Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect on urinary electrolyte excretion, renin release and plasma norepinephrine of single oral doses of 400 mg etozolin (E) and of 40 mg furosemide (F) were studied in hypertensive patients with normal (n = 6) and impaired kidney function (n = 6). E caused a marked saluresis up to 24 hours, showing its long duration of action. F, however, displayed a brief, brisk peak diuresis, followed by a rebound from the 4th to the 24th hours. The brisk peak diuresis induced by F was associated with pronounced release of renin, almost twice that induced by E. In chronic renal failure the renin release in relation to the magnitude of the diuresis was increased, i.e. the sensitivity of these patients to changes in water homeostasis was increased. E and F stimulated the sympathetic system to roughly the same extent. Patients with essential hypertension had higher plasma levels of norepinephrine than hypertensive patients with chronic renal failure. In addition, hypertensive patients with normal renal function (n = 4) and varying degrees of renal impairment (n = 11) were also given 400 mg daily for 2 weeks. Effects on blood pressure and electrolyte homeostasis were monitored, as well as the plasma kinetics of metabolite I, ozolinone. At the end of the 2 week treatment E had significantly lowered systolic (-12 mm Hg) and diastolic (-9 mm Hg) blood pressure, and had produced a significant loss of body weight, without altering plasma electrolytes or blood chemistry. There was no accumulation of the effective metabolite ozolinone under conditions of severe impairment of kidney function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pharmacodynamics and kinetics of etozolin/ozolinone in hypertensive patients with normal and impaired kidney function. 638 84

By inhibiting ACE, captopril blocks the conversion of AI or AII and augments the effects of bradykinin both in vitro and in vivo. In rats, dogs, and monkeys with 2-kidney renal hypertension, orally administered captopril rapidly and markedly reduces blood pressure; this antihypertensive effect apparently occurs via a renin-dependent mechanism; that is, the inhibition of ACE. In 1-kidney renal hypertension studies in rats and dogs, it was determined that oral doses of captopril markedly lowered blood pressure, but only after several days of dosing; the mechanism is thought to be non-renin dependent. In SHR, daily oral doses of captopril progressively lowered blood pressure; normal levels were attained by the sixth month. In all species studied, the reduction in blood pressure resulted from a reduction in total peripheral resistance; cardiac output remained unchanged or increased. In humans, captopril reduces blood pressure in patients with essential hypertension with low, normal, and high renin levels, and in patients with renovascular hypertension and hypertension associated with chronic renal failure. In hypertensive patients with high plasma renin activity, captopril apparently exerts most of its pharmacologic effects through inhibition of ACE. The means by which captopril reduces high blood pressure associated with low or normal PRA is not known, but it is clear that captopril does not act on an overactive plasma renin-angiotensin system in these cases. The antihypertensive effect of captopril is enhanced when it is given in combination with a diuretic or after salt depletion. Captopril was rapidly and well absorbed in all species tested, including man. Studies in rodents indicated that ingestion of food caused a reduction in the extent of absorption and bioavailability of captopril. Captopril and/or its metabolites were distributed extensively and rapidly throughout most tissues of normal rats; no radioactivity was detected in the brain. In vitro and in vivo, captopril formed disulfide bonds with albumin and other proteins. This binding was reversible in nature. In vitro studies in blood indicates that the disulfide dimer of captopril and mixed disulfides of captopril with L-cysteine and glutathione were formed. In intact blood cells, captopril remained in the reduced form (sulfhydryl), whereas in whole blood or plasma, captopril was converted to its disulfide dimer and other oxidative products. Biotransformation of captopril may involve both enzymatic and nonenzymatic processes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Captopril: pharmacology, metabolism and disposition. 643 80

Calcium antagonists are increasingly used in the treatment of primary and secondary hypertension. A new substance of this group, isobutyl methyl 1,4-dihydro-2,6-dimethyl-4-(2-nitrophenyl)-3,5-pyridinecarboxylate (nisoldipine, Bay k 5552) inhibits the calcium-induced contraction of arteries and veins in concentrations 5-20 times lower compared to those of nifedipine in vitro. The effect of nisoldipine (10 mg orally) on blood pressure and heart rate in supine and upright position, on serum electrolytes (Na+, K+, Ca2+) and on serum aldosterone and serum hydrocortisone (cortisol) was comparatively studied in patients with essential hypertension (n = 6, 57 +/- 7 years), in patients with hypertension and chronic renal failure (n = 6, 46 +/- 4 years, serum creatinine 2.1 +/- 0.5 mg/100 ml) and in 6 patients with unilateral renal artery stenosis. In patients with essential hypertension, systolic blood pressure (BP) dropped by 26 mmHg; diastolic BP was lowered by 17 mmHg after 150 min compared to placebo. In patients with chronic renal failure, decrement in BP was 25/16 mmHg (systolic and diastolic BP, respectively). In patients with renal artery stenosis, blood pressure declined by 31/18 mmHg after nisoldipine. Serum electrolytes (Na+, K+ and Ca2+) and serum aldosterone as well as serum hydrocortisone remained unchanged. The hypotensive action of nisoldipine seems to be independent of the type of hypertension. However, the hypotensive activity correlates with the level of the baseline blood pressure.
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PMID:[Hypotensive properties of nisoldipine. Comparative study in essential, renal and renovascular hypertension]. 654 May 81

Total kininogen (Kgn), kallikrein, and prekallikrein were measured in patients with malignant hypertension (MH), essential hypertension (EH), normotensive control (NC), and hypertension and chronic renal failure (HRF). These components of the kallikrein-kinin system were related to the levels of creatinine and fibrinogen. High molecular weight Kgn and low molecular weight Kgn were also measured in blood samples from a peripheral vein, arterial blood, and suprahepatic vein in NC, EH, and MH. Results showed that total Kgn levels were diminished in MH and this diminution could not be ascribed to decreases in renal function, hematocrit, or fibrinogen levels. Appropriate antihypertensive treatment for over 1 year did not normalize Kgn levels in 10 of 11 patients. High molecular weight Kgn and low molecular weight Kgn were both diminished in MH (0.26 +/- 0.04 nmol bradykinin/ml and 0.93 +/- 0.12 nmol lysyl-bradykinin/ml, respectively) as compared to NC (0.39 +/- 0.07 and 1.92 +/- 0.16) and EH (0.51 +/- 0.07 and 1.65 +/- 0.13). Higher concentrations of high molecular weight Kgn were demonstrated in the suprahepatic vein as compared to arterial blood, demonstrating its synthesis by the liver. However, patients with MH had a diminished capacity to synthetize high molecular weight Kgn. A decrease in synthesis of high molecular weight Kgn may be a partial explanation for low levels of total Kgn. It is suggested that a lack of Kgn may play a role in the pathogenesis of MH.
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PMID:Malignant hypertension: a syndrome accompanied by plasmatic diminution of low and high molecular weight kininogens. 655 4

Muscle biopsy specimens form 22 patients with primary hypertension, 10 patients with chronic renal failure and 21 healthy normotensive controls were analyzed using a Kevex 0600 X-ray spectrometer. Muscle potassium (MK), calcium (MCa), sulphur (MS) and phosphorus (MP) were determined. In the patients with primary hypertension, MK was decreased compared to the controls (p less than 0.001), MCa was increased (p less than 0.05), MS was decreased (p less than 0.05) and no difference was seen in MP. In the patients with chronic renal failure, MK was decreased compared to the controls (p less than 0.001), MCa showed no difference compared to the controls, whereas both MP and MS were lower (p less than 0.05 and p less than 0.001). It was concluded that intracellular potassium is low both in primary hypertension and chronic renal failure. In chronic renal failure the potassium decrease is probably secondary to loss of cellular potassium capacity, whereas in primary hypertension an inhibition of the sodium, potassium, adenosine triphosphatase is suggested as the cause of the low potassium.
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PMID:Potassium in skeletal muscle in untreated primary hypertension and in chronic renal failure, studied by X-ray fluorescence technique. 673 Oct 36

Antihypertensive effect of an orally active angiotensin I-Converting enzyme inhibitor, SQ 14225 (Captopril) was assessed in 18 hypertensive patients, of whom 13 had essential hypertension, 2 had malignant hypertension, 2 had hypertension associated with chronic renal failure, and 1 had renovascular hypertension. Blood pressure decreased markedly not only in patients with high renin levels but also in those with low renin levels. Nevertheless, the magnitude of blood pressure reduction was correlated with the pre-treatment plasma renin activity (r =-0.64, p less than 0.01 systolic, r =- 0.60, p less than 0.05 diastolic). There was a significant correlation between the fall in mean blood pressure and the decrease in plasma aldosterone concentration 3 weeks after treatment (r = 0.64, p less than 0.05). The serum potassium elevated from 4.2 +/- 0.4 to 4.8 +/-0.9 mEq/L (p less than 0.05), and the change correlated inversely with the reduction of plasma aldosterone concentration (r = 0.71, p less than 0.02), while serum sodium slightly decreased from 140-+/- 2 to 138 +/- 3 mEq/L. There was neither finding of orthostatic hypotension nor escape from the antihypertensive effect. These results indicate that chronic inhibition of angiotensin I-converting enzyme with an orally active compound offers an effective and well-tolerated approach to treatment of hypertension.
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PMID:Antihypertensive effect of the oral angiotensin I-converting enzyme inhibitor in long-term treatment of hypertensive patients. 704 Jul 24

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.
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PMID:Treatment of hypertension in dialysis and essential hypertension patients with nifedipine. 718 89

The cardiac function in Hegglin syndrome (HS; prolonged QT interval and shortened QS2) remains unclear. In order to estimate cardiac function of HS, left ventricular echocardiographic parameters and systolic time intervals (STI) were analyzed, and compared with those of normal subjects (N) (n = 20). Forty-six patients (pts) of HS are constituted of 23 pts with chronic renal failure, 7 with cardiomyopathy, 5 with ischemic heart disease, 5 with essential hypertension, 4 with acquired valvular disease, 1 with effusive pericarditis and 1 with Romano-Ward syndrome. Corrected preejection period (PEPc) and PEP/ET were significantly larger (0.15 +/- 0.02 vs 0.13 +/- 0.01, p less than 0.001; 0.48 +/- 0.13 vs 0.35 +/- 0.04, p less than 0.001, respectively) in HS. Corrected ejection time (ETc) was significantly smaller (0.37 +/- 0.02 vs 0.41 +/- 0.01, p less than 0.001) in HS. Mitral EF slope (DDR), ejection fraction (EF), and mean ventricular circumferential fiber shortening (mVCF) were significantly decreased (58 +/- 29 vs 92 +/- 25, p less than 0.001; 0.52 +/- 0.15 vs 0.62 +/- 0.07; p less than 0.005; 0.98 +/- 0.33 vs 1.18 +/- 0.20; p less than 0.05, respectively) in HS, but cardiac index (C.I.) did not differ. Thus, patients with Hegglin syndrome showed heart failure pattern in STI and hypodynamic cardiac function in echocardiographic parameters, and our data suggest that hypodynamic cardiac function of HS is caused by both lowered pump function and decreased myocardial contractility.
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PMID:[Systolic time intervals and echocardiographic parameters in Hegglin syndrome (author's transl)]. 732 May 60

The responses in the left ventricular systolic time intervals following digoxin administration (0.5 mg i.v.) were studied in 11 patients with chronic renal failure and hypertension. The control group comprised 11 patients with mild essential hypertension. There were no clinical signs of congestive heart failure in any of the patients. Before digoxin administration total electromechanical systole (QS2), the pre-ejection period (PEP) and the PEP/LVET ratio were greater, while the left ventricular ejection time (LVET) was shorter than in the control group (P < 0.001). In patients with chronic renal failure digoxin administration induced a reduction in QS2, PEP and PEP/LVET ratio and a prolongation of LVET (P < 0.001). These data suggest latent heart failure in the group of patients studied with chronic renal failure. It seems to be advisable to use digitalis preparations in patients with chronic renal failure despite the absence of clinical signs of heart failure.
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PMID:The left ventricular systolic function after digoxin administration in patients with chronic renal failure. 739 45

Calcium antagonists such as verapamil are among the antihypertensive agents categorised as first line treatments for essential hypertension. They have also shown efficacy in secondary forms of hypertension, including hypertension associated with chronic renal failure, irrespective of the degree of renal impairment. Systemic and renal haemodynamic parameters, and renal function were analysed in 15 hypertensive patients with mild to severe chronic renal failure after a 2-week placebo period and after 4 weeks of administration of verapamil sustained release (SR) 240 mg/day. After 4 weeks of treatment with verapamil SR, blood pressure was normalised in all patients. Arterial pressure decreased as a result of the decrease in systemic vascular resistance, while cardiac output and heart rate remained unchanged. Verapamil therapy did not significantly affect left cardiac function curves. The normalisation of arterial pressure did not result in changes in the glomerular filtration rate; however, renal vascular resistance decreased significantly, although the filtration fraction remained unchanged. Renal blood flow increased significantly and there was a significant increase in uricosuria and a subsequent decrease in plasma uric acid levels. In conclusion, verapamil SR is an effective and well tolerated treatment for hypertension associated with chronic renal failure.
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PMID:Long term effects of sustained release verapamil on the renal and systemic haemodynamic parameters in hypertensive patients with mild to severe chronic renal failure. 751 64


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