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PubMed2002

[The use of enalaprilat for the treatment of uncomplicated hypertensive crises in patients with hypertensive disease (essential hypertension)].

When used for the treatment of hypertensive crises enalaprilat produced pronounced lowering of both systolic and diastolic blood pressures. Lowering of blood pressure was accompanied by regression of clinical symptoms. There were no episodes of excessive blood pressure drop. The use of enalaprilat was associated with normalization of parameters of central and cerebral hemodynamics, lessening of degree of strain of regulatory systems of the body. Diminishment of left atrial dilatation and augmentation of left ventricular ejection fraction occurred in patients with initially dilated left atrium.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1983

[Mathematical analysis of informative criteria for the differential diagnosis of renovascular hypertension and essential hypertension].

Retrospective clinical and mathematical analysis of 168 parameters was performed in 188 patients with arterial hypertension, using standard programmed case history format designed specifically for the purpose. A number of differential criteria were identified and their diagnostic informative value was assessed for each form of arterial hypertension. The isolated criteria were grouped into anamnestic, clinical-laboratory, radioroentgenographic and roentgenoangiographic ones. Anamnestic and clinical-laboratory groups of diagnostic criteria were shown to be acceptable for health services. Their use in prehospital screening of patients is expected to contribute to the diagnosis of basic disease provoking arterial hypertension.

Adult↗
PubMed1997

Lacidipine restores endothelium-dependent vasodilation in essential hypertensive patients.

Essential hypertension is characterized by impaired endothelium-dependent vasodilation. The present study was designed to test whether antihypertensive treatment with the calcium antagonist lacidipine can improve endothelium-dependent vasodilation in essential hypertensive patients. In 12 normotensive subjects (mean age, 47.8+/-8.6 years; blood pressure, 118.6+/-4.2/76.7+/-3.9 mm Hg) and 19 hypertensive patients (mean age, 49.4+/-10.2 years; blood pressure; 153.5+/-13.3/101.3+/-6.4 mm Hg), we studied forearm blood flow modifications (strain-gauge plethysmography) induced by intrabrachial infusion of acetylcholine (0.15, 0.45, 1.5, 4.5, and 15 microg/100 mL per minute) and bradykinin (5, 15, and 50 ng/100 mL per minute), two endothelium-dependent vasodilators that act through different receptors and signal transduction pathways, and sodium nitroprusside (1, 2, and 4 microg/100 mL per minute), an endothelium-independent vasodilator. In essential hypertensive patients, vascular reactivity was repeated during prolonged (8 weeks of oral treatment at 6 mg/d) lacidipine administration and 2 weeks after withdrawal of chronic (32-week) treatment. Hypertensive patients showed significantly (P<.01) blunted vasodilation in response to acetylcholine (vascular resistance, 31.5+/-4.9 to 7.6+/-2.4 SU) and bradykinin (vascular resistance, 32.3+/-5.8 to 8.5+/-3.0 SU) compared with control subjects (vascular resistance: acetylcholine, 24.3+/-3.9 to 3.7+/-1.2 SU; bradykinin, 24.7+/-0.4 to 4.1+/-1.3 SU), whereas the response to sodium nitroprusside was similar. After either 8 or 32 weeks of lacidipine treatment, the vasodilation in response to acetylcholine (30.6+/-7.7 to 5.7+/-1.5 and 34.3+/-6.6 to 5.9+/-1.9 SU, respectively) and bradykinin (31.3+/-7.2 to 6.4+/-1.6 and 33.7+/-5.4 to 6.1+/-1.5 SU, respectively), but not to sodium nitroprusside, proved to be significantly (P<.05) increased compared with baseline. In essential hypertensive patients, oral treatment with lacidipine increased forearm vasodilation in response to acetylcholine and bradykinin, suggesting that this drug can improve endothelial function in patients with essential hypertension.

Acetylcholine↗
PubMed1996

Influence of humoral and neurohormonal factors on cardiovascular hypertrophy in untreated essential hypertensives.

In essential hypertension, cardiovascular structure is believed to be influenced by hormonal and by hemodynamic factors. The objective of the present study was, in essential hypertensives, to investigate the relationship between blood pressure (BP) level as well as circulating hormones on the one hand and cardiovascular structure on the other. Seventy-nine untreated essential hypertensives were examined by 24-h ambulatory BP monitoring, echocardiography, microscopy of subcutaneous resistance vessels and analyzes of plasma for angiotensin II (P-Ang II), aldosterone, atrial natriuretic factor and 24-h urinary excretion of catecholamines. Multiple regression analysis showed a statistically significant correlation between P-Ang II and the end diastolic interventricular septal diameter (IVSDd) (R = 0.32, P = .005) and a weak correlation between P-Ang II and the left ventricular posterior wall diameter (R = 0.22, P = .049). These correlations were closer in the subgroup of patients (N = 54) who had never received antihypertensive treatment (R = 0.42/0.32, respectively). A weak, though statistically significant, correlation was found between the catecholamine excretion and systolic BP (R = 0.26, P = .03). A statistically negative correlation existed between catecholamines and end-diastolic left ventricular internal diameter index (R = -0.36, P = .001). No significant relationship was found between hormonal levels and the tunica media structure of the resistance arteries. In conclusion, P-Ang II was in this study significantly correlated to IVSDd, but not to resistance artery structure. In essential hypertension a complex relationship exists between humoral and hemodynamic factors and cardiovascular remodeling.

Adult↗
PubMed2004

Sulfhydryl angiotensin-converting enzyme inhibition induces sustained reduction of systemic oxidative stress and improves the nitric oxide pathway in patients with essential hypertension.

BACKGROUND: Essential hypertension is associated with enhanced LDL oxidation and impaired endothelium-dependent vasodilation. The antioxidant status is linked to the nitric oxide (NO) pathway. Sulfhydryl angiotensin-converting enzyme (ACE) inhibitors inhibit oxidative stress and atherogenesis in experimental models; therefore we tested whether this beneficial antioxidant activity could be also clinically relevant in patients with essential hypertension. METHODS: Plasma LDL oxidizability was investigated initially in untreated normocholesterolemic patients with moderate essential hypertension without clinically evident target organ damage (n = 96) and in control normotensive subjects (n = 46). Patients were then randomly assigned into two age- and sex-matched groups to receive the new sulfhydryl ACE inhibitor zofenopril (15 to 30 mg/d; n = 48) or enalapril (20 mg/d, n = 48). LDL oxidizability was evaluated (generation of malondialdehyde, MDA) and systemic oxidative stress was evaluated by isoprostanes (8-isoPGF2alpha). Asymmetrical dimethyl-L-arginine (ADMA), a competitive inhibitor of endothelial NO synthase, and plasma nitrite and nitrates (NOx) were also measured. RESULTS: LDL from hypertensive subjects had enhanced susceptibility to oxidation in vitro compared with that in control subjects (P <.05). Similarly, isoprostanes were significantly increased (P <.01) in hypertensive subjects versus control subjects. After 12-week treatment, MDA levels were significantly reduced by zofenopril (P <.05) but not enalapril treatment (P = not significant). Isoprostanes were normalized after zofenopril treatment (P <.03), whereas enalapril was ineffective. After treatment with both ACE inhibitors, plasma NOx concentrations were significantly reduced (P <.05). Similarly, hypertension increased ADMA concentration compared with the normotensive state, whereas ACE inihibition elicited a significant decrease. However, the reduction of ADMA concentration was significantly higher in patients receiving sulfhydryl ACE inhibition (P <.05 vs enalapril). CONCLUSIONS: The sulfhydryl ACE inhibitor zofenopril reduces oxidative stress and improves the NO pathway in patients with essential hypertension. If confirmed in a large multicenter clinical trial, our data suggest a possible vasculoprotective effect of the compound in retarding vascular dysfunction and atherogenesis that often develops rapidly in hypertensive patients.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

Impaired suppression of plasma free fatty acids and triglycerides by acute hyperglycaemia-induced hyperinsulinaemia and alterations in high density lipoproteins in essential hypertension.

OBJECTIVES: Essential hypertension may be associated with abnormalities in free fatty acids (FFA) and triglyceride metabolism, which could lead to alterations in high density lipoproteins (HDL). Lecithin: cholesterol acyltransferase (LCAT) and cholesteryl ester transfer protein (CETP) are key factors in the esterification of cholesterol and the subsequent transfer of cholesteryl ester from HDL towards triglyceride-rich lipoproteins. We compared baseline plasma lipids, HDL lipids, plasma LCAT and CETP activity as well as the lowering of plasma FFA and triglycerides by acute hyperglycaemia-induced hyperinsulinaemia in patients with essential hypertension and control subjects. SETTING: University Hospital, Groningen. SUBJECTS AND DESIGN: Eight patients with essential hypertension and eight control subjects were studied during a 3-h hyperglycaemic glucose clamp (blood glucose, 10 mmol L-1). MAIN OUTCOME MEASURES: Plasma insulin, FFA, triglycerides and HDL lipids, plasma LCAT and CETP. RESULTS: Baseline plasma FFA, total cholesterol and HDL cholesterol were not different between the groups, but plasma triglycerides tended to be higher in the hypertensive patients (P < 0.10). The baseline HDL free cholesterol content and the HDL free cholesterol/cholesteryl ester ratio were lower (P < 0.05 for both) in the hypertensive than in the control group. Although baseline plasma LCAT and CETP activity were not significantly different between the groups, the plasma LCAT/CETP ratio, reflecting the amount of active LCAT compared to that of CETP, was higher in the hypertensive patients (P < 0.05). In the combined subjects and in the hypertensive group, the HDL free cholesterol content was negatively related to plasma triglycerides and to the LCAT/CETP ratio, whereas this ratio was positively correlated with plasma triglycerides (P < or = 0.01 for all correlations). During a 3-h hyperglycaemic clamp (blood glucose 10 mmol L-1) plasma FFA and triglycerides decreased to a lesser extent (P < 0.02 and P = 0.05) and remained higher (P < 0.05 for both) in the hypertensive patients, despite similar plasma insulin levels. CONCLUSION: The action of insulin on FFA metabolism is impaired which is likely to contribute to higher plasma triglycerides in essential hypertension. In turn, higher triglycerides influence the HDL lipid composition, either directly or via an effect on the plasma LCAT/CETP ratio.

Acute Disease↗
PubMed1982

Treatment of hypertension in dialysis and essential hypertension patients with nifedipine.

The immediate antihypertensive effect of 10 mg nifedipine sublingually (nifedipine test), was measured in 19 chronic renal failure hypertensive patients on dialysis and 34 essential hypertensive patients with normal kidney function. The blood pressure decreased significantly in both groups. The minimal values were observed between 30 and 60 minutes after the sublingual administration of nifedipine. The blood pressure decreased from 178 +/- 3.3/104.0 +/- 3.9 to 136.0 +/- 4.7/87.5 +/- 5.1 mm Hg (p less than 0.001) in dialysis patients and from 176.8 +/- 4.5/107.1 +/- 2.4 to 133.0 +/- 3.0/81.7 +/- 2.2 mm Hg in essential hypertension patients (p less than 0.001). The decrease in blood pressure during the test had a significant positive correlation with the pre-test values. Thirteen hypertensive patients on dialysis and 20 essential hypertensive patients completed 2 weeks of daily oral nifedipine therapy, with a dose of 30 to 40 mg per day. The mean blood pressure at the end of the 2 weeks of treatment decreased from 179.5 +/- 4.5/108.5 +/- 5.3 mm Hg to 154.4 +/- 6.3/82.3 +/- 2.6 mm Hg (p less than 0.001) in dialysis patients, and from 176.8 +/- 5.8/110.3 +/- 2.9 to 151.3 +/- 5.3/93.5 +/- 2.6 mm Hg (p less than 0.001) in essential hypertension patients. The present results reveal that nifedipine has a powerful immediate as well as a long-term antihypertensive action in dialysis patients with high blood pressure. This effect is similar to that obtained in essential hypertensive patients.

Humans↗
PubMed1995

Role of angiotensinogen in the genetics of essential hypertension.

Although essential hypertension has long been recognized to involve a strong genetic predisposition, the genes that increase susceptibility remain virtually unknown. With recent advances in molecular biology and statistical methods, it has become feasible to study candidate genes which may contribute to the pathogenesis of essential hypertension in humans. Recently, the angiotensinogen (AGT) locus was demonstrated to exhibit genetic linkage and association to essential hypertension and to preeclampsia. While the statistical evidence that mutations of the AGT gene or a neighboring gene contribute to the development of hypertension is strong, the exact mechanism(s) by which these mutations affect the regulation of blood pressure (BP) is unknown. Increasing attention is now being focused on elucidating this mechanism(s).

Amino Acid Sequence↗
PubMed1992

Increased norepinephrine spillover into the jugular veins in essential hypertension.

In essential hypertension sympathetic nerve firing is commonly increased. A central nervous system origin has been presumed but not tested directly. To estimate cerebral norepinephrine release in essential hypertension, spillover of norepinephrine into the cerebrovascular circulation was measured by isotope dilution, with high internal jugular venous sampling. Norepinephrine was released into the cerebrovascular circulation in both hypertensive patients and healthy volunteers and was present after administration of the ganglion blocker trimethaphan and in patients with sympathetic nervous failure, indicating that brain neurons and not cerebrovascular sympathetic nerves were the probable source. Although differing among hypertensive patients, norepinephrine spillover on average was higher in the hypertensive patients (153 +/- 41 pmol/min) than in healthy subjects (59 +/- 12 pmol/min; p less than 0.05), and was elevated in six of 17 patients, in whom the accompanying whole body norepinephrine spillover rate was higher than in the remaining 11 patients (p less than 0.01). To test for a possible link between brain norepinephrine release and human sympathetic nervous function, the effect of the tricyclic antidepressant desipramine (0.3 mg/kg i.v.) on both brain and whole body norepinephrine spillover was measured in healthy volunteers. Desipramine lowered the cerebrovascular spillover of norepinephrine, its precursor dihydroxyphenylalanine, and its metabolite dihydroxyphenylglycol by 50-80% and produced a mean fall of 35% in whole body norepinephrine spillover. One interpretation of these results is that human sympathetic nerve firing is dependent on norepinephrine release within the brain and that increased cerebral norepinephrine release may possibly be present in some patients with essential hypertension, underlying their higher sympathetic nerve firing rates.

Cerebrovascular Circulation↗
PubMed1991

Aspirin test for differentiation of unilateral renovascular hypertension from hyperreninemic essential hypertension.

Responses of renin release and blood pressure to aspirin DL-lysine (ASP) were examined to find out if the responses could help in the differentiation between unilateral renovascular hypertension (RVH) and hyperreninemic essential hypertension (EHT). The two studies involved ten patients with unilateral RVH, eight with hyperreninemic EHT, and five with hyporeninemic EHT. In a radiological study, before and 30 min after an intravenous injection of ASP (18 mg/kg), renal venous and abdominal aortic plasma was sampled and assayed for prostaglandin (PG) E2 and plasma renin activity (PRA). Systemic blood pressure was measured serially. The reproducibility of the responses to ASP was confirmed in a bedside study. In unilateral RVH, ASP suppressed renin release from the stenotic kidney and reduced the renal vein PRA ratio to less than 1.5 via the inhibition of PG synthesis, which is accelerated in that kidney. The mean suppression of aortic PRA at this dose of ASP was 35% in these patients, and their blood pressure decreased in proportion to the suppression of PRA. However, in the two EHT groups, ASP elevated the mean blood pressure. The renal synthesis of PGE2 was inhibited by ASP in all patients, but the suppression of PRA, while small, was significant (19% in the aorta) in the patients with hyperreninemic EHT, and not significant in patients with hyporeninemic EHT. The different responses of blood pressure and PRA to ASP between RVH and EHT were reproducible in the bedside study.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

[Experimental types of hypertension--models for essential hypertension in the human?].

Since the pathogenesis of essential hypertension is multifactorial, the causal therapy of primary arterial hypertension remains a great challenge. At a given genetic predisposition, the manifestation of hypertension depends critically on lifestyle factors. It is thus essential to study the molecular consequences of various deleterious lifestyle factors. We demonstrated by radiotelemetric measurements that an increased caloric intake raises both systolic and diastolic blood pressure as well as heart rate in spontaneously hypertensive rats (SHR). This model is comparable to hyperkinetic hypertension in hypertensive persons which, if it persists, will lead to established hypertension. Overfeeding also results in the characteristic metabolic derangements (hyperinsulinemia, hypertriglyceridemia) of insulin resistant hypertensive persons. The enhanced sympathetic outflow of the brain can be potentiated by lifestyle factors such as high sodium intake and psychological stress. In contrast to sodium intake, psychological stress (e.g. schedule-induced stress) is difficult to mimic in animal experiments. In view of the recent progress in the characterization of imidazoline receptors in the rostral ventrolateral medulla and the development of antihypertensive drugs with a high selectivity (moxonidine) for imidazoline receptors, efforts should be made to elucidate key regulatory mechanisms involved in brain insulin sensitivity and appetite regulation. Such an approach could help in pharmacologically reducing the influence of deleterious lifestyle factors at a given genetic predisposition.

Animals↗
PubMed2001

Thyrotropin-releasing hormone receptor (TRHR) gene is associated with essential hypertension.

In essential hypertension, a polygenic and multifactorial syndrome, several genes interact with the environment to produce high blood pressure. Thyrotropin-releasing hormone (TRH) plays an important role in central cardiovascular regulation. We have described that TRH overexpression induces hypertension in a normal rat, which was reversed by TRH antisense treatment. This treatment also reduces the central TRH hyperactivity in spontaneously hypertensive rats and normalizes blood pressure. Human TRH receptor (TRHR) belongs to the G protein-coupled seven-transmembrane domain receptor superfamily. Mutations of these receptors may result in constitutive activation. As it has been demonstrated that hypertensive patients have a blunted TSH response to TRH injection, suggesting a defect in the TRHR, we postulate that the TRHR gene is involved in human hypertension. We studied 2 independent populations from different geographic regions of our country: a sample of adult subjects from a referral clinic and a population-based sample of high school students. In search of molecular variants of TRHR, we disclosed that a polymorphic TG dinucleotide repeat (STR) at -68 bp and a novel single nucleotide polymorphism, a G-->C conversion at -221 located in the promoter of the TRHR are associated with essential hypertension. As STRs detected in gene promoters are potential Z-DNA-forming sequences and seem to affect gene expression, we studied the potentially different transcriptional activity of these TRHR promoter variants and found that the S/-221C allele has a higher affinity than does the L/G-221 allele to nuclear protein factor(s). Our findings support the hypothesis that the TRHR gene participates in the etiopathogenesis of essential hypertension.

Adolescent↗
PubMed1997

Comparison of clinical efficacy and adverse effects between extended-release felodipine and atenolol in patients with mild and moderate essential hypertension.

BACKGROUND: Essential hypertension is a risk factor for cardiovascular disease. Atenolol, a cardio-selective beta-blocker, has been shown to be a safe and effective antihypertensive agent. The extended-release form of felodipine (felodipine ER), a vascular-selective dihydropyridine calcium blocker, is extensively used in Caucasians. However, its effectiveness, tolerability and adverse side-effect have not been assessed in Chinese populations. METHODS: Sitting blood pressure (BP), heart rate, body weight, adverse reaction and serum biochemistry were assessed in 70 patients with mild-moderate essential hypertension treated either with felodipine ER (37 patients), or atenolol (33 patients) for 10 weeks. Each patient was prescribed 5 mg of felodipine ER or 50 mg of atenolol once daily and this daily dosage was doubled to twice daily if necessary. RESULTS: Six patients who received felodipine ER and 3 who received atenolol withdrew from the treatment because of intolerable side effects. Within ten weeks, 81.1% of the patients had responded to a total daily dosage of 5-10 mg of felodipine ER and 81.8% to a daily dose of 50-100 mg of atenolol. By the end of treatment, the mean BP in the felodipine ER group had decreased from 176/104 mmHg at baseline to 145/85 mmHg, while the BP in the atenolol group had dropped from 173/103 mmHg to 145/84 mmHg (NS between the two groups). Heart rate declined in the atenolol group but did not change in patients who received felodipine ER. Overall, patients in the felodipine ER group had a higher rate of adverse reaction (70.3% vs. 39.4%; p < 0.001), and 16.2% of the patients in the felodipine ER group experienced symptoms of hypotension. CONCLUSION: Equivalent doses of felodipine ER and atenolol are effective first-line monotherapeutic agents for the treatment of mild-moderate essential hypertension.

Adrenergic beta-Antagonists↗
PubMed1985

Cytoplasmic free [Ca2+] is increased in the platelets of spontaneously hypertensive rats and essential hypertensive patients.

The cytoplasmic free calcium concentration [( Ca2+]i) was assessed with the fluorescent dye Quin 2 in platelets and lymphocytes of spontaneously hypertensive rats (SHR), normotensive Wistar-Kyoto rats (WKY), essential hypertensive patients (EHP) and normotensive human control subjects (NCS). [Ca2+]i was significantly higher in the platelets of 8- and 20-week-old SHR in comparison with WKY. However, no difference was evident after weaning. Changes of cellular calcium in hypertensive rats apparently evolved simultaneously with the development of high arterial pressure. [Ca2+]i was significantly higher in platelets of EHP than in NCS. In lymphocytes of SHR, [Ca2+]i was not different from WKY at 4 and 8 weeks, but was increased at 14 weeks and at older ages. In EHP, intralymphocytic [Ca2+] was only modestly higher than in controls. On the whole, the results suggest that control of cytoplasmic calcium in these blood cells is similarly affected in human and animal models of primary hypertension.

Adult↗
PubMed1995

Effects of angiotensin receptor antagonist and angiotensin converting enzyme inhibitor on insulin sensitivity in fructose-fed hypertensive rats and essential hypertensives.

This study was designed to investigate the effects of angiotensin II (AII) receptor antagonist and angiotensin converting enzyme (ACE) inhibitor on insulin resistance, and the mechanism by which ACE inhibitor improves insulin-dependent glucose uptake (insulin sensitivity) in an insulin-resistant hypertensive rat model (fructose-fed rats, FFR) and in essential hypertensives (EHT). Male Sprague-Dawley rats were fed on fructose-rich or standard chow for 4 weeks and treated either with 10 mg/kg/day of delapril (n = 8), 1 mg/kg/day of TCV-116 (AII receptor antagonist; n = 13), or vehicle (n = 9) for the latter 2 weeks. Steady-state plasma glucose (SSPG) was measured with the subjects in the conscious state; simultaneously, we infused insulin (2.5 mU/kg/min) and glucose (8 mg/kg/min) to determine insulin sensitivity in each group. Thirteen EHT were hospitalized and the 2-h euglycemic hyperinsulinemic glucose clamp (GC) method was performed in a fasting condition before and after 2 weeks' administration of TCV-116 (8 mg/day) in 7 EHT and of delapril (120 mg/day) in 6 EHT. Insulin sensitivity was evaluated as M-value calculated from the infusion rate of glucose. Mean blood pressure (MBP) was higher in FFR (137.7 +/- 73.8 mm Hg, P < .05) compared to controls (120.8 +/- 2.7 mm Hg), and was lower in both the delapril (108.1 +/- 6.3 mm Hg, P < .05) and TCV-116 (112.8 +/- 4.3 mm Hg, P < .05) groups than in FFR.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗