[Hypertensive crises].
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Antihypertensive Agents↗
Biomedical subjects
S Strandgaard
Publications and source records attributed to S Strandgaard.
The influence of angiotensin-converting enzyme inhibition on renal tubular function in progressive chronic nephropathy.
The influence of angiotensin-converting enzyme (ACE) inhibition on renal tubular function in progressive chronic nephropathy was investigated in 69 patients by the lithium clearance (C(Li)) method. Studies were done repeatedly for up to 2 years during a controlled trial on the effect of enalapril on progression of renal failure. The pattern of proteinuria was followed over the first 9 months. At baseline, the glomerular filtration rate (GFR) was 5 to 68 mL/min. Absolute proximal tubular reabsorption rate of fluid (APR), estimated as the difference between GFR and C(Li), was 1 to 54 mL/min. Calculated fractional proximal reabsorption (FPR) was moderately subnormal. During the study, GFR decreased and sodium clearance was unchanged; fractional excretion of sodium therefore increased. In the group of patients randomized to treatment with enalapril (n = 34), GFR at 1 month was 83% (P < 0.001) and C(Li) was 88% (P < 0.01) of the baseline values, APR and FPR had not changed significantly, and potassium clearance was significantly decreased. Through the rest of the study period, APR remained nearly unchanged and FPR even increased in the enalapril group. In the group of patients randomized to treatment with conventional antihypertensive drugs (n = 35), C(Li) was unchanged until severe reduction in GFR, APR and FPR decreased gradually, and potassium clearance was almost unchanged. These differences in tubular function between the two treatment regimens were significant (P < 0.05). An unchanged or increased APR in either treatment regimen was associated with a long-term slower progression of renal failure. Over 9 months, the 24-hour fractional clearance of albumin decreased in the ACE inhibitor group (P < 0.01), whereas the clearances of immunoglobulin G and retinol-binding protein were unchanged in this group. In the conventional group, the fractional clearances of these three plasma proteins all increased. It is concluded that in progressive chronic nephropathy ACE-inhibitor treatment was associated with different adaptive tubular changes in the handling of sodium, water, and protein compared with conventional antihypertensive therapy. During ACE inhibition, the reabsorptive capacity of the proximal tubule appeared to be better preserved, which might be of importance for the beneficial effect of this treatment in chronic renal disease.
Absorption↗
Endogenous versus exogenous lithium clearance for evaluation of dopamine-induced changes in renal tubular function.
1. The present randomized, double-blind cross-over study compared endogenous and exogenous lithium clearance (CLi) for estimation of the effect of dopamine on tubular sodium reabsorption. Twelve normal, salt-repleted male subjects were investigated on three different occasions with either placebo or 450 mg or 600 mg of lithium given in random order at 22.00 hours. After an overnight fast, renal clearance studies were performed during a 1 h baseline period and subsequently during the second hour of an infusion of 3 micrograms min-1 kg-1 of dopamine. 2. Baseline values of endogenous CLi and fractional excretion of lithium (FELi) [27.0 (23.5-30.5) ml/min and 24.2 (20.3-28.2)% (means with 95% confidence interval)] were lower than exogenous values [lithium, 450 mg: 32.7 (29.9-35.4) ml/min (P < 0.05) and 27.4 (25.2-29.6)% (P < 0.05); lithium, 600 mg: 33.4 (29.2-37.6)ml/min (P < 0.05) and 28.6 (26.3-31.0)% (P < 0.01)]. Both test doses of lithium increased the baseline sodium clearance (CNa), but glomerular filtration rate and urine flow rate remained unchanged. 3. Dopamine increased CNa to similar values on the three study days. CLi increased to 40.9 (35.5-46.5) ml/min (endogenous lithium, P < 0.001), 43.2 (40.8-45.6) ml/min (450 mg of lithium, P < 0.01) and 44.9 (41.3-48.4) ml/min (600 mg of lithium, P < 0.001), respectively. FELi increased to 32.2 (27.5-37.0)% (P < 0.01), 35.4 (33.0-37.7)% (P < 0.01) and 35.9 (32.8-38.9)% (P < 0.01), respectively. Values during dopamine infusion did not differ significantly. 4. The lower baseline values of endogenous CLi and FELi compared with exogenous values suggest that CLi in humans depends on the plasma concentrations of lithium. However, the effect of dopamine on CLi and FELi was expressed to the same extent with endogenous and exogenous lithium, indicating that the two methods are interchangeable for estimation of dopamine-induced changes in tubular function.
Adult↗
Effects of the prostacyclin analogue iloprost on cyclosporin-induced renal hypoperfusion in stable renal transplant recipients.
BACKGROUND: The synthetic prostacyclin analogues have been proposed to protect against cyclosporin A (CsA) nephrotoxicity. The present study investigated the effect of infusion of the prostacyclin analogue iloprost on the acute CsA-induced renal hypoperfusion and hypofiltration in stable renal-transplant recipients. METHODS: The study included 10 stable renal-transplant recipients with good graft function (s-creatinine 90-170 micromol/l). Renal function and the acute renal haemodynamic and tubular response to an oral CsA-dose (Sandimmun Neoral, 3 mg.kg-1) were investigated with an infusion of iloprost (1 ng.kg-1.min-1) or placebo on 2 separate days. After an overnight fast, seven 30-min renal clearance periods were performed, two before infusion, three during infusion, and two recovery periods. An additional control clearance study without CsA intake or iloprost/placebo infusion was done in eight of the patients. RESULTS: CsA ingestion decreased ERPF and GFR significantly with a maximum decline at the end of the clearance study. Iloprost infusion abolished the CsA-induced decrease in ERPF, but had no effect on the CsA-induced decrease in GFR, leading to a significant decline in FF. Renal clearance of lithium (CLi)), used as an index of proximal tulbular outflow, decreased in parallel with GFR after CsA intake, with no additional effects of iloprost. Iloprost infusion decreased blood pressure and increased heart rate. CONCLUSION: Infusion of iloprost causes systemic and renal vasodilation, but has no effect on the CsA-induced decrease in GFR and CLi in stable renal transplant recipients.
Adult↗
Hypertension and stroke.
HYPERTENSION AND STROKE: Hypertension is a major risk factor for stroke, and stroke prevention is the most important achievement of modern antihypertensive treatment. In controlled trials, a few years of this treatment can eliminate the entire excess stroke risk associated with hypertension. In observational studies, stroke risk appears to be not always fully reversible when the blood pressure is lowered with drugs. Hypertension is associated with an increased incidence of both haemorrhagic, ischaemic and lacunar stroke. It is likely that antihypertensive treatment prevents all these types of strokes as well as transient ischaemic attacks. ACUTE STROKE: In acute stroke, a transient rise in blood pressure is common, in some cases superimposed on chronic hypertension. No major controlled trials have reported findings on whether blood pressure should be lowered acutely in such patients. On the basis of observational studies and haemodynamic considerations, it seems prudent to leave all but the highest blood pressures in acute stroke to settle spontaneously. ISCHAEMIC STROKE: Ischaemic stroke may occasionally be precipitated by overzealous blood pressure reduction. This has been reported in particular in the initial treatment of very severe hypertension, and occasionally in the elderly hypertensive. It may also occur in the rare cases where transient cerebral ischaemia is haemodynamically induced.
Antihypertensive Agents↗
Antihypertensive drugs and cerebral circulation.
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Angiotensin II↗
Marked hepatotoxicity associated with losartan treatment.
Losartan represent a novel approach in the treatment of hypertension. Clinical trials have reported a very low incidence of side effects. We describe two patients who developed increases in alanine/aspartate amino transferase of 8 and 15 times the upper normal limit, as well as thoracic pain, after a short time of treatment with losartan. The increase resolved after discontinuing losartan treatment.
Angiotensin Receptor Antagonists↗
Brief report: acute renal failure after losartan treatment in a patient with bilateral renal artery stenosis.
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Acute Kidney Injury↗
Insulin resistance and hyperinsulinaemia in mild to moderate progressive chronic renal failure and its association with aerobic work capacity.
Tissue sensitivity to insulin and aerobic work capacity was measured in patients with mild to moderate progressive chronic renal failure. Twenty-nine non-diabetic patients with a glomerular filtration rate of 25 ml.min-1.1.73 m-2 (11-43) (median, range) and 15 sex, age, and body mass index matched control subjects with normal renal function were studied. Fasting blood glucose was comparable and in the non-diabetic range in the two groups as was the oral glucose tolerance test. Patients demonstrated hyperinsulinaemia both during fasting (p < 0.01) and during the test (p < 0.02). The tissue sensitivity to insulin, expressed by the amount of glucose infused during the last 60 min of a 120-min hyperinsulinaemia euglycaemic clamp (M-value) and the M/I ratio, was significantly lower in the patients than in the control subjects (M-value 404 +/- 118 vs 494 +/- 85 mg glucose/kg body weight, p < 0.02) (M/I ratio 1.77 +/- 0.71 vs 2.57 +/- 0.70 (mg/(kgBW.min) per pmol/l.100, p < 0.001). The maximal aerobic work capacity was significantly lower in the patients than in the control subjects (24 +/- 8 vs 32 +/- 11 ml O2/(kg body weight.min), p < 0.02) and positively correlated to the M-value and the M/I ratio in both groups. In conclusion, not only patients with end-stage chronic renal failure but also those with mild to moderate progressive chronic renal failure are insulin resistant and hyperinsulinaemic. The tissue sensitivity to insulin is correlated to the maximal aerobic work capacity suggesting that these patients might benefit from physical training programmes.
Adult↗
Cerebral blood flow in untreated and treated hypertension.
Cerebral blood flow (CBF) is the same in hypertensive and normotensive man without neurological deficit. Chronic hypertension shifts the lower and upper blood pressure limits of CBF autoregulation towards higher pressure. Acute blood pressure reduction will lower CBF only if the pressure is taken below the lower limit of autoregulation. Added to this, some drugs are cerebral vasodilatators and have the potential for paralysing autoregulation and raising intracranial pressure, an effect also seen with at least some calcium antagonists. Converting enzyme inhibitors improve autoregulation during hypotension, probably by releasing angiotensin II dependent tone in the larger cerebral resistance vessels. With chronic antihypertensive treatment, CBF autoregulation may re-adapt towards normal. Converting enzyme inhibitors when given chronically probably retain their beneficial effect on the lower limit of autoregulation. Apart from this, it is uncertain whether there are chronic pharmacological effects of antihypertensive drugs directly on the cerebral circulation.
Antihypertensive Agents↗
Urinary excretion of epidermal growth factor in living human kidney donors and their recipients.
Epidermal growth factor (EGF) is a growth-promoting peptide that is synthesized in the distal tubules of the kidney and excreted in urine. EGF has been suggested to play a role in the repair after renal tissue damage, as well as in compensatory growth of the remaining kidney after uninephrectomy. The present study examined the urinary EGF excretion after uninephrectomy and transplantation among relatives. The urinary EGF excretion rate and the glomerular filtration rate (GFR) were followed for 26-54 days in 16 healthy kidney donors and nine recipients. After uninephrectomy the median urinary EGF excretion rate in the donors was not 50% of the pre-operative value, but around 65% (95% confidence limits of the median on the fifth post-operative day: 59-72%). This suggests that there is a compensatory increase in the EGF excretion rate from the remaining kidney of around 30% after uninephrectomy. A similar compensatory increase was demonstrated for GFR, indicating that the compensatory changes in EGF excretion rate and GFR might be correlated. In the transplanted kidneys, GFR was consistently around 15% lower and EGF excretion rate around 40% lower than in the corresponding kidneys remaining in the donors. This might reflect ischaemic and drug-induced damage of the transplanted kidneys. The present study demonstrated a compensatory increase of around 30% in urinary EGF excretion from the remaining kidney after uninephrectomy in healthy humans. Whether EGF plays a role in the adaptive processes in the remaining kidney or whether changes in EGF excretion are merely of a secondary nature is still uncertain.
Adult↗
Hypertension and left ventricular hypertrophy in patients with spontaneous subarachnoid hemorrhage.
One hundred eighteen consecutive cases of spontaneous subarachnoid hemorrhage seen at one hospital during a 3-year period were examined to assess the prevalence of hypertension and the correlation between the presence of hypertension and the risk of early death. Eighty-seven of the patients had intracerebral aneurysms. The diagnosis of hypertension was determined by means of three complementary criteria: a history of treatment with antihypertensive drugs; systolic and/or diastolic blood pressure levels > or = 160 and 95 mm Hg, respectively, measured by the general practitioners of the patients before the onset of the subarachnoid hemorrhage; and the presence of left ventricular hypertrophy determined by echocardiography and/or necropsy. The major findings were as follows: 1) hypertension was present in at least 41% of the patients; 2) in 37% of 51 patients with no history of hypertension before the hemorrhage, left ventricular hypertrophy was diagnosed; and 3) the frequency of hypertension and left ventricular hypertrophy was significantly higher in patients who died within 14 days after the bleeding episode compared with patients surviving this period.
Adolescent↗
No effect of dietary fish oil on renal hemodynamics, tubular function, and renal functional reserve in long-term renal transplant recipients.
Dietary supplementation with fish oil rich in n-3 polyunsaturated fatty acids has been suggested to protect the kidney against cyclosporin A (CsA) toxicity. This study investigated the effects of a 10-wk dietary supplementation with fish oil on renal function and renal functional reserve in healthy volunteers (N = 9) and two groups of stable long-term kidney-transplanted patients treated with maintenance low-dose CsA (3.0 +/- 0.6 mg/kg; N = 9) or without CsA (N = 9). After an overnight fast, the subjects were water loaded, and clearance studies were performed, postponing morning medication. GFR and effective RPF were measured as the renal clearances of (99mTc)DTPA and (131I)hippuran, respectively. Renal tubular function was evaluated by use of the renal clearance of lithium and the urinary excretion of beta 2-microglobulin. Fish oil did not change baseline values of effective RPF, GFR, lithium clearance, and urinary excretion of beta 2-microglobulin in any of the groups. The infusion of amino acids induced a comparable increase in GFR, lithium clearance, and the urinary excretion rate of beta 2-microglobulin in all three groups with no additional effect of fish oil. Thus, long-term renal transplant recipients treated with a low maintenance dose of CsA had a well-preserved renal functional reserve, and dietary supplementation with fish oil in these patients did not improve renal function.
Adult↗
Vascular endothelial cell function and cardiovascular risk factors in patients with chronic renal failure.
Cardiovascular risk factors and markers of endothelial cell function were studied in nondiabetic patients with mild to moderate chronic renal failure. The transcapillary escape rate of albumin and the plasma concentrations of von Willebrand factor, fibrinogen, and plasma lipids were measured in 29 nondiabetic patients (GFR of 25 (11-44) mL/min x 1.73 m2 (median and range)) and 14 normal subjects. The proportion of smokers was similar between the groups. In the patients, the plasma concentration of von Willebrand factor was elevated by 61% (1.27 +/- 0.44 versus 0.79 +/- 0.28 U/mL; P < 0.01) (mean +/- SD) and that of fibrinogen was elevated by 72% (10.18 +/- 4.14 versus 5.92 +/- 2.01 mumol/L; P < 0.01). The plasma concentrations of lipoproteins showed an atherogenic pattern in the patients with increased levels of very low-density lipoprotein cholesterol (0.57 +/- 0.31 versus 0.33 +/- 0.13 mmol/L; P < 0.01) and triglycerides (1.26 +/- 0.25 versus 0.71 +/- 0.28 mmol/L; P < 0.01), but a decreased level of high-density lipoprotein cholesterol (1.23 +/- 0.33 versus 1.46 +/- 0.35 mmol/L; P < 0.05). Total cholesterol and low-density lipoprotein cholesterol were similar in the groups. The observed differences were further aggravated among smoking patients, particularly with respect to von Willebrand factor and triglycerides. The transcapillary escape rate of albumin was similar in the patients and the controls and was not correlated to the level of albuminuria.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Late outcome of a controlled trial of enalapril treatment in progressive chronic renal failure. Hard end-points and influence of proteinuria.
An earlier controlled trial showed that over an average of 26 months, enalapril slowed the progression of chronic renal failure. Following completion of the trial, the patients continued to receive antihypertensive treatment according to ordinary clinical criteria. All but four patients in the enalapril group remained on that drug, and two patients in the control group were switched to an angiotensin-converting enzyme (ACE) inhibitor. In the present study the fate of the 70 patients 44 months after termination of the trial was investigated, with a total follow-up of around 7 years. In the original enalapril group, 12 of the 35 patients (34%) were alive without renal replacement therapy versus five of the 35 patients (14%) in the control group. This difference of 20% in favour of having been in the enalapril group in the original trial was significant (P = 0.05; 95% confidence limits 0.5-39.5%). The influence of baseline proteinuria on clinical outcome was analysed. In the original control group, baseline renal clearances of albumin (Calb) and immunoglobulin G (CIgG) were significantly lower in patients surviving without renal replacement therapy at follow-up than in patients who ultimately developed end-stage renal failure (ESRF) (P < 0.05). In the original enalapril group, these baseline clearances were equal in the two renal outcome groups. In all patients, baseline Calb and CIgG were negatively correlated with the rate of change in GFR during the controlled trial (r = -0.37, P < 0.01 and r = -0.28, P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Angiotensin II receptor antagonist CV-11974 and cerebral blood flow autoregulation.
OBJECTIVE: To investigate whether the angiotensin II (Ang II) subtype 1 receptor (AT1) antagonist CV-11974 had a similar effect to angiotensin converting enzyme inhibitors on cerebral blood flow autoregulation in normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). METHODS: Sixteen WKY rats and 16 SHR were given CV-11974 0.1 mg/kg intravenously and compared with two control groups (n = 16). Their cerebral blood flow was measured with the intracarotid xenon-133 injection method and blood pressure was raised by noradrenaline infusion and lowered by controlled haemorrhage in separate groups of rats. The limits of autoregulation were determined by computed least-sum-of-squares analysis. RESULTS: The dose of CV-11974 given lowered blood pressure but did not influence baseline cerebral blood flow. In WKY rats the lower limit of autoregulation in control rats was 60 +/- 3 mmHg, whereas after CV-11974 administration it was 48 +/- 2 mmHg (P < 0.01). In SHR the corresponding values were 85 +/- 2 and 78 +/- 2 mmHg, respectively (P < 0.05). In WKY rats the upper limit of autoregulation in control rats was 144 +/- 5 mmHg, whereas after CV-11974 administration it was 126 +/- 7 mmHg (P < 0.05). In SHR the corresponding figures were 174 +/- 8 and 144 +/- 6 mmHg, respectively (P < 0.01). CONCLUSION: Thus, the AT1 receptor antagonist, although it did not influence baseline cerebral blood flow, shifted the autoregulation curve towards lower blood pressure. This effect is similar to that of angiotensin converting enzyme inhibitors, and might be due to release of Ang II-dependent tone in the larger cerebral resistance vessels.
Angiotensin II↗
Cerebrovascular damage in hypertension.
Hypertension causes marked adaptive changes in the cerebral circulation. The excess risk of stroke associated with hypertension is eliminated in controlled trials of antihypertensive treatment. Such treatment may even prevent transient ischaemic attacks in the elderly. In rare cases, overzealous antihypertensive treatment may cause cerebral ischaemia, especially in the initial treatment of very severe hypertension. Headache may occasionally be caused by severe hypertension, which may also lead to the rare syndrome of acute hypertensive encephalopathy. Finally, the importance of white-matter lesions, or leukoaraiosis, in hypertension is not yet fully established.
Aged↗
Fish oil and cyclosporin A-induced renal hypoperfusion in kidney-transplanted patients.
BACKGROUND: Dietary supplementation with fish oil has been said to improve renal function in cyclosporin A (CsA)-treated subjects. METHODS: Renal function and the acute renal haemodynamic and tubular response to an oral CsA-dose (3 mg/kg) were investigated before and after 12 weeks of fish oil supplementation (6 g/day) in 12 low-dose CsA-treated kidney-transplanted patients (s-creatinine, 124 +/- 24 mumol/l, mean +/- SD). After an overnight fast, ten l-h renal clearance periods were performed, two periods before and eight after CsA-ingestion. An additional control clearance study without CsA intake was performed in six subjects. RESULTS: Fish oil did not change baseline values of the effective renal plasma flow (ERPF) or the glomerular filtration rate (GFR). Compared to the control study, CsA decreased GFR and ERPF significantly on average 20 +/- 3% (P < 0.01) and 23 +/- 3% (P < 0.01) respectively, 4-6 h after peak CsA blood concentration with no additional effect of fish oil. CsA also significantly decreased the renal clearance of lithium, used as an index of proximal tubular outflow, with no impact of dietary fish oil. CONCLUSION: Fish oil supplementation had no effect on baseline renal function or CsA-induced hypoperfusion in stable renal transplant recipients treated with a low maintenance dose of CsA.
Adult↗