Search PubMed⌕ Search

Biomedical subjects

L M Ruilope

Publications and source records attributed to L M Ruilope.

At least 145 records · Page 8Linked to original sources
PubMed1993

Natriuretic effects of dopamine agonist drugs in models of reduced renal mass.

In addition to recognized neurotransmitter properties in the central nervous system, dopamine (DA) plays a role in the physiological activity of the kidney through its hemodynamic and natriuretic effects. On the basis of these data, some pharmacological interventions have focused their attention on the use of DA-related drugs to improve renal sodium handling. We summarize the data obtained from two studies using two DA agonist drugs, lisuride (LIS) and fenoldopam (FEN), in two situations of reduced renal mass. During an intravenous sodium load performed on 10 uninephrectomized dogs, LIS induced a significant blockade of the concomitant pressor response, estimated by lower blood pressure and norepinephrine levels. Under these same conditions, FEN significantly decreased blood pressure and elevated the natriuretic response. In a second study, when FEN was administered at nonhypotensive doses to chronic renal failure patients, it evoked an enhancement of diuresis, natriuresis, and creatinine clearance. These data seem to confirm the involvement of DA in the regulation of cardiovascular homeostasis and its role in renal sodium handling. Furthermore, these beneficial effects support the use of DA-related drugs in the field of hypertension.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1993

Clinical relevance of proteinuria and microalbuminuria.

Proteinuria (protein excretion > 300 mg/d) is an independent risk factor for the development of cardiovascular disease and renal failure. The finding of persistent proteinuria in otherwise asymptomatic patients often precedes the development of arterial hypertension and renal failure. When proteinuria is accompanied by arterial hypertension, blood pressure control can decrease the quantity of protein excretion but not the incidence of proteinuria. In this sense, converting enzyme inhibitors seem to possess a higher capacity to reduce proteinuria. Nevertheless, the effects of reducing proteinuria on renal function and cardiovascular risk remain to be elucidated. Microalbuminuria (urine albumin excretion oscillating between 30 and 300 mg/d) seems to be a predictor of cardiovascular disease in diabetic and nondiabetic subjects and has been established as a predictor for the development of diabetic nephropathy. Blood pressure levels and urinary albumin excretion correlate positively, and antihypertensive therapy of any kind decreases the quantity of albumin present in the urine. The role of increased albumin excretion in essential hypertension and in renal failure remains to be elucidated.

Albuminuria↗
PubMed1993

Exogenous cGMP prevents decrease in diuresis and natriuresis induced by inhibition of NO synthesis.

We previously demonstrated that the intravenous infusion of the specific inhibitor of nitric oxide (NO) synthesis, NG-nitro-L-arginine methyl ester (L-NAME), over a period of 60 min elevates mean arterial pressure (MAP) and reduces renal hemodynamics and excretory function. The objective of the present study was to determine the ability of a guanosine 3',5'-cyclic monophosphate (cGMP) analogue, 8-bromo-cGMP (8-BrcGMP), in preventing the increase in MAP and the reductions in renal plasma flow (RPF), glomerular filtration rate (GFR), urine flow (UV), and sodium excretion rate (UNaV) induced by intravenous infusion of L-NAME in rats. As expected, the infusion of L-NAME (50 micrograms.kg-1.min-1) increased (P < 0.05) MAP and reduced (P < 0.05) RPF, GFR, UV, and UNaV. The administration of 8-BrcGMP (100 micrograms.kg-1.min-1) and L-NAME resulted in no change in MAP, RPF, and GFR. However, decreased (P < 0.05) UV and UNaV were still observed. When 8-BrcGMP (200 micrograms.kg-1.min-1) and L-NAME were infused together, no significant changes in MAP or in renal function were observed. To prove the specificity of the 8-BrcGMP preventive effects, dibutyryl cAMP (200 micrograms.kg-1.min-1) and L-NAME (50 micrograms.kg-1.min-1) were infused together. Under these conditions, MAP, RPF, GFR, UV, and UNaV were modified in a manner similar to that observed during the infusion of L-NAME.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

The kidney and arterial hypertension.

It has been known for some time that a relationship exists between the kidney and blood pressure. The renal origin of arterial hypertension has been demonstrated in different animal models resembling human hypertension, with data from humans seeming to confirm this hypothesis. On the other hand, the renal vasculature also suffers the consequences of arterial hypertension, and renal insufficiency can develop as a result of elevated blood pressure levels. Antihypertensive therapy can prevent the development of renal damage secondary to hypertension. For example, calcium antagonists possess specific renal effects that not only facilitate their antihypertensive capacity but also protect the kidney from the development of renal failure.

Animals↗
PubMed1993

Antihypertensive effect of nitrendipine in the hypertensive patient with renal impairment.

Calcium antagonists exert several characteristic effects on the kidney that potentiate their antihypertensive effect. The objective of the present study was to investigate the effectiveness of nitrendipine in the presence of different degrees of renal impairment. Two groups of hypertensive patients were included in the study. Group 1:10 patients with arterial hypertension secondary to chronic renal parenchymatous disease and adequately controlled with a diuretic and/or a beta-blocker who were switched to nitrendipine. These patients were then followed monthly for 1 year. Group 2:24 patients diagnosed as having essential hypertension who presented values of urinary albumin excretion above 30 mg/day after a minimum of 3 years of adequate blood pressure control with a diuretic and/or a beta-blocker. Patients were randomly assigned to continue with the same therapy or to switch to nitrendipine for 1 year. In both groups nitrendipine was as efficacious as standard therapy for controlling blood pressure and did not induce changes in renal hemodynamics. Nitrendipine did not modify the level of proteinuria in group 1, nor the urinary excretion of albumin in group 2. These results seem to indicate that nitrendipine can be safely used in patients with arterial hypertension and different degrees of renal function impairment.

Adult↗
PubMed1993

Angiotensin-converting enzyme inhibitors in the treatment of mild arterial hypertension.

Angiotensin-converting enzyme inhibitors are nowadays widely employed for the treatment of arterial hypertension. They exhibit comparable levels of efficacy and better tolerability when compared with the other antihypertensive agents. In mild arterial hypertension they have been shown to be more efficacious than nonpharmacological therapy that is recommended as the first-step therapeutic approach for most cases of this type of hypertension. Potential advantages for the control of associated metabolic risk factors and specific renal and cardiac effects make these drugs suitable for the first step pharmacological therapy on mild hypertension.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Influence of salt intake on the antihypertensive effect of carvedilol.

AIM: To investigate whether moderate sodium restriction can increase the proven antihypertensive effect of carvedilol, a newly developed beta-blocker with vasodilating properties. METHOD: A randomly allocated double-blind crossover in 19 patients. RESULTS: Lowering dietary salt increased the fall in blood pressure obtained with carvedilol.

Adrenergic beta-Antagonists↗
PubMed1993

Lipophilic dihydropyridines provide renal protection from cyclosporin toxicity.

AIM: To review cyclosporin nephrotoxicity and its prevention by calcium antagonists. METHOD: Review of published and unpublished studies. RESULTS: Cyclosporin A nephrotoxicity is the most important side effect of this potent immunosuppressive drug. Several mechanisms have been implicated in the production of this adverse effect but elevated endothelin release is perhaps the most frequently cited cause. Calcium antagonists have demonstrated a beneficial effect in preventing cyclosporin A nephrotoxicity in renal cadaveric transplants, during both short- and long-term follow-up. Lacidipine, a lipophilic dihydropyridine calcium antagonist, prevents the reductions in the glomerular filtration rate and renal plasma flow that are often seen after cyclosporin A administration. This effect is not related to endothelin suppression. CONCLUSIONS: Calcium antagonists can provide renal protection in patients who undergo renal cadaveric transplantation and are treated with cyclosporin.

Antihypertensive Agents↗
PubMed1993

Kidney and aetiology, pathology and management of essential hypertension.

The existence of a relationship between the kidney and arterial hypertension has long been known. Renal participation in the development of arterial hypertension has been clearly shown in different animal models that mimic human essential hypertension. Some data obtained in hypertensive humans also seem to support the prevalence of the kidney in the initiation of this particular type of arterial hypertension. On the other hand, renal vasculature can also suffer the consequences of essential hypertension and, as a result, chronic renal failure can develop. The role of antihypertensive therapy in preventing renal damage has been sufficiently addressed. However, investigation of the potential for facilitating the antihypertensive capacity of drugs through their renal effects and investigation of the differing abilities of particular groups of antihypertensive agents to prevent or slow the progression of renal damage constitutes a challenge for future research.

Animals↗
PubMed1992

Long-term beneficial effects of angiotensin-converting enzyme inhibition in patients with nephrotic proteinuria.

Angiotensin-converting enzyme inhibitors (ACEI) can reduce proteinuria in diabetic and nondiabetic nephropathy. However, no studies have determined whether this antiproteinuric effect modifies the progression of renal insufficiency. We studied the evolution of 46 nondiabetic patients with nephrotic proteinuria treated with captopril for a minimum of 12 months. The follow-up period before captopril treatment was 12 to 18 months. At the end of follow-up, after captopril introduction (24.4 +/- 7.6 months), proteinuria had decreased from 6.3 +/- 2.5 to 3.9 +/- 3.1 g/24 h (P less than 0.001), with a mean decrease of 45% +/- 28%. The proteinuria decrease was higher in patients with reflux nephropathy, proteinuria associated with reduction of renal mass, inactive crescentic glomerulonephritis, nephroangiosclerosis, and IgA nephropathy, whereas patients with membranous glomerulonephritis and idiopathic focal glomerulosclerosis showed a poorer response. Patients were separated according to a proteinuria reduction greater (group A, 23 patients) or lower (group B, 23 patients) than 45% of the initial value. At the end of follow-up, renal function had not significantly changed in group A with respect to values at the start of treatment: serum creatinine (SCr) was 229 +/- 167 mumol/L (2.6 +/- 1.9 mg/dL) versus 203 +/- 97 mumol/L (2.3 +/- 1.1 mg/dL), and creatinine clearance (CrCl) was 0.80 +/- 0.52 mL/s (48 +/- 31 mL/min) versus 0.87 +/- 0.47 mL/s (52 +/- 28 mL/min). The slope of the reciprocal of Scr (1/SCr) showed a significantly beneficial change after captopril introduction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Additive antiproteinuric effect of converting enzyme inhibition and a low protein intake.

The hypothesis that converting enzyme inhibition and a protein-restricted diet could have additive antiproteinuric effects has been tested. A group of 17 patients with proteinuria in excess of 3 g/24 h per 1.73 m2 of body surface area were submitted to a 3-wk period of study, after a 4-wk wash-out period during which protein intake was 1.0 g/kg per day and in the absence of any medication. During the first and second weeks of the study, protein intake was lowered to 0.3 g/kg per day, and in the third week, it returned to 1.0 g/kg per day. Enalapril (20 mg daily) was administered during the second and third weeks of the study. Initially and at the end of each week thereafter, we determined blood pressure, GFR (inulin clearance), RPF (para-aminohippurate clearance), plasma sodium and potassium, PRA and aldosterone, and the 24-h urine excretion of sodium potassium, protein, and urea. The low protein intake during the first week induced a significant fall of proteinuria (P < 0.01), GFR (P < 0.01), and RPF (P < 0.01) in the absence of changes in filtration fraction. The addition of enalapril induced a further decrease of proteinuria (P < 0.01) and a fall in filtration fraction (P < 0.05), whereas plasma potassium, PRA, GFR, and RPF values increased (P < 0.01). The rise in protein intake during the last week of the study induced a significant rise in proteinuria, GFR, and RPF (P < 0.01), although the first of these parameters attained values significantly lower (P < 0.05) than those observed initially.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Sodium intake does not influence the effect of verapamil in hypertensive patients with mild renal insufficiency.

Information is limited regarding the efficacy of antihypertensive drugs in patients with hypertension associated with renal insufficiency. To address this question, a group of 14 outpatients with essential hypertension and mild renal insufficiency received slow release verapamil 240 mg/day for 14 days after a 4-week washout period. Patients were randomly assigned to a low (4 g/day) or high (11 g/day) salt diet, and crossed over to the alternative diet after 7 days. 24-Hour blood pressure monitoring was performed at the end of the washout period and after 7 and 14 days during verapamil treatment. Verapamil induced a significant fall in mean 24-hour blood pressure that was similar for patients on both diets (p < 0.01). As expected, natriuresis increased significantly during high sodium intake (p < 0.01), and bodyweight fell significantly when sodium intake was reduced (p < 0.05). Meanwhile, serum creatinine and creatinine clearance remained stable. These results indicate that the antihypertensive effect of verapamil is independent of sodium intake even in the presence of mild renal insufficiency.

Blood Pressure↗
PubMed1992

The antihypertensive effect of verapamil in patients with chronic renal failure.

The calcium antagonist verapamil has been demonstrated to be effective in reducing hypertension in patients in whom sodium intake was not restricted. The present study evaluated the effect of verapamil in reducing hypertension in patients with chronic renal failure on low or high sodium diets. Also, the present study evaluated the effect of verapamil on proteinuria in chronic renal failure patients who were administered a normal and low protein diet. The results reveal that verapamil-SR 240 mg daily is effective in reducing hypertension in patients with chronic renal failure and the effect of verapamil is equal in patients on a high or low sodium intake. In addition, verapamil-SR 240 mg daily is effective in maintaining reduced proteinuria in chronic renal failure patients on low protein diet and may prevent proteinuria in such patients on a normal protein diet. Therefore, verapamil-SR 240 mg daily appears to be an excellent choice for the treatment of hypertensive chronic renal failure patients.

Antihypertensive Agents↗
PubMed1992

Renal consequences of arterial hypertension.

AIM: To seek ways of improving the prognosis for renal function in the presence of arterial hypertension. BACKGROUND: Nephrosclerosis is a term used to define the renal damage induced by arterial hypertension. The renal vasculature can participate in the genesis of essential hypertension and can suffer the consequences of elevated blood pressure. There is no doubt that antihypertensive therapy has dramatically improved the prognosis for renal function in the presence of arterial hypertension. RESULTS OF LITERATURE REVIEW: There appears to be a need for a further improvement in the prognosis for renal hypertension. At present, the prevalence of nephrosclerosis as a cause of terminal renal failure may be increasing and a progressive fall in renal function in treated hypertensive patients compared to normotensives has been described. CONCLUSIONS: It is not yet clear whether improvements in renal hypertension depend merely on the effectiveness of antihypertensive therapy in reducing arterial blood pressure or whether it will be necessary to improve the metabolic disturbances that accompany hypertension or the renal hemodynamic effects of different drugs before the prognosis for nephrosclerosis can be improved.

Antihypertensive Agents↗
PubMed1992

Abnormalities of renal function in essential hypertension with increased circulating levels of insulin-like growth factor I.

An increase in glomerular filtration rate and in tubular Na+ reabsorption from the parenteral administration of insulin-like growth factor I (IGF-I) have been reported in human subjects. To evaluate whether glomerular hyperfiltration and Na+ hyper-reabsorption present in some essential hypertensives are associated to an excess of IGF-I, the plasma levels of this factor and several parameters of renal function were studied in 30 non-treated essential hypertensives and in 30 normotensive controls. IGF-I levels were higher in hypertensive as compared to controls. With the 95% (upper) limit of the normotensive population as a cut-off point, a subgroup of six hypertensives had an abnormally high IGF-I level. Mean blood pressure was slightly lower in these six patients (112 +/- 7 mmHg) than in the remaining patients (120 +/- 2 mmHg). As compared to normotensives and hypertensives with normal IGF-I levels, patients with increased IGF-I levels were characterized by lower (P < 0.01) fractional Na+ excretion and higher (P < 0.05) creatinine clearance. The analysis of the relation of plasma renin activity and the concurrent daily rate of Na+ excretion showed that patients with increased IGF-I were low-renin hypertensives and patients with normal IGF-I were normal-renin hypertensives. These results indicate that an association exists between exaggerated circulating levels of IGF-I and abnormalities of renal function present in some patients with essential hypertension. It is suggested that IGF-I can play a role in low-renin essential hypertension.

Absorption↗