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Diabetes hypertension treatment, Az angiotenzinreceptor-blokkoló telmisartan kardiometabolikus hatásai | Semantic Scholar

Search Menu Abstract Background. Remikiren is an orally active renin inhibitor with established antihypertensive efficacy.

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As a single dose it induces renal vasodilatation, suggesting specific renal actions. Data on the renal effects of continued treatment by renin inhibition are not available, either in subjects with normal, or in subjects with impaired renal function.

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The effect of 8 days of treatment with remikiren mg o. Remikiren induced a significant peak fall in mean arterial pressure of Continued treatment with remikiren induced a sustained fall diabetes hypertension treatment blood diabetes hypertension treatment, renal vasodilatation, negative sodium balance, and a reduction in glomerular protein leakage. These data are consistent with a renoprotective potential of renin inhibition. When administered systemically, renin inhibitors reduce blood pressure in healthy volunteers and hypertensive patients more or less similarly to ACEi [ 4—7 ].

The renal haemodynamic actions of renin inhibitors so far have been consistent with a renoprotective potential.

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Remarkably, in accordance with earlier animal data [ 1516 ], the renal vasodilator response to renin inhibition was reported to exceed the response to ACE inhibition [ 17 ].

As the clinical application of renin inhibitors has been hampered by their low bioavailability, the experience with these compounds during maintenance treatment in man is very limited.

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No data are available thus far on the renal effects of continued treatment with remikiren, or on the renal effects of renin inhibition in patients with renal function impairment and proteinuria. In the present study, therefore, we report on the renal and systemic effects of continued treatment for 8 days the renin inhibitor remikiren in hypertensive patients with normal renal function, as well as in patients with impaired renal function and proteinuria.

Subjects and methods Patients and protocol Fourteen caucasian patients with mild to moderate hypertension diastolic blood pressure between 90 and mmHg were included. No other clinical relevant target organ damage was allowed.

All subjects gave their informed consent and the study was approved by the Ethical Committee of the Hospital. Median age of the patients was 53 years range 32— The median body mass index a cukorbetegség eloszlása ​​és kezelése baseline was Histological diagnoses were glomerulosclerosis 3 ; membranous glomerulopathy 2and IgA nephropathy 1.

Systolic blood pressure at entry was ±2 mmHg range — and diabetes hypertension treatment blood pressure was ±2 mmHg range 90— ; these values were similar for the essential hypertensives and the renal patients. In the essential hypertensives median albuminuria at entry was In the renal patients nephrotic range proteinuria was present, with a median of All antihypertensives had been withdrawn at least 3 weeks prior to the study, with the exception of one proteinuric patient in whom diuretic treatment was necessary.

The dose of the diuretic was kept constant throughout the protocol. This patient was excluded from the analysis of electrolyte balance. During hospitalization they received a diet containing 50 mmol sodium, mmol potassium, 60 g protein, and ml fluids daily. During this baseline period, stabilization of blood pressure, proteinuria, and electrolyte excretion was established.

Subsequently, remikiren treatment mg orally o. Blood pressure was measured daily between 11 and 12 a. Renal haemodynamic measurements were performed pretreatment and on the fifth day of remikiren treatment. On the first and the last treatment day timed blood samples were drawn for measurement of plasma renin activity PRAimmunoreactive renin irRand angII. For each hour the mean value was calculated. Urinary protein was measured by the pyrogallol red—molybdate method. This method has a coefficient of diabetes hypertension treatment of During analysis plasma was first separated from plasma proteins by ethanol extraction.

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The lower limit of detection is 3. Circulating levels of remikiren were determined by the radioinhibitor assay of Cumin et al.

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Glomerular filtration 1rate GFR and effective renal plasma flow ERPF were measured as the renal clearances of constantly infused [I]iothalamate and [I]hippuran respectively. Correction for urine collection errors was applied as described previously [ 19 ]. Values are normalized for body surface area. Data analysis Results are presented as means±SEM. Data sets that are not normally distributed are presented as medians and ranges. Data on hormonal responses, blood pressure, renal haemodynamics, and electrolyte balance are presented for all patients taken together.

Data on the responses of proteinuria and albuminuria are presented for the renal patients and the essential hypertensives separately. Results The efficacy of remikiren in diabetes hypertension treatment the RAS, as well as the drug levels, are shown in Figure 1. PRA fell maximally within 30 min after the first dose of remikiren and remained suppressed during the 12 h following.

After dosing, a further decrease to almost undetectable levels occurred. Remikiren plasma levels reached their peak within 30 min after oral administration both on the first median Cmax Remikiren was rapidly cleared from the plasma thereafter.

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It shows that MAP fell significantly, from ±2 to 96±2 mmHg. The effect on diurnal blood pressure profile is given in Figure 3. It shows that MAP is reduced throughout 24 h and that heart rate did not change. The fall in blood pressure was similar for systolic and diastolic blood pressure. This resulted in a trough to peak ratio of 0. The renal haemodynamic effects are shown for individual patients in Figure 4. Mean MAP was lowered from Remikiren diabetes hypertension treatment significant effects on the renal excretion of sodium and potassium Figure 5.

This negative sodium balance corresponded to a decrease in body weight of 0.

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During these 8 days, a transient fall in diabetes hypertension treatment was observed with a return to values not different from baseline as of day 4 Figure 5.

The effect of remikiren on proteinuria in the six renal patients is shown in Figure 6together with the effect on MAP in these patients.

H Pécs, Hungary. Patients and Methods: Forty-seven hypertensive patients who underwent transcutaneous CO2 therapy were enrolled. Thirty healthy individuals were recruited for the control group. Blood samples were taken one hour before, as well as one hour, 24 hours and 3 weeks after the first CO2 treatment. Controls did not undergo CO2 treatment.

Median baseline value was 5. In the essential hypertensive patients a reduction in renal protein leakage was found as well.

No significant effects on serum electrolytes, albumin or cholesterol were observed during treatment. Mean arterial pressure mean±SEM during baseline and 8 days treatment with remikiren, mg o. Discussion Continued treatment for diabetes hypertension treatment days with renin inhibitor remikiren induced distinct systemic as well as renal effects in hypertensive patients with normal and impaired renal function. A fall in blood pressure was observed that is sustained throughout the day.

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GFR was unchanged, resulting in a fall in FF. Finally, a net negative sodium balance was observed, associated with a positive potassium balance. This dissociation is in line with previous studies [ 20 ]. The peak drug levels immediately after dosing as well as the rapid clearance from the plasma therafter confirms the pharmacokinetic profile of remikiren, as described earlier [ 91121 ].

Experimental data have shown that remikiren levels in tissue exceed those in plasma [ 2223 ].

Az angiotenzinreceptor-blokkoló telmisartan kardiometabolikus hatásai

It has been hypothesized that the kidney is the main target tissue for remikiren and that retention of the drug sikerek diabétesz kezelésére this organ may provide a reservoir of drug within the body [ 23 ]. This would explain the sustained pharmacodynamic effects after single doses of remikiren despite undetectable plasma drug levels [ 8—10 ].

Thus it is likely, in spite of the low diabetes hypertension treatment bioavailability, that enough drug is available at the target level. We questioned whether an impaired renal function would lead to plasma accumulation of the drug. This in accordance with rapid biliary elimination of the drug, but does not rule out the possibility of higher tissue concentrations in patients with impaired renal function.

In line diabetes hypertension treatment the measurements of PRA and irR, this indicates efficacy throughout 24 h. A previous study in essential hypertensive patients [ 8 ] found a somewhat less pronounced blood pressure response with renin inhibition. Several factors could account for the more pronounced blood pressure response in our study. Whether this is due to pharmacokinetic factors i.

SUMMARY Metabolic syndrome is made up of a cluster of conditions including obesity, impaired insulin sensitivity, hypertension, and altered lipid profile. These conditions are also considered as risk factors for type 2 diabetes and cardiovascular disease.

Hormonal parameters were similar for the renal patients and the essential hypertensive patients, but this does not exclude differences in activity of tissue RAS. Our study is the first to provide data on the renal effects of continued treatment with renin inhibition.

This allowed an assessment of the effects on sodium and potassium balance.

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Remikiren induced a net negative sodium balance—in spite of the fall in blood pressure—and a concomitant positive potassium balance in both essential hypertensive and renal patients. The combination of sodium loss and potassium gain was also reported for ACE inhibition, and is usually attributed to a suppression of aldosterone.

The gradual return to baseline values of aldosterone after its initial decline—a feature that we have previously reported to occur with ACE inhibition as well [ 24 ]—presumably reflects stimulation of aldosterone by the positive potassium balance, as the persistently elevated PRA indicates an ongoing drug effect on RAS activity.

Diabetes and Blood Pressure: What To Know

Remikiren induced renal vasodilatation, with a significant rise in ERPF despite the fall in blood pressure. The renal haemodynamic profile, with a fall in FF, suggests that efferent cukorbetegség 1 típusú kezelés a hónapban vasodilatation predominates over afferent vasodilatation.

Such renal vasodilatation may well have facilitated renal sodium diabetes hypertension treatment. Interestingly, this renal profile occurred irrespective the presence of renal functional impairment. In renal patients this renal haemodynamic profile may contribute diabetes hypertension treatment long term renoprotection [ 26 ]. However, diabetes hypertension treatment study design does not allow the conclusion that the antiproteinuric effect is specifically due to RAS blockade, as the lower blood pressure may have played a role.

Could there be advantages of renin inhibition as compared to other modes of RAS blockade? However, we only treated for 8 diabetes hypertension treatment, whereas it takes approximately 4 weeks before the maximum antiproteinuric effect of ACEi and AT1 blockade is reached [ 29 ].

It would be of interest, therefore, to investigate whether more prolonged renin inhibition would further reduce proteinuria. Moreover, it might be of interest to investigate whether additive therapy with renin inhibition could provide a strategy to circumvent treatment resistance to ACE inhibition or AT1 blockade by precluding the reactive rise in renin activity with those modes of RAS blockade [ 30 ].

In conclusion, continued treatment with remikiren reduces blood pressure in hypertensive patients with normal and impaired renal function.

The precise mechanism of the renoprotective action of RAS blockade is still incompletely known. Whereas the clinical application of renin inhibitors has been hampered by their poor bioavailability, the data presented here suggest that renin inhibition can be a useful tool to unravel the mechanisms of the renoprotective action of RAS blockade.

Fischli, and Mw G.