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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a double-blind, double-dummy, placebo-controlled crossover design, the renal hemodynamic and tubular effects of 2-month specific vasodilation with a converting enzyme inhibitor (enalapril, 40 mg once daily) was compared with that of a calcium antagonist (verapamil slow release, 240 mg twice daily) in 15 patients with established essential hypertension. Enalapril and verapamil treatment induced a 9% reduction in mean blood pressure (BP). Heart rate (HR) was similar after placebo (66 beats/min), enalapril (63 beats/min), and verapamil (63 beats/min). Plasma norepinephrine (P-NE) was unaltered after enalapril and verapamil as compared with placebo (0.92, 0.88, and 1.33 nM, respectively). Plasma angiotensin II and aldosterone decreased and plasma renin activity (PRA) increased after enalapril but were unaltered after verapamil. Glomerular filtration rate (51Cr-EDTA) was not altered by either enalapril or verapamil, whereas renal blood flow (125I-hippurate) was reduced 9% by verapamil. Renal vascular resistance (RVR) was unchanged after enalapril as well as verapamil. Fractional excretion of electrolytes and diuresis were unaltered and body weight was similar after enalapril, verapamil, and placebo (81.0, 82.5, and 80.2 kg, respectively). Long-term treatment with enalapril and verapamil had a comparable antihypertensive effect. Neither enalapril nor verapamil appeared to induce reflex activation of the sympathetic nervous system. Renal hemodynamic and tubular function was well preserved with both drugs without signs of sodium and water retention.
J Cardiovasc Pharmacol 1990 Mar
PMID:Renal and endocrine effects of long-term converting enzyme inhibition as compared with calcium antagonism in essential hypertension. 169 57

The effects of A-64662, a new specific renin inhibitor, on plasma renin activity (PRA) and blood pressure (BP) were studied for the first time in patients with essential hypertension. A single intravenous bolus of vehicle, 0.001, 0.003, 0.01, 0.03, and 0.1 mg/kg was given to the first four patients, maintained on a constant 100 mEq Na diet. PRA was promptly reduced from 3.4 +/- 2.9 (mean +/- SEM) to 0.2 +/- 0.06 ng/ml/h, a 94% inhibition with the smallest dose, and to undetectable levels (less than 0.1 ng/ml/h) with the larger ones. However, BP did not change within this dose range. The subsequent seven patients received larger doses ranging from 0.2 to 1.0 mg/kg. In three cases, there was reduction in BP on the second dosing day, at doses of 0.4, 0.7, and 1 mg/kg. All responses were late (at 110 min after the injection), transient, and unrelated to baseline PRA. These results strongly suggest that there is a dissociation between the effectiveness of A-64662 in inhibiting PRA and its blood pressure lowering effect in hypertensive patients.
J Cardiovasc Pharmacol 1990 Mar
PMID:Effects of a novel renin inhibitor in patients with essential hypertension. 169 75

Renal effects of 4-week fixed maintenance doses of bunazosin three times daily (2.0 mg t.i.d., n = 8) and propranolol (40 mg t.i.d., n = 8) were evaluated in patients with mild-to-moderate essential hypertension [World Health Organization (WHO) stages I and II]. Both bunazosin and propranolol decreased blood pressure (BP) significantly (p less than 0.05), but the magnitude of reduction in diastolic BP (DBP) was greater with bunazosin (p less than 0.05) than with propranolol. Bunazosin produced a nonsignificant increase in renal blood flow (RBF) by 14%, a significant increase in glomerular filtration rate (GFR) 11% (p less than 0.05), and a decrease in total renal vascular resistance (TRR) by 15% (p less than 0.05), whereas propranolol caused no significant changes in these parameters. Urinary sodium excretion rate and the fractional excretion of sodium were unchanged by either of the drugs. The results of this short-term study suggest that bunazosin may be a drug that will increase RBF and GFR and decrease TRR with a concomitant hypotensive action in patients with mild-to-moderate essential hypertension. Whether these renal functional effects of the drug would benefit such patients must be determined in long-term studies.
J Cardiovasc Pharmacol 1990 May
PMID:Renal effects of bunazosin, a new alpha 1-adrenoceptor blocker, in patients with mild-to-moderate essential hypertension. 169 44

The antihypertensive action of OPC-13340, a new dihydropyridine, was studied in rats and compared with the action of nicardipine and other dihydropyridines. OPC-13340 showed more potent and longer hypotensive action than nicardipine when administered either intravenously (i.v.) or orally in normotensive and hypertensive rats. Among 6 compounds tested, (OPC-13340, nifedipine, nitrendipine, nisoldipine, nicardipine and diltiazem), OPC-13340 was the most potent and long-acting when administered orally to spontaneously hypertensive rats (SHR). Tachycardia after administration of OPC-13340 was less or diminished earlier than that of nicardipine. Oral administration of OPC-13340 (3 mg/kg) once daily for 13 days did not cause any rebound phenomena in SHR. The compound inhibited Ca- or K-induced contractions in isolated rat aorta and shortened action potential duration in guinea pig papillary muscle, suggesting Ca channel blocking action. OPC-13340 might be useful as a drug for once-daily therapy of essential hypertension.
J Cardiovasc Pharmacol 1990 May
PMID:Antihypertensive activity of OPC-13340, a new potent and long-acting dihydropyridine calcium antagonist, in rats. 169 46

Felodipine, a dihydropyridine calcium antagonist, was used to treat eight patients with severe uncontrolled hypertension: five had essential hypertension, two had renovascular disease, and one chronic pyelonephritis. Mean blood pressure (BP) was 221 +/- 14/120 +/- 4 mm Hg despite treatment with three or more antihypertensive drugs. All patients experienced an immediate and pronounced lowering of BP after adding felodipine, which persisted during long-term treatment in combination with previous medication except for vasodilating drugs. In all cases, an increase in glomerular filtration rate (51Cr-EDTA clearance) after 6 and 12 months of felodipine treatment was seen (59 +/- 10 to 63 +/- 7 and 70 +/- 6 ml/min, respectively, p less than 0.05). Renal plasma flow (PAH clearance) exhibited only a slight increase (315 +/- 68 to 340 +/- 63 and 314 +/- 69 ml/min), giving a nonsignificant rise in filtration fraction (18 +/- 1 to 21 +/- 1 and 20 +/- 1%, respectively). It is concluded that felodipine decreases BP dramatically in patients with previously refractory hypertension and that the drug causes an improved renal function in these patients.
J Cardiovasc Pharmacol 1990
PMID:Long-term effects of felodipine on blood pressure and renal hemodynamics in severe hypertension. 169 10

Felodipine is a new calcium antagonist that was developed aiming particularly at reduction in vascular resistance-without any decrease in heart pump function. Studies in animals have demonstrated that felodipine given intravenously induces an acute fall in total peripheral resistance and blood pressure (BP), associated with acute reflex tachycardia and an increase in cardiac output (CO). During chronic treatment, the reflex tachycardia is abolished, while resistance and BP remain reduced. Acute vasodilatation has been demonstrated in the heart, kidneys, intestines, and skeletal muscles. Increased blood flow has also been demonstrated in the coronary arteries. Acute studies in humans with essential hypertension have demonstrated similar effects to what has been observed in the spontaneously hypertensive rat (SHR): a marked fall in total peripheral resistance and BP-associated with reflex tachycardia and increased CO. There is also an increase in coronary renal, and forearm blood flow. Catheterization studies have indicated that felodipine also dilates large coronary arteries. During chronic treatment in 16 males with initial diastolic BP of 100-120 mm Hg, felodipine reduced total peripheral resistance approximately 15% at rest and during exercise without significant changes in cardiac index (CI), heart rate (HR), and stroke volume (SV). As in animals, no reflex tachycardia is seen during chronic treatment. It is concluded that felodipine reduces BP in hypertensive animals and humans because of the marked effect on total peripheral resistance. CO is not reduced either at rest or during exercise. During chronic treatment, reflex tachycardia is abolished.
J Cardiovasc Pharmacol 1990
PMID:Hemodynamic effects of felodipine in hypertension: a review. 169 23

Calcium antagonists demonstrate a close relationship between plasma drug level and effect on blood pressure (BP). Thus, the intensity and duration of action can be influenced by dose and disposition. Felodipine has a dose-related effect on diastolic BP whether given alone or with a beta-blocker. The latter combination reduces adverse effects and improves tolerability, particularly at higher (20 mg/day) doses of felodipine. Felodipine 5 or 10 mg/day in an extended release formulation could be predicted to lower BP throughout a 24-h period. The results of formal prospective clinical trials confirm the predictions and indicate that felodipine can be used as a once-daily agent in essential hypertension.
J Cardiovasc Pharmacol 1990
PMID:Dose-plasma concentration--effect relationship of felodipine in essential hypertension: a review. 169 28

Epidemiological evidence supports a link between hyperinsulinemia and blood pressure. In nondiabetic, normotensive individuals, the male sex, age, obesity, and body fat distribution all are associated with higher systolic and diastolic blood pressure and with higher plasma insulin concentrations. Nevertheless, when accounting for the above physiological variables, blood pressure still is independently related to plasma insulin. In the general population, hypertensive individuals have multiple metabolic abnormalities (glucose intolerance, hyperinsulinemia, and dyslipidemia). A striking pattern of overlap exists among obesity, diabetes, and hypertension. Physiological studies (euglycemic insulin clamp) have shown that essential hypertension per se is a state of insulin resistance: lean, nondiabetic subjects with untreated hypertension have a mean 40% reduction in the ability of physiological hyperinsulinemia to stimulate whole-body glucose uptake. Other insulin actions (suppression of hepatic glucose output, lipolysis, lipid oxidation, and promotion of K+ uptake) are conspicuously preserved. In perfused forearm studies, local (intra-arterial) hyperinsulinemia induces subnormal rates of glucose uptake and glycogen synthesis in the skeletal muscle of individuals with essential hypertension. In the San Antonio Heart Study, parental history of non-insulin-dependent diabetes mellitus (NIDDM) is associated with hyperinsulinemia and higher blood pressure and serum lipid levels in nondiabetic probands. In this biethnic population, however, hyperinsulinemia and NIDDM are more prevalent (approximately threefold) among Mexican-Americans than non-Hispanic whites, but hypertension is more prevalent among the latter.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1990
PMID:Essential hypertension: an insulin-resistant state. 169 27

Seventeen middle-aged males with sustained essential hypertension (WHO stage II) and diastolic blood pressures (BP) exceeding 100 mm Hg during a placebo run-in period completed a trial to assess the hemodynamic effects of isradipine, a new dihydropyridine calcium antagonist. The study was double-blind and placebo-controlled with a crossover design. Brachial artery compliance was assessed as the ratio of stroke volumes and simultaneous pulse pressure. During therapy with isradipine (all patients received 7.5 mg b.i.d.), highly significant reductions in supine systolic BP [from 184 +/- 16 to 162 +/- 20 mm Hg (mean +/- S.D.)] and diastolic BP (from 96 +/- 8 to 83 +/- 8 mm Hg) were observed. Heart rate was unchanged (69 +/- 3 vs. 73 +/- 2 beats/min) during chronic therapy. Total peripheral resistance was significantly reduced (from 24.8 +/- 9 to 17.4 +/- 5 units) while cardiac output was unchanged (6.0 +/- 1.9 vs. 7.2 +/- 1.8 L/min). Stroke volume was unchanged (92 +/- 25 vs. 100 +/- 25 ml/beat), and a significant (p less than 0.05) increase in brachial artery compliance (from 1.05 +/- 0.25 to 1.26 +/- 0.35 ml/mm Hg) was observed.
J Cardiovasc Pharmacol 1990
PMID:Central hemodynamics and brachial artery compliance during therapy with isradipine, a new calcium antagonist. 169 12

Lipid profiles were determined in 56 elderly patients with benign essential hypertension during an open-label 1-year study of the safety and efficacy of isradipine, a new calcium antagonist, in controlling blood pressure. Patients with diastolic blood pressures between 96 and 115 mm Hg were titrated with isradipine (mean dose of 11 mg/day) to reduce blood pressure to less than 90 mm Hg. Ten of these patients received concomitant hydrochlorothiazide (HCTZ) 50 mg/day for additional control. Sera were analyzed using standard methods at the end of a 2- to 4-week washout period, and at the end of Months 6 and 12, for total cholesterol (CHOL) and HDL- and LDL-cholesterol. Changes in lipid values (mg/dl) from baseline to 12 months with isradipine alone (n = 38) were as follows: CHOL, -7.5; HDL, +3.9 (p less than 0.05); LDL, -6.2; CHOL/HDL, -0.6 (p less than 0.05). For patients receiving concomitant HCTZ (n = 9), the changes were as follows: CHOL, -4.9; HDL, +3.4; LDL, -16.8; CHOL/HDL, -0.4. In conclusion, isradipine alone was associated with significant improvements in HDL cholesterol and total CHOL/HDL ratio. Lipid profiles of patients receiving isradipine and HCTZ were minimally affected. Favorable lipid changes with isradipine suggest that it may have advantages in the treatment of hypertensive patients.
J Cardiovasc Pharmacol 1990
PMID:Long-term lipid profiles with isradipine and hydrochlorothiazide treatment in elderly hypertensive patients. 169 13


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