Search PubMed⌕ Search

Biomedical subjects

M B Murphy

Publications and source records attributed to M B Murphy.

At least 109 records · Page 6Linked to original sources
PubMed1983

Blood pressure and plasma norepinephrine concentrations after endogenous norepinephrine release by tyramine.

To determine whether small changes in sympathetic activity would cause detectable changes in plasma norepinephrine (NE) levels, and whether the effects of endogenously released and exogenous NE differ, we injected tyramine infusions and l-norepinephrine (l-NE), into six healthy subjects, and the changes in blood pressure (BP) and plasma NE were related. The mean increase in systolic BP was approximately 17 mm Hg with both infusions; diastolic BP increased with l-NE but did not rise significantly with tyramine. Heart rate fell more with l-NE than with tyramine infusions. The maximum increase in plasma NE levels was more than 500% during l-NE infusions but less than 200% with tyramine. There was no correlation between plasma NE and absolute levels of systolic BP when individual data were plotted for tyramine infusions, whereas mean group changes in systolic BP correlated strongly with mean group plasma NE, both during tyramine and l-NE infusions. The slope of the relationship was much steeper for tyramine than for l-NE. We conclude that the use of plasma NE to measure small differences in sympathetic activity among individuals is limited by interindividual variability, whereas changes in sympathetic activity within groups are more likely to be detected.

Adult↗
PubMed1983

The effects of pentolinium on sympathetic activity in hypertensives and normotensive controls.

The effects of pentolinium tartrate 2.5 mg i.v. on blood pressure, heart rate and plasma noradrenaline and adrenaline concentrations were studied in 21 hypertensives and in 20 normal controls. Mean basal catecholamine concentrations and the extent of their suppression by pentolinium were similar in both groups. The reductions in both plasma catecholamine levels correlated with the prepentolinium values. Supine systolic blood pressure was significantly reduced and there was a small increase in heart rate. These data support the use of plasma noradrenaline as an index of sympathetic activity but are inconsistent with the hypothesis that essential hypertension is associated with hyperactivity of the sympathetic nervous system.

Adult↗
PubMed1982

The effects of nifedipine and hydralazine induced hypotension on sympathetic activity.

To determine whether inhibition of sympathetic activity is a factor in calcium antagonist induced hypotension, plasma noradrenaline was measured after intravenous infusion of hydralazine (25 mg) and the calcium antagonist nifedipine (4 mg) in 6 hypertensive males. The resultant reduction in mean blood pressure (12.4% and 14.2% respectively) was accompanied by similar increases in heart rate and plasma noradrenaline concentration. These results suggest that calcium slow channel blockade does not inhibit noradrenaline release from sympathetic nerves and that nifedipine induced hypotension is independent of such a mechanism.

Adult↗
PubMedDate not supplied

Changes in blood pressure and plasma catecholamines caused by tyramine and cold exposure.

Tyramine may be used to stimulate release of endogenous norepinephrine. We have compared the increases in blood pressure and plasma catecholamines in normal volunteers during (a) tyramine infusions, and (b) the more physiological sympathetic stimulus of cold exposure. In a second study, the cardiac component of the pressor effect of tyramine was assessed by measuring systolic time intervals, and by infusing tyramine in beta-blocked subjects. Tyramine, 15.0 micrograms/kg/min for 30 min, elevated systolic BP from 122 +/- 11 to 149 +/- 4 mm Hg, without increasing diastolic BP or heart rate. Plasma norepinephrine rose from 0.547 +/- 0.184 to 0.836 +/- 0.096 ng/ml; plasma epinephrine was unchanged. Thirty-min exposure to 4 degrees C elevated both systolic BP (from 105 +/- 8 to 116 +/- 9 mm Hg) and diastolic BP (from 72 +/- 4 to 81 +/- 6 mm Hg). This was associated with a greater rise in plasma norepinephrine, from 0.357 +/- 0.131 to 1.143 +/- 0.393 ng/ml; plasma epinephrine was again unchanged. A single oral dose of propranolol 160 mg caused approximately a two-fold right shift in the systolic BP dose response to tyramine, and blocked the tyramine-induced shortening of the presystolic ejection period. Tyramine appears to exert its pressor effect mainly by stimulation of cardiac beta-receptors. This may account for the relatively small rise in plasma norepinephrine (relative to cold exposure) since the heart does not contribute a high proportion of circulating norepinephrine.

Adult↗
PubMedDate not supplied

Efficacy of nifedipine as a step 3 antihypertensive drug.

The efficacy of nifedipine (N) as a "step 3" antihypertensive drug was assessed in 15 patients who remained hypertensive in spite of atenolol 100 mg and bendrofluazide 5 mg daily. Nifedipine was added in doses of 10, 20, and 30 mg three times daily in a placebo-controlled double-blind trial. Supine mean blood pressure was reduced by 11.9% +/- 6.2% by N 10 mg three times daily, by 13.9% +/- 7.6% by N 20 mg three times daily and by 20.3% +/- 6.2% by N 30 mg three times daily. Plasma potassium was reduced from 3.9 +/- 0.5 mEq/liter on placebo to 3.6 +/- 0.5 mEq/liter on N 10 mg three times daily, 3.6 +/- 0.4 mEq/liter on N 20 mg three times daily (p less than 0.05), and 3.5 +/- 0.5 mEq/liter on N 30 mg three times daily (p less than 0.05). Heart rate, body weight, renal function, and plasma glucose were not altered. Nifedipine is thus a useful third-line hypotensive agent that should be used in combination with a potassium-sparing diuretic.

Adult↗
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

Long-term preservation of renal function in hypertensive heart transplant recipients treated with enalapril and a diuretic.

Hypertension and progressive deterioration in renal function are commonly seen in heart transplant recipients treated for the long term with cyclosporine. Because angiotensin converting enzyme inhibitors have been associated with amelioration of renal dysfunction in some patients with hypertension and preexisting mild-moderate kidney failure, we treated nine hypertensive recipients of orthotopic heart transplants with enalapril (11 +/- 2 mg/day) and furosemide (62 +/- 15 mg/day) for 23 +/- 4 months. Most of the enalapril dose was given at bedtime, which minimized nocturnal and early morning hypertension. In addition to controlling blood pressure (154 +/- 6/100 +/- 2 mm Hg before enalapril vs 120 +/- 5/81 +/- 2 mm Hg currently; p less than 0.001 for both systolic and diastolic blood pressures by paired t test), there has been no increase in serum creatinine level over 684 +/- 102 days of follow-up (1.88 +/- 0.20 mg/dl before enalapril vs 1.81 +/- 0.17 mg/dl currently; p greater than 0.70). This is unlikely to be caused by the reduction in daily cyclosporine dose (492 +/- 60 mg/day before enalapril to 305 +/- 47 mg/day currently) because there were no significant changes in mean blood cyclosporine level (which has been maintained between 100 and 500 ng/ml). Treatment of hypertension with enalapril and a diuretic after heart transplantation may help prevent or delay the impairment of renal function often seen during prolonged cyclosporine therapy.

Adult↗