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Biomedical subjects

A D Struthers

Publications and source records attributed to A D Struthers.

278 records · Page 16Linked to original sources
PubMed1982

Effect of nifedipine on blood pressure and adrenocortical responses to trophic stimuli in humans.

The effect of nifedipine on blood pressure and aldosterone and cortisol responses to both angiotensin II and adrenocorticotrophin (ACTH) was studied in two groups of normal male subjects. Nifedipine (20 mg by mouth) caused a significant fall in diastolic blood pressure in both groups, from 71 +/- 8 (SEM) to 60 +/- 10 mm Hg after 30 min (p greater than 0.005; n = 15; paired t test), and a reflex tachycardia. During graded infusion of angiotensin II at 5, 10, and 20 ng/kg/min each for 30 min, there was a significant decrease in both the pressor and aldosterone responses after administration of nifedipine (p less than 0.05; n = 6; paired Wilcoxon test); the pressor and aldosterone response ratios at 10 ng/kg/min were 0.5 and 0.25, respectively. However, in a second study, no inhibition of either cortisol or aldosterone responses to ACTH (250 microgram intramuscularly) was observed. These data indicate that aldosterone release in humans is calcium dependent, and that nifedipine decreases the sensitivity of the zona glomerulosa to angiotensin II, but has no effect on the aldosterone or cortisol responses to ACTH.

Adrenal Cortex↗
PubMedDate not supplied

Importance of potassium in cardiovascular disease.

The pivotal role of potassium (K+) in cardiovascular disease and the importance of preserving potassium balance have become clinical hot points, particularly as relates to new and emerging cardioprotective and renoprotective therapies that promote potassium retention. Although clinicians may be aware of the critical nature of this relationship, quite frequently there is some uncertainty as to the best way to monitor potassium levels in the face of a host of pathologic states and/or accompanying drug therapies that affect serum levels and/or total body potassium balance. Moreover, guidelines for monitoring of serum potassium levels are at best tentative and oftentimes are translated according to the level of concern of the respective physician. To address these uncertainties, an expert group was convened that included representatives from multiple disciplines. They attempted to reach consensus on the importance of K+ in hypertension, stroke, and arrhythmias as well as practical issues on maintaining K+ balance and avoiding K+ depletion. Because of the complexity of this topic, issues of hyperkalemia will be addressed in a forthcoming manuscript.

Cardiovascular Diseases↗
PubMedDate not supplied

Nonadherence with ACE inhibitors is common and can be detected in clinical practice by routine serum ACE activity.

Our objective was to assess whether serum angiotensin-converting enzyme (ACE) activity during routine clinical practice accurately reflects patient adherence to ACE inhibitor treatment in chronic heart failure (CHF). During 1994-95, ACE was measured in 73 CHF patients who were routinely attending the heart failure clinic at Ninewells Hospital. At the same time, the Medicines Monitoring Unit collected data on whether and when prescriptions for ACE inhibitors were redeemed at community pharmacies, which enabled each patient's adherence over a prolonged period to be assessed. We then correlated whether an elevation in serum ACE was associated with poor adherence with ACE inhibitor treatment. In total, 18% of CHF patients appeared to exhibit less than 70% adherence with their ACE inhibitor treatment, with 34% exhibiting less than 85%adherence and 58% exhibiting less than 100% adherence. A serum ACE activity of more than 12 U/L gave 91% positive predictive accuracy that the patient was less than 100% adherent with his or her ACE inhibitor treatment. At the other extreme, a serum ACE less than 6.5 U/L gave 81% positive predictive accuracy that the patient was more than 85% adherent with ACE inhibitor treatment. Nonadherence with ACE inhibitor treatment, therefore, was found to be common in patients with CHF. The simple, inexpensive test of serum ACE activity can be used in CHF patients to identify many, although not all, nonadherent patients so that adherence-enhancing strategies can be targeted toward them. Further work is clearly required to explore the precise clinical utility of this promising test. (c)2001 by CHF, Inc.

Journal Article↗
PubMedDate not supplied

Effect of centrally acting alpha-adrenergic agonists on sympathetic nervous system function in humans.

Three studies were undertaken to reevaluate whether there is a peripheral component in the reduction of sympathetic activity caused by centrally acting drugs; and whether the antihypertensive effect of these drugs is due entirely to this reduction. Plasma growth hormone and norepinephrine concentrations were used as respective markers of central alpha-adrenoceptor stimulation and peripheral sympathetic activity. In six normal volunteers, intravenous infusion of 0.2 mg clonidine and 2 mg guanfacine was compared. The falls in systolic blood pressure and plasma norepinephrine concentration were slightly greater after clonidine (18 mm Hg and 0.22 ng/ml) than after guanfacine (12 mm Hg and 0.13 ng/ml) administration. These falls occurred earlier than the rise in growth hormone, which rose to a maximum of 23 and 20 IU/ml respectively at 45 minutes after dosing. In six patients with essential hypertension clonidine and alpha-methyldopa caused similar falls in blood pressure and plasma norepinephrine concentration although these changes occurred later with alpha-methyldopa. Plasma growth hormone levels remained undetectable in most patients. In Wistar rats the effect of central and peripheral alpha 2-blockade on clonidine-induced changes was compared. Two groups of six rats received intravenous RX 781094, 0.3 mg/kg, or vehicle 10 minutes before receiving clonidine, 5 micrograms/kg i.v. In the latter, control group, clonidine reduced mean blood pressure by 30.7 +/- 1.9 mm Hg and heart rate by 46 +/- 6.7 beats/min. Plasma norepinephrine fell from 0.22 +/- 0.023 ng/ml to 0.116 +/- 0.013 ng/ml. After pretreatment with RX 781094, blood pressure did not change and heart rate fell by 18 +/- 2.7 beats/min.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMedDate not supplied

Glucose tolerance during antihypertensive therapy in patients with diabetes mellitus.

Many antihypertensive drugs have adverse effects on glycemic control when they are used in diabetic patients. This was noted for thiazide diuretics in 1960, and the mechanism of the effects remains uncertain. Indirect evidence suggests that changes in the serum potassium are at least contributory, although the principal mechanism of thiazide-induced hyperglycemia is probably a reduction in the insulin response to glucose. Beta blockers also adversely affect blood sugar control but only by a small margin. The main cause for concern with beta blockers, however, is their effect during hypoglycemia in which nonselective agents delay blood sugar recovery. In diabetic patients, the institution of antihypertensive therapy should be followed by a reassessment to note any changes in sugar, potassium, and lipids, or side effects.

Adrenergic alpha-Agonists↗
PubMedDate not supplied

Cyclosporin-induced nephrotoxicity and hypertension.

The use of cyclosporin in therapeutics is increasing. Unfortunately, cyclosporin has important detrimental effects on kidney function and blood pressure. Based on the pathogenesis of these side effects, different drug groups have been studied, but with variable success.

Angiotensin-Converting Enzyme Inhibitors↗