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Showing papers by "Luis M. Ruilope published in 1996"



Journal ArticleDOI
TL;DR: In patients with predominantly moderate to severe essential hypertension, the addition of HCTZ 12.5 mg or 25 mg toLosartan 50 mg produced effective control of blood pressure in a substantial majority of patients who only partially responded to losartan monotherapy.
Abstract: Ruilope LM, Simpson RL, Toh J, Arcuri KE, Goldberg AI, Sweet CS. Controlled trial of losartran given concomitantly with different doses of hydrochlorothiazide in hypertensive patients.The purpose o...

75 citations


Journal ArticleDOI
TL;DR: Data demonstrate that Ang II potentiates the vasoconstriction induced by phenylephrine through the stimulation of AT1 receptors, and AT2 receptors and nitric oxide appear to be involved in this effect.
Abstract: Nitric oxide seems to be involved in the mechanisms underlying the antihypertensive and renal responses of losartan in spontaneously hypertensive rats (SHR). We investigated the contribution of nitric oxide to the effect of this angiotensin II (Ang II) type 1 (AT1) receptor antagonist on the constrictor response of phenylephrine in aortic rings from SHR. Furthermore, since it has been suggested that Ang II could bind to unblocked AT2 receptors, during administration of an AT1 receptor antagonist, we also studied the effect of the AT2 receptor antagonist PD 123319 on the contractile response to phenylephrine in aortic rings from SHR. To this end, we studied dose-response curves of phenylephrine (10(-9) to 10(-5) mol/L) in the presence and absence of losartan (10(-9), 10(-7), and 10(-5) mol/L) in SHR aortic rings. Preincubation with losartan reduced the constrictor response to phenylephrine but not to KCl (10 to 120 mmol/L) in a dose-dependent manner. On the other hand, the presence of captopril (10(-5) mol/L) in the incubation medium did not alter the response to phenylephrine, even at the dose of 10(-3) mol/L. The reduced response to phenylephrine in the presence of losartan was abolished in both endothelium-denuded rings and rings treated with a nitric oxide synthesis inhibitor. A similar situation was observed in PD 123319-pretreated rings, in which the effect of losartan on the contractile response to phenylephrine was reversed. Losartan was not able to stimulate the production of aortic cGMP compared with the control group. Likewise, losartan did not modify the relaxing responses to either acetylcholine or sodium nitroprusside in phenylephrine-preconstricted aortic rings. Furthermore, losartan did not alter isometric tension in aortic rings in either basal or phenylephrine-preconstricted conditions. These data demonstrate that Ang II potentiates the vasoconstriction induced by phenylephrine through the stimulation of AT1 receptors. Moreover, AT2 receptors and nitric oxide appear to be involved in this effect.

65 citations


Journal ArticleDOI
TL;DR: A high percentage of patients with gout, hypertension, and CRF have an excessive Pb burden, and about 15% of the patients diagnosed as 'essential' hypertensives also show high Pb burdens.
Abstract: Background. The true incidence of lead (Pb) overload as a cause of chronic renal failure (CRF) is unknown. Also, it is unclear if CRF per se could generate an increment in the body Pb burden. Most studies of chronic Pb intoxication have been performed on cohorts or patients with a past history of occupational exposure. Therefore we studied the body Pb burden in CRF of known aetiology versus those patients with CRF with gout and hypertension of unclear aetiology without a past history of Pb exposure. In addition we studied patients diagnosed with essential hypertension. Methods. We studied 296 patients lacking a past history of Pb exposure, who were subdivided into four groups : group I (n=30), normal control subjects ; group II (n=104), patients with 'essential' hypertension and normal renal function ; group III (n=132), patients with CRF of uncertain aetiology in association with hypertension and/or gout, and group IV (n=30), patients with CRF of known aetiology. The blood and urine Pb levels were assessed before and after an EDTA test. Results. No abnormal test results were obtained for patients in groups I and IV. The EDTA test was abnormal in 16 patients (15.4%) in group II and in 74 patients (56.1%) in group III. A positive correlation was observed between plasma creatinine levels and post-EDTA urinary Pb in group III, but not in group I. No correlation regarding plasma creatinine and the duration of hypertension or gout were demonstrated. The bone Pb levels, measured in 12 patients with pathological EDTA test results, were positively correlated to the plasma creatinine levels. Conclusions. A high percentage of patients with gout, hypertension, and CRF have an excessive Pb burden, and about 15% of the patients diagnosed as 'essential' hypertensives also show high Pb burdens. It is remarkable that a history of overt Pb exposure was lacking in the whole study population.

52 citations


Journal ArticleDOI
TL;DR: Both quinapril and diltiazem are not only able to reduce BP elevation induced by the chronic administration of LNAME in rats, but also to prevent the renal damage and the hyperresponsiveness to phenylephrine induced by this NO synthesis inhibitor.

41 citations


Journal Article
TL;DR: The objective of the study is to compare fatal and nonfatal cardiovascular endpoints in hypertensive patients randomised to the calcium-channel blocker, nifedipine GITS or a thiazide diuretic, co-amilozide.
Abstract: The objective of the study is to compare fatal and nonfatal cardiovascular endpoints in hypertensive patients randomised to the calcium-channel blocker, nifedipine GITS or a thiazide diuretic, co-amilozide. A total of 6592 patients from nine countries (UK, France, Israel, Spain, Italy, The Netherlands, Sweden, Denmark and Norway) will be recruited, aged 55-80 and with a blood pressure (BP) > or = 150/95 or > or = 160 mm Hg (systolic). All patients will have at least one other major cardiovascular risk factor. Patients will be minimised by country and risk factors and randomised to double-blind treatment with either nifedipine GITS or diuretic. After a single dose titration, additional treatment will be atenolol or enalapril (where beta-blockade is contra-indicated). After achieving a target BP of 140/90 mm Hg patients will be followed for a total of 3 years. Primary endpoints are myocardial infarction, stroke, subarachnoid haemorrhage, heart failure and sudden cardiac death. The study has a power of 80% at 5% significance to detect a difference between 8% event rate over 3 years in diuretic-treated patients and 6% in those receiving nifedipine.

35 citations


Journal Article
TL;DR: Results indicate that aging produces a derangement of endothelial function in essential hypertension in young and aged essential hypertension.

26 citations



Journal ArticleDOI
01 Jan 1996-Nephron
TL;DR: The results suggest that patients with the highest levels of Lp(a) are at risk of developing complications in their vascular accesses, and they also have lower vascular access survival.
Abstract: Lipoprotein(a) [Lp(a)] is an independent risk factor for atherosclerotic and cardiovascular complications in the general population and in hemodialysis patients. Increased Lp(a) levels have been also

17 citations


Journal ArticleDOI
TL;DR: Both quinapril and diltiazem were able to prevent BP elevation levels in the fructose-fed rat, and reduced the exaggerated response to an oral glucose tolerance test in these animals.

15 citations


Journal ArticleDOI
TL;DR: The data suggest that a sustained hyperinsulinemic state can interact with the physiological vasoactive mechanisms involved in the regulation of renal vasculature, and may be pertinent to human disease, especially in pathological conditions in which insulin resistance is present.

01 Jan 1996
TL;DR: The measurement of urinary albumin excretion, initially and during the follow-up, in a subset of patients of the ELSA Study will be able to know which is the prevalence of microalbuminuria in the type of patients entering the ELsa Study.
Abstract: Microalbuminuria constitutes a good predictor of cardiovascular risk in general population and also in hypertensive and diabetic patients. This reason led us to consider of interest the measurement of urinary albumin excretion, initially and during the follow-up, in a subset of patients of the ELSA Study. By doing so we will be able to know which is the prevalence of microalbuminuria in the type of patients entering the ELSA Study. The evolution of microalbuminuria with the two different therapies and its correlation with the changes observed by ultrasonography in the carotid wall will also be investigated.