Plasma renin and blood pressure during treatment with methyldopa

Blood pressure and plasma renin activity and concentration were studied before and during administration of alpha methyldopa to normal and hypertensive subjects. Methyldopa produced no significant decrease in renin levels and caused only inconsistent changes in blood pressure in subjects with normal pressure, patients with low renin essential hypertension regardless of severity, or patients with normal renin essential hypertension of mild degree. In contrast, a significant reduction in blood pressure and marked lowering of plasma renin levels were observed after administration of methyldopa in patients with normal renin essential hypertension of moderate to severe degree and in those with hypertensive terminal renal failure. In moderate to severe essential hypertension, methyldopa-lnduced decreases in blood pressure and plasma renin activity were significantly correlated. These data are consistent with the possibility that the hypotensive action of methyldopa may be partially related to Its effect on the renin-angiotensin system. They also lend support to the value of plasma renln determinations In selecting appropriate antlhypertensive drugs for individual patients.     

Coronary arteriography in acute transmural myocardial infarction

Coronary arteriography was performed 16 ± 3 days (range 7 to 21 days) in 106 patients with acute transmural myocardial infarction (61 posterior infarct, 45 anterior infarct). Coronary arteriography was performed without serious complications. Only 44 per cent of patients with anterior infarct had total occlusion of the left anterior descending artery while a significant stenosis of the vessel was observed in the others ?27 per cent had a single vessel disease, 49 per cent had two lesions and 22 per cent had three lesions; one patient had angiographically normal coronary arteries. Among the patients with posterior infarction, 21 per cent had one vessel disease and double or triple lesions accounted for 39 per cent of each.Sixty per cent of patients with anterior infarction and 45 per cent with posterior infarction had no collateral vessels. In the others patients collateral circulation had a protective effect only in anterior infarction. Age has no effect on the distribution and number of lesions nor on the development of a collateral circulation. The location and severity of the lesions were not different in patients who presented with arrythmias and those who did not.     

Effect of sodium depletion on plasma renin concentration before and during adrenergic beta-receptor blockade with propranolol in normotensive man.

Plasma renin levels have been used to discriminate between different forms of hypertension, but how to define the normal range of plasma renin levels has not been agreed upon. Sodium depletion stimulates renin release. Evaluation of plasma renin would, therefore seem possible only in relation to sodium balance. Plasma renin concentration and concurrent daily sodium excretion were determined in 33 healthy normotensive subjects (control group) ingesting high, normal and low sodium diets. A well-defined hyperbolic relationship was found between the two variables indicating that the physiologic level of plasma renin concentration depends on the state of sodium balance. An increase in plasma potassium concentration may reduce plasma renin concentration, but this appeared to be overruled by the stimulating effect of sodium depletion. To examine whether beta-adrenergic stimulation contributes to the increase in plasma renin concentration during sodium depletion, the relationship between plasma renin concentration and concurrent sodium excretion was studied during beta-receptor blockade with propranolol. In 20 healthy normotensive subjects in whom beta-receptor blockade was verified by a significant reduction in pulse rate, the same hyperbolic relationship was found between plasma renin concentration and sodium excretion as in the control group showing that sodium depletion stimulates renin release independent of sympathetic nervous activity.     

Left ventricular compliance: mechanisms and clinical implications.

Left ventricular diastolic compliance is determined by the level of operating pressure and the diastolic pressure-volume relation. This relation is curvillinear and the slope of a tangent (operative chamber stiffness) to the pressure-volume curve increases as the chamber progressively fills. Such preload-dependent changes in compliance occur during any acute alteration in ventricular volume. At a given diastolic pressure, operative chamber stiffness (or its reciprocal, operative chamber compliance) is determined by the relative values for ventricular volume and muscle mass and by the stiffness of a unit of myocardium. Thus, there may be a leftward shift of the diastolic pressure-volume curve (increase in the modulus of chamber stiffness) as a consequence of ventricular hypertrophy or an increase in the stiffness of heart muscle itself (increase in modulus of muscle stiffness). To distinguish between hypertrophy and stiff muscle, it is useful to examine the modulus of chamber stiffness, derived from pressure-volume data, together with the volume/mass ratio of the ventricle. In this fashion, changes in the modulus of chamber stiffness that are inappropriate for a given volume/mass ratio may be attributed to changes in the material properties of the heart muscle. Examples of clinical and experimental pressure-volume studies are presented to illustrate the variety of mechanisms by which acute and chronic changes in ventricular chamber compliance evolve during the course of clinical heart disease. The pathophysiology of pulmonary congestion is best understood by considering the factors responsible for producing changes in chamber stiffness of the ventricle, whereas an examination of muscle stiffness is likely to provide more insight into the extent of irreversible functional and structural defects of the myocardium.     

Disappearance of abnormal Q waves after aortocoronary bypass surgery

Sixty-one patients were selected from 100 consecutive patients undergoing aortocoronary artery bypass. The number of vessels diseased as defined by coronary arteriography and the number of bypass grafts were recorded. Review of the preoperative electrocardiograms showed an infarct pattern in 26 of the 61 patients and analysis of the postoperative electrocardiograms revealed loss of abnormal Q waves in 3 of the 26. The pre- and postoperative clinical course of these three patients is analyzed and the extent of their coronary artery disease and number of bypass grafts compared with those of the 23 patients who had persistence of the infarction pattern and the 17 patients who manifested new Q waves. Possible explanations for the disappearance of abnormal Q waves are discussed.     

Blood pressure crisis following withdrawal of clonidine (Catapres, Catapresan), with special reference to arterial and urinary catecholamine levels, and suggestions for acute management

In five patients with severe essential hypertension, placebo was substituted after 24 to 48 months of treatment with clonidine and a diuretic. In the present study, four of the patients developed a marked blood pressure rise following withdrawal of clonidine which was rapidly reversed by intravenous administration of propranolol 0.2 mg. per kilogram of body weight and phentolamine 20 to 30 mg. The fifth patient was pretreated with reserpine 2.0 mg. intramuscularly for three days prior to withdrawal of clonidine, and the blood pressure rise which he experienced was far less impressive. All patients experienced similar “withdrawal” symptoms, consisting of headaches, insomnia, restlessness, tremor, and nausea.Catecholamines were determined in arterial blood and urine, before and during the overshoot. They revealed a marked increase, particularly in the urine samples, consistent with the appearance of a hyperadrenergic state.