Showing papers by "Luis M. Ruilope published in 1994"

Are renal hemodynamics a key factor in the development and maintenance of arterial hypertension in humans

Abstract: The kidney plays a key role in the control of body fluids and blood pressure. Evidence has shown that impairment of renal function can lead to the development of arterial hypertension. The regulation of renal blood flow appears to be a key element in the pathophysiology of the hypertensive process, because multiple evidence suggests the existence of a functional enhancement of renal vascular tone in this disorder. The existence of renal vasoconstriction and of an inherited defect in the regulation of renal blood flow has been proposed in the prehypertensive stage. The mechanisms responsible for this alteration include a lack of modulation of the renal vasculature to angiotensin II, increased sympathetic activity, or suppressed renal dopaminergic activity. Established hypertension is characterized by elevated renal vascular resistance, decreased renal blood flow, sustained glomerular filtration rate, and increased filtration fraction. The increase in renal vascular resistance is initially due to elevations in renal vascular tone and is reversible, whereas later it becomes irreversible because of structural changes involved in nephrosclerosis. Antihypertensive drugs are able to decrease blood pressure and to prevent the development of further renal vascular damage independently of variable effects on renal hemodynamics.

Hormonal, renal, and metabolic alterations during hypertension induced by chronic inhibition of NO in rats

Abstract: The evolution of renal excretory function and circulating vasoactive systems was studied during progressive increases in blood pressure (BP) induced in rats by oral administration of NG-nitro-L-arginine methyl ester (L-NAME; 5-30 mg/100 ml) for 5 wk. L-NAME induced a stepped elevation (P < 0.05) in BP levels without changing creatinine clearance, urine flow, or sodium excretion rate along the study. Reductions (P < 0.05) in plasma renin activity and plasma aldosterone concentration were found only during treatment with 30 mg/100 ml of L-NAME. Plasma norepinephrine and epinephrine concentrations were elevated (P < 0.05) in the last week of the study. Plasma concentrations of endothelin-1 and urinary excretion of prostaglandin E2, 6-ketoprostaglandin F1 alpha, and thromboxane B2 were not significantly affected by L-NAME. Similarly, no changes in plasma concentrations of glucose, insulin, total cholesterol, or triglycerides were observed. In summary, during long-term administration of L-NAME, progressive increases in BP levels were observed without changes in either sodium excretion or enhanced circulating vasoconstrictor activity. Thus, it is likely that inhibition of synthesis of nitric oxide (NO) in the vasculature leads to an imbalance between the tonic relaxing action of NO and the influences of vasoconstrictor agents even when the latter remain at normal levels.

Relationship between blood pressure and renal function.

Abstract: UNLABELLED RENAL DAMAGE CAUSED BY HYPERTENSION: Renal vasoconstriction seems to be a key factor in the origin of arterial hypertension and accounts for the decrease in renal blood flow commonly observed in patients with hypertension. An inverse correlation has been found between renal blood flow and clinic blood pressure levels in established hypertension. Other features of renal damage attributable to high blood pressure have also been correlated with clinic blood pressure levels. Microalbuminuria is a good example of an alteration in renal function that depends in part on blood pressure levels. EFFECTS OF ANTIHYPERTENSIVE AGENTS Antihypertensive agents can prevent or ameliorate renal vascular damage secondary to arterial hypertension, including renal failure. Ambulatory blood pressure monitoring is an excellent method of studying blood pressure levels in relation to end-organ damage and the blood pressure response to antihypertensive agents. Preliminary studies using this technique indicate that changes in renal function are closely correlated with the average daily blood pressure in arterial hypertension. CONCLUSIONS Further studies are needed on the mechanisms of renal deterioration and on how to preserve renal function in arterial hypertension.

Randomly allocated study of the effects of standard therapy versus ACE inhibition on micro-albuminuria in essential hypertension.

Abstract: OBJECTIVE To compare the effects of standard therapy (diuretic, beta-blocker or both) with those of angiotensin converting enzyme (ACE) inhibition with quinapril on renal function and urinary albumin excretion in patients with essential hypertension. METHODS A 1-year, placebo-controlled, randomly allocated study was conducted in a group of 40 patients with essential hypertension. Before beginning the active treatment phase, all patients were given a matched placebo for quinapril for at least 14 days. At baseline and after 1, 3, 6 and 12 months of treatment, blood pressure, heart rate, body weight, renal plasma flow, glomerular filtration rate, plasma renin activity, plasma aldosterone and urinary albumin excretion were measured. RESULTS Both the standard therapy and quinapril produced similar decreases in blood pressure, but only quinapril produced a significant decrease in micro-albuminuria, from 68.5 +/- 16.7 to 47.2 +/- 14.9 mg/24 h (P < 0.05). The renal plasma flow remained constant in both study groups while the glomerular filtration rate and filtration fraction decreased significantly (P < 0.05) in the quinapril group. CONCLUSIONS The results of this study indicate that long-term therapy for essential hypertension with ACE inhibition has a more favorable effect on micro-albuminuria than standard therapy for an equal level of blood pressure control.

Evaluation of the renal effects of calcium antagonists.

Abstract: Calcium antagonists exert renal effects consisting mainly of renal vasodilation and facilitation of renal excretion of sodium through a direct action on renal tubules. These effects facilitate the antihypertensive action of this class of drugs and make them suitable for therapy of different forms of human hypertension, including that accompanying chronic renal failure. At the same time, renal vasodilation and enhanced natriuresis could also be of value for correcting the renal defect that initiates essential hypertension. Renal effects of calcium antagonists have also fostered the concept of a renoprotective effect of these drugs in different situations. A demonstration of this concept has been shown in cyclosporine-related nephrotoxicity. Calcium antagonists can improve the short- and long-term prognosis for renal function in human transplantation through their effects in avoiding cyclosporine-induced renal vasoconstriction and in facilitating renal sodium output.

How Much Does the Kidney Participate in the Origin of Primary Hypertension

Abstract: 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. Different theories have tried to explain the mechanism(s) underlying the renal participation in human hypertension. According to the data contained in the literature renal vasoconstriction is present in the kidney since the very early stages of the hypertensive disease and could constitute the mechanism facilitating the development of arterial hypertension.