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Biomedical subjects

H P Nast

Publications and source records attributed to H P Nast.

16 recordsLinked to original sources
PubMed1998

A comparison of the antihypertensive efficacy and safety of felodipine IV and nifedipine IV in patients with hypertensive crisis or emergency not responding to oral nifedipine.

OBJECTIVE: A clinical definition of a hypertensive emergency is excessively high blood pressure in the presence of symptoms indicating end organ damage. Equally high blood pressure without symptoms is called a hypertensive crisis. Patients with hypertensive crisis or emergency need prompt, effective, and specific therapy and a controlled reduction of blood pressure. METHODS: We performed a randomized, double-blind multi-centre study, to compare the safety, efficacy and tolerability of an intravenous (i.v.) infusion of two dihydropyridine calcium channel blockers (either nifedipine or felodipine) in 122 patients, of whom 63 were diagnosed as hypertensive emergencies and 59 as hypertensive crisis, who had not reacted adequately (diastolic blood pressure <115 mmHg) to 5 mg of nifedipine PO. RESULTS: Both drugs lowered blood pressure adequately in more than 90% of the patients and were well tolerated. Only one patient had to be withdrawn, because of an excessive decrease in blood pressure. CONCLUSION: Patients with excessively high blood pressure who do not react to oral nifedipine can be treated equally effectively with felodipine and nifedipine IV. Felodipine is easier to handle because of its lack of light sensitivity.

Administration, Oral↗
PubMed1993

[Nitroglycerin in comparison with nifedipine in patients with hypertensive crisis].

To determine whether nitroglycerin is just as effective as nifedipine in lowering the blood pressure in excessive hypertension and hypertensive crisis, two groups of 20 patients received in random sequence either 1.2 mg of nitroglycerin sublingually or a 10 mg nifedipine capsule, which was chewed and swallowed. The blood pressure fell after 5 min in the nitroglycerin group from 211/122 mm Hg to 171/95 mm Hg and after nifedipine from 210/118 to 185/102 mm Hg. The greater effect of nitroglycerin results from faster absorption through the oral mucosa than through the small intestinal mucosa where nifedipine is primarily absorbed. After 15 to 20 min a satisfactory reduction in blood pressure was reached in both groups: 157/91 and 158/92 mm Hg, respectively. After 30 min the heart rate in the nitroglycerin group had decreased from 83 to 80/min, but in the nifedipine group it had increased from 84 to 90/min. The reduction in blood pressure persisted up to 6 h. No significant difference in side-effects was determined. Since a hypertensive crisis is usually accompanied by left-ventricular failure, pulmonary edema or angina pectoris and infarction, and nitroglycerin has been definitively shown to positively influence these conditions, preference should be given to nitroglycerin in the treatment of hypertensive crisis.

Administration, Oral↗
PubMed1992

Comparison of nitroglycerin with nifedipine in patients with hypertensive crisis or severe hypertension.

To determine whether nitroglycerin is as effective as nifedipine in lowering the blood pressure in severe hypertension and hypertensive crisis, two groups of 20 patients received in random sequence either 1.2 mg nitroglycerin sublingually or a 10-mg nifedipine capsule, which was chewed and swallowed. The blood pressure fell after 5 min in the nitroglycerin group from 211/122 mmHg to 171/95 mmHg and after nifedipine from 210/118 to 185/102 mmHg. The greater effect of nitroglycerin may result from faster absorption through the oral mucosa than through the small intestinal mucosa where nifedipine is primarily absorbed. After 15-20 min a satisfactory reduction in blood pressure was reached in both groups: 157/91 and 158/92 mmHg, respectively. After 30 min the heart rate in the nitroglycerin group had decreased from 83 to 80/min, but in the nifedipine group it had increased from 84 to 90/min. The reduction in blood pressure persisted up to 6 h. No significant differences in side effects were determined. Since a hypertensive crisis is usually accompanied by left ventricular failure, pulmonary edema, angina pectoris, or infarction, nitroglycerin has been definitively shown positively to influence these conditions, and preference should be given to nitroglycerin in the treatment of hypertensive crises.

Acute Disease↗
PubMed1977

Low renin hypertension.

Low renin hypertension probably does not represent a clinical entity. In many patients with low renin hypertension blood pressure is normalized by treatment with diuretics only; in these patients a (genetic?) sensitivity to salt might play a predominant role in the pathogenesis of hypertension and renin suppression. In another group of patients renin suppression appears to be secondary to the hypertensive process. This is indicated by the observation that prevalence of low renin hypertension increases with age and that it is more frequent in advanced stages of hypertension. Also a diminished sympathetic tone might play a part in the renin unresponsiveness. Finally, although no positive evidence was found, the possibility cannot be excluded that, at least in some cases, a mineralocorticoid other than aldosterone is involved. Neither in normotensive subjects nor in hypertensive patients, both with normal and with low plasma renin was a correlation between plasma renin concentration and plasma aldosterone concentration following stimulation by upright posture found. More detailed studies will be necessary to clarify the relationship between the renin-angiotensin system and aldosterone secretion during upright posture, in particular in patients with low renin hypertension.

Adrenal Cortex↗
PubMed1976

[Studies on the pH-dependence, inhibition and reactivation of angiotension II-amide splitting enzymes in human erythrocytes (author's transl)].

Aminopeptidase activity of three fractions of human erythrocytes (membranes free of hemoglobin; hemolysate free of membranes; enzyme protein fraction made free of hemoglobin by DEAE-cellulose) was measured by a NADH dependent optical test using asparaginyl1-angiotension II-amide as substrate. 1. From the enzyme protein fraction 6 subfractions were obtained by (NH4)2SO4 precipitation. By measuring enzyme kinetics at three different pH-values (pH 5,0; 7,0; 8,0) with and without addition of the effectors Na2EDTA and Ca++ the existence of 6 different enzymes could be demonstrated. 2. The aminopeptidase activity of the hemolysate made free of membranes could be inhibited by diisopropylfluorphosphate and p-chloromercuribenzoate at three different pH-values (pH 5,0; 6,5; 7,0; 8,0 and 6,5; 7,0; 8,0 respectively). 3. A reduction of enzymatic activity of 20% was found after incubation at 37degreesC for two hours.

Calcium↗
PubMed1976

[Diurnal profiles of plasma aldosterone, cortisol, renin, angiotensinogen and angiotensinases in normal subjects (author's transl)].

Plasma cortisol and renin were estimated in 1 h intervals, plasma aldosterone, angiotensinogen and angiotensinases in 3 h intervals over periods of 24 h in six normal volunteers (age 20-26) under control conditions and subsequently under suppression of ACTH release by dexamethasone. Highest cortisol levels were found around 7 a.m., minimum levels between 9 p.m. and 1 a.m. Dexamethasone reduced cortisol to constantly low concentrations. Aldosterone was highest around 4 a.m. under control conditions and under dexamethasone, and showed lowest concentrations between 4 and 10 p.m. There were no significant differences between mean aldosterone concentrations at corresponding time points of the control and the dexamethasone period. Similar to aldosterone, renen showed peak values around 4 a.m. All mean values at corresponding time points between 7 a.m. and 11 p.m. and the 24 hour mean values of each subject were significantly increased under the influence of dexamethasone. No evidence could be achieved for the existence of circadian rhythms of angiotensinogen and angiotensinases. Dexamethasone did not cause significant changes of these parameters.

Adrenocorticotropic Hormone↗
PubMed1975

[Metabolism of angiotensin II during angiotensin infusion and following sodium depletion].

1. Angiotensin II (A II) and angiotensin (3--8)-hexapeptide (H) were measured by radioimmunoassay in arterial and venous plasma before and during infusion of angiotensin II-amide in five normotensive subjects, both in sodium-replete and sodium-depleted states. The separation of the oligopeptides was performed by thin layer chromatography. 2. Before sodium-depletion the mean ratio of arterial to venous A II was 1.14+/-0.11:1, corresponding to an A II-extraction of approximately 12% during a single forearm passage. Infusion of A II-amide increased extraction of A II. The mean ratio of arterial to venous A II increased to 1.68+/-0.3:1, corresponding to an extraction of approximately 39% when 8 ng-min-1-kg-1 were infused. 3. Sodium depletion increased arterial and venous concentrations of A II and H. During infusion of angiotensin II-amide the arterial and venous concentrations of A II and H increased approximately parallel to the concentrations before sodium depletion. The extraction of A II did not differ significantly in both states. 4. The augmented extraction extraction of A II observed during infusion of angiotensin II-amide suggest an overproportional increase of the metabolism of A II under the latter condition. Sodium depletion, however, does not appear to cause a percent change in A II metabolism.

Adult↗