urinary excretion and plasma concentration of prostaglandins E and F were significantly reduced during aspirin therapy. Plasma-renin activity declined from 85 to 20 ng/ml/h (normal 1-5-4 mg/ml/h) and hyperaldosteronism was corrected. These results suggest that overproduction of prostaglandins has a central role in the pathogenesis of Bartter's syndrome.

Aldosterone↗