Thirty-six haemodialysis patients on treatment for more than six months were studied for residual renal function (RRF). Twenty patients were anuric. The remaining 16 patients with RRF excreted 35-1600 ml urine/day with creatinine clearance ranging 0.17-6.95 ml/min. Patients with RRF were on dialysis therapy for shorter periods than those with anuria (25.5 +/- 18.5 vs. 101.7 +/- 14.2 months, p = 0.001). Twelve out of 20 anuric patients had had previous renal transplantation, whereas none of those with RRF had been transplanted (p = 0.0006). Interdialytic weight gain, serum potassium and phosphate were lower in patients with RRF. Serum phosphate and uric acid were correlated with their respective urinary excretion rates (p = 0.013 and 0.005, respectively), but interdialytic weight gain could not be correlated with urinary output. Creatinine clearance significantly correlated with urinary excretion of potassium, sodium, phosphate and uric acid. In this series of patients a previous unsuccessful renal transplantation was an important factor in the loss of RRF. The presence of RRF contributed to the regulation of the blood levels of phosphate and the excretion rate of potassium, sodium and uric acid.
The immediate and long‐term effects of enalapril (MK421) and its lysine analogue (MK521) in once‐daily dosage, were compared in a study of 12 normal subjects. Both compounds lowered blood pressure equally throughout 24 h without causing tachycardia. The biochemical changes with MK521 were more sustained than with MK421, but this did not affect the magnitude of blood pressure reduction. Twenty‐four hours after the previous dose, with both active drugs, plasma renin concentration was significantly higher on day 8 than on day 1, though angiotensin I did not increase in proportion; this probably reflects a fall in renin‐ substrate with prolonged converting enzyme inhibition. There was an early natriuresis with each compound but this effect was no longer apparent after 8 days of continuous therapy. Both MK421 and MK521 were well tolerated with no serious side effects.
Plasma epinephrine may be increased in some patients with essential hypertension, and prolonged infusion of this catecholamine has been claimed to raise blood pressure. The objectives of our experiments were to determine whether continuous intravenous infusion of epinephrine raised blood pressure in a rat preparation known to respond in this way to angiotensin II in low dose and, if so, the plasma concentration of epinephrine required to raise pressure in comparison to the physiological range of plasma catecholamine concentration in the rat. Intravenous infusion of epinephrine at a rate of 400 ng X kg-1. min-1 or less for 30 min into Wistar rats did not increase mean arterial pressure (MAP); pressure did rise when the rate was increased to 800 ng X kg-1. min-1. However, when rats were given epinephrine at 400 ng X kg-1. min-1 for 4 days with continuous blood pressure recording, average MAP showed a progressive rise on successive days of infusion, reaching a maximum increase of 12 mmHg on the 4th and final day of infusion (P less than 0.02). Blood pressure did not change significantly during epinephrine infusion at 10 and 70 ng X kg-1. min-1. Plasma epinephrine was raised more than 13 times basal at the highest rate of infusion. In comparison, blood pressure and catecholamine concentrations increased only slightly although significantly during a period of restraint. We confirm the existence of a slowly developing pressor effect of epinephrine, but it is small and requires a large sustained increase of plasma epinephrine for its development.
1 Ketanserin, a 5-HT type 2 receptor antagonist, was administered intravenously to nine patients with essential hypertension in a double-blind placebo controlled study to investigate the drug's effects on blood pressure, heart rate, the renin-angiotensin system and sympatho-adrenal function. 2 Average blood-pressure for the group prior to injection of the drug was 150 + 7/94 + 4 (s.e. mean) mm Hg and decreased significantly (P < 0.01) to 137 + 8/88 + 5 mm Hg during the 2 h after injection; heart rate increased immediately after injection of ketanserin, reaching a maximum of 81 + 4 beats/min. 3 After drug administration systolic and diastolic blood pressure decreased on tilting, but the heart rate response was not different from that with placebo. 4 Ketanserin did not affect the blood pressure response to graded infusion of the ocl-adrenoceptor agonist phenylephrine.5 Plasma active renin, angiotensin II and aldosterone concentrations increased slightly but not significantly after the drug; plasma noradrenaline increased transiently. 6 5-HT may be important in the maintenance of blood pressure but alternative mechanisms for the action of ketanserin in reducing blood pressure require investigation.
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