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Biomedical subjects

M Aurell

Publications and source records attributed to M Aurell.

At least 73 records · Page 4Linked to original sources
PubMed1990

Plasma noradrenaline and dopamine in renin-mediated hypertension.

Noradrenaline (NA) and dopamine (DA) have opposite effects on the kidney; NA causes vasoconstriction and increased sodium reabsorption while DA promotes vasodilation and natriuresis. In 15 patients investigated for renin-mediated hypertension measurements of plasma renin activity (PRA), NA and DA concentrations were made in arterial and renal venous blood from both kidneys before and after acute stimulation of renin release by i.v. dihydralazine. Nine patients had unilateral renin secretion and were classified as renin-positive, while the remaining six patients were renin-negative. Renin-positive patients had higher arterial and renal venous PRA, NA and DA levels than the negative ones. In the renin-positive group V-A differences for NA and DA were present on both sides despite unilateral secretion of renin. NA but not DA levels were higher in the renin-secreting kidney, which can partly be explained by the reduced plasma flow to the involved kidney. After dihydralazine the arterial NA and DA rose similarly in renin-positive and renin-negative patients, while PRA rose only in the renin-positive cases. In the renin-positive patients where stimulation of renin secretion caused a marked increase of the PRA gradient on the affected side only, renal gradients for NA and DA increased bilaterally. The increase in DA was more pronounced than that of NA yielding a rise in DA/NA ratio on the affected side. Arterial PRA was positively correlated to the plasma concentrations of NA and DA. V-A differences for PRA and NA or DA were positively correlated on the involved renin-secreting side. In summary, patients with renin-dependent hypertension have elevated plasma NA and DA concentrations. Stimulation of renin release by dihydralazine increases the DA/NA ratio in arterial and renal venous blood indicating release of 'precursor dopamine' from noradrenergic fibres and/or activation of dopaminergic nerves. There seems to be a relationship between renal nerve activity and renin release in renin-dependent hypertension.

Adolescent↗
PubMed1990

Diabetes mellitus, the renin-angiotensin system, and angiotensin-converting enzyme inhibition.

Many traditional antihypertensive drugs are linked to various effects that may cause concern in the hypertensive diabetic patient. The favorable tolerability of angiotensin-converting enzyme (ACE) inhibitors in essential hypertension makes it likely that they will be well tolerated when used in diabetic patients. Data from ongoing studies support the theory that ACE inhibitors lower blood pressure to the same extent in hypertensive diabetics as in patients with essential hypertension. ACE inhibitors do not seem to affect glucose homeostasis adversely; they may even improve glucose tolerance to a small degree. The renal effects of ACE inhibitors in animal experiments suggest a renal-protective effect that can make them especially valuable.

Aldosterone↗
PubMed1990

Effect of acute vascular fluid volume expansion on erythrocyte sodium transport in essential hypertension.

Evidence exists that volume expansion is associated with the appearance of a circulating sodium transport inhibitor. We have evaluated intra-arterial blood pressure (BP), central venous pressure (CVP), plasma renin activity (PRA), intraerythrocyte sodium content, erythrocyte sodium influx and rate constant of sodium efflux in 10 untreated primary hypertensive men (WHO stages I and II). The investigations were done during baseline conditions and after rapid intravenous infusion of 1 litre of saline (0.9% NaCl solution) over 15-20 min. Volume expansion caused an increase in CVP by 6.0 +/- 0.5 cmH2O (p less than 0.01), while BP only exhibited a slight increase. No significant changes in intraerythrocyte sodium content, sodium influx, sodium efflux rate constant or PRA were found after volume expansion compared to baseline. All patients with low normal PRA experienced a decrease in sodium efflux rate constant after volume expansion. We found a positive correlation between baseline PRA and change in sodium efflux rate constant after volume expansion (r = 0.62, p less than 0.05). At baseline the relationship between PRA and intraerythrocyte sodium content nearly reached statistical significance (r = 0.63, p = 0.054). These results may indicate that acute volume expansion influences the release of a circulating factor, modulating sodium transport in low-renin hypertension.

Adult↗
PubMed1990

Angiotensin-converting enzyme inhibitors in diabetes: effect on the kidney and on blood pressure.

In diabetes mellitus, studies on the renin angiotensin system conflict. Among type I diabetic patients, we have found normal plasma renin activity and angiotensin II levels. In these patients, low-dose angiotensin II infusion resulted in the same effect on renal hemodynamics as that observed in healthy controls. In patients with diabetic nephropathy, a disease usually regarded as a low-renin condition, we have found elevated levels of plasma renin activity as compared with that seen in healthy persons and control subjects with other renal diseases that result in a similar degree of renal failure. In patients with diabetic nephropathy, interruption of the renin angiotensin system with angiotensin-converting enzyme inhibitors has been associated with a reduction in proteinuria. It is not clear whether this is a result of blood pressure reduction or a specific effect of these drugs. In a randomized trial with patients with diabetic nephropathy, we found that enalapril treatment reduced proteinuria to less than half the level obtained in a metoprolol-treated group during equally effective blood pressure control. In a long-term prospective study of captopril in patients with diabetic nephropathy, the rate of decline in kidney function was reduced to half the value that was calculated during a retrospective period. The renin angiotensin system, therefore, can be normally active in patients with diabetic nephropathy, and angiotensin-converting enzyme inhibitors can reduce proteinuria by mechanisms independent of their effect on blood pressure. Long-term treatment may protect renal function to a greater degree than might be expected from the blood pressure-lowering effect.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

Renal sensitivity to angiotensin II in type 1 diabetes.

The role of the renin angiotensin system for the regulation of kidney function in diabetes mellitus is uncertain. Results from studies in diabetic animals suggest that a reduced activity in this system contributes to the renal hyperperfusion and hyperfiltration in diabetes. The renal sensitivity to angiotensin II in diabetic patients is also unknown. Changes in renal hemodynamics were measured after infusion of two low doses of angiotensin II in ten young type 1 diabetic patients without complications and in ten healthy controls. The renin and angiotensin II levels were found to be the same in both groups. The baseline glomerular filtration rate was higher in the diabetics. During the highest angiotensin II dose, the 51Cr-EDTA and PAH clearance decreased 14 +/- 15 and 157 +/- 118 ml/min in the diabetics and 14 +/- 15 and 146 +/- 109 in the controls respectively. The changes in blood pressure and renal vascular resistance or sodium excretion did not differ between the groups. A malfunction of the renin angiotensin system is thus unlikely as a cause of the glomerular hyperfiltration in type 1 diabetes.

Adult↗
PubMed1989

Angiotensin converting enzyme inhibitors and progressive renal insufficiency. Current experience and future directions.

STUDY OBJECTIVE: To review the rationale for using angiotensin converting enzyme (ACE) inhibitors in progressive renal disease, and to evaluate the experience with these agents in patients with hypertension and renal insufficiency. DATA IDENTIFICATION: Experimental and clinical studies published from January 1977 to November 1988 were identified by searching the literature and by extensive hand searching of bibliographies of identified articles. STUDY SELECTION: Experimental studies of glomerular function during therapy with ACE inhibitors or other antihypertensive regimens were reviewed. Series using ACE inhibitors for treating hypertensive patients with renal disease were evaluated and reports of adverse events were studied. RESULTS OF DATA SYNTHESIS: Experimentally, ACE inhibitors seem to decrease glomerular injury by reducing both systemic and glomerular hypertension. Clinically, ACE inhibitors reduce systemic blood pressure in hypertensive patients with diabetic and nondiabetic renal disease without causing dramatic changes in glomerular filtration rate or renal blood flow. Most studies of nondiabetic renal insufficiency suggest that proteinuria is reduced in most patients. However, no long-term controlled study on the effect of ACE inhibitors on the progression rate of nondiabetic renal disease has been completed. ACE inhibitors have not yet been approved by the Food and Drug Administration (FDA) for treating or preventing progressive renal disease. Such use would therefore be considered "innovative" therapy. CONCLUSIONS: ACE inhibitors are tolerated by azotemic patients, although transient reductions in renal function can occur. Patients with bilateral renal insufficiency or low cardiac output are at increased risk for developing reversible acute renal insufficiency. Hyperkalemia may occur, particularly in patients with diabetes or severe renal insufficiency. In many patients with renal disease, ACE inhibitors dramatically reduce proteinuria, but whether they also reduce the rate of progression of renal disease remains unproved.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

Renal and hemodynamic effects of isradipine in essential hypertension.

Twenty-three men with essential hypertension participated in a double-blind placebo-controlled study with a crossover design to evaluate the long-term (nine weeks) effects of isradipine on central and renal hemodynamics. Isradipine as monotherapy was titrated from 2.5 to 5 and then to 7.5 mg twice daily. At the end of the crossover periods, cardiac output (dye-dilution) and intraarterial blood pressure were assessed. Compared with placebo, isradipine reduced ambulatory blood pressure from 174/104 to 154/91 (p less than 0.001), whereas the heart rate was unchanged. The reduction of blood pressure was entirely due to a reduction (36 percent; p less than 0.001) of the peripheral resistance. The baroreceptor sensitivity did not change (RR intervals during infusion of phenylephrine) but, with isradipine, the setpoint was shifted to lower blood pressure levels. Renal plasma flow (para-amino hippurate clearance) increased (465 versus 391 ml/minute; p less than 0.05), but glomerular filtration rate ([51Cr]ethylenediaminetetraacetic acid clearance) did not change. Hence, the filtration fraction decreased. With isradipine, there was a post-dose increase in natriuresis (0.45 to 0.34 mmol/minute; p = 0.06). Side effects were mild.

Antihypertensive Agents↗
PubMed1989

Blood pressure control and haemodynamic adaptation with the dihydropyridine calcium antagonist isradipine: a controlled study in middle-aged hypertensive men.

Twenty-three middle-aged men (59 +/- 2 years) with sustained, essential hypertension (WHO Stage II) and with diastolic blood pressure exceeding 100 mmHg during a run-in placebo month were included in a trial designed to assess the clinical and haemodynamic effects of isradipine, a novel dihydropyridine calcium antagonist. The study was double-blind with a placebo-controlled crossover design. Isradipine as monotherapy was titrated in three, 3-week periods in doses of 2.5, 5 and 7.5 mg twice daily, or as apparently identical placebo capsules. A 3-week placebo wash-out period separated the two phases of the study. Clinical characteristics were followed during each treatment phase and an invasive haemodynamic examination was performed on the last day of the final active or placebo dose. In the haemodynamic investigation, cardiac output was measured using a dye-dilution technique and blood pressure via a catheter in the brachial artery. Plasma renin activity (PRA) was assessed by radio-immunoassay of generated angiotensin I and arterial noradrenaline concentrations using high-performance liquid chromatography (HPLC). Baroreceptor sensitivity was calculated from R-R intervals of the ECG and beat-to-beat systolic blood pressure during increasing bolus injections of phenylephrine. During optimal therapy with isradipine (7.5 mg twice daily), highly significant decreases in supine systolic (from 174 +/- 4 to 154 +/- 3 mmHg) and diastolic blood pressures (from 104 +/- 2 to 91 +/- 1 mmHg) were observed. Heart rate was unchanged (79 +/- 3 versus 81 +/- 2 beats/min) during chronic therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1989

Pharmacokinetics of felodipine in patients with impaired renal function.

1. The pharmacokinetics of felodipine and its effects on blood pressure and heart rate were studied in eight male patients aged between 28 and 57 years with a glomerular filtration rate, GFR, between 8 and 68 ml min-1, following single i.v. and oral administration. 2. Clearance, Cmax, AUC, Vss and V, of felodipine were unaffected by the renal disease. The metabolite excretion (14C-labelled) was slower than in healthy subjects. Initial renal clearance of these metabolites correlated with individual GFR values. The total amount of the dose excreted in the urine was also decreased.

Administration, Oral↗
PubMed1988

Long-term followup of maximum concentrating ability and glomerular filtration rate in adult obstructed kidneys after pyeloplasty.

We investigated 34 patients with obstructed kidneys preoperatively and 8 to 10 years postoperatively concerning the separate glomerular filtration rate and maximum concentration ability. The mean glomerular filtration rate for the obstructed kidneys was approximately 10 per cent lower compared to that for the contralateral kidneys preoperatively and at followup. Although the mean value for obstructed kidneys was not improved at followup, kidneys with a decreased glomerular filtration rate preoperatively improved significantly after pyeloplasty. The maximum concentration ability was low preoperatively for the obstructed kidneys compared to the contralateral kidneys. The lowest maximum concentration ability was found in patients with a history of repeated upper urinary tract infections. At followup marked improvement was noted, which was most obvious for kidneys with severely reduced concentration ability preoperatively. However, the restoration was not total. There was a positive correlation between the improvement in glomerular filtration rate and improvement in maximum concentration ability.

Adult↗
PubMed1988

Low urinary calcium excretion in Bartter's syndrome.

The urinary calcium excretion has been determined in 19 patients with Bartter's syndrome and found to be significantly lower than the calcium excretion in 92 healthy subjects (1.16 +/- 0.82 vs. 4.36 +/- 2.71 mmol/24 h, p less than 0.001). There were no differences in height, weight, glomerular filtration rate, urinary sodium excretion or serum calcium concentration between the patients and the control subjects to account for the disparity in calcium excretion. In the patients, the concentrations for ionized calcium, PTH, 25-OH vitamin D and 1,25-(OH)2 vitamin D were normal. A low urinary calcium excretion appears to be a characteristic feature of Bartter's syndrome. The cause remains unexplained.

Adolescent↗
PubMed1988

Acute renal failure after analgesic drugs including paracetamol (acetaminophen).

Seven patients with acute renal failure after ingestion of analgesic drug combinations including paracetamol were seen. They presented with oliguric renal failure and restitution of renal function was complete. Only 2 patients had severe liver damage and 2 patients had no signs of liver abnormality. Renal biopsies, studied by light and electron microscopy, in 3 patients showed focal tubular epithelial cell necrosis. Focal vascular damage, predominantly of endothelial cells, was also present in all specimens. This vascular injury was found in various locations in the kidney, including the glomerular and peritubular capillaries and small arterioles. This suggests that microvascular damage is an important mechanism for the renal injury after analgesic drugs.

Acetaminophen↗
PubMed1988

Aspects of the role of intraglomerular pressure as a cause of progressive renal damage.

Renal damage in hypertension was thought to be a result of excessive renal arteriolar constriction leading to ischaemia and nephron damage. However, more recent studies have shown that in animal models the aetiology is one of increased intraglomerular pressure, and there is strong evidence that this is also the case in patients with essential hypertension. The problem is therefore one of inadequate constriction of afferent arterioles allowing increased systemic pressure to be transmitted to the glomerular capillaries. Since angiotensin II preferentially constricts the efferent arterioles, and since hypertensive patients have increased renovascular sensitivity to angiotensin II, this may explain why angiotensin-converting enzyme inhibitors are the only drugs which actually lower intraglomerular pressure and why they reduce renal damage in hypertensive disease.

Humans↗
PubMed1988

Renal function before and after withdrawal of long term antihypertensive treatment in primary hypertension.

Glomerular filtration rate (GFR) and renal plasma flow (inulin and para-aminohippurate clearance) were measured in a random sample of 17 normotensive and 20 untreated patients with primary hypertension. At the 7-year follow-up, 19 patients were on metoprolol (as the sole drug or in combination with either hydrochlorothiazide or hydralazine) and 1 patient was on hydrochlorothiazide. They were re-examined after withdrawal of treatment and return of hypertension. At the 7-year follow-up GFR was more reduced in the hypertensive (-17%) than in the normotensive group (-9%). The percentage decrease in renal blood flow was the same in both groups. No significant renal function changes appeared after withdrawal of treatment. In conclusion, there was a slightly greater deterioration in GFR in the hypertensive patients after long term treatment with metoprolol than can be explained by normal ageing.

Antihypertensive Agents↗