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Biomedical subjects

G S Stokes

Publications and source records attributed to G S Stokes.

At least 73 records · Page 4Linked to original sources
PubMed1980

Prediction of response to antihypertensive therapy with prazosin.

Blood-pressure responses and changes in plasma drug concentration were studied in 11 hypertensive patients after an initial oral dose of 2 mg of prazosin. Subsequently, blood pressure was monitored during long-term treatment with prazosin. The prazosin reactivity index, a value derived during the first-dose study, appeared to predict the long-term antihypertensive effect of prazosin alone or prazosin combined with bendrofluazide.

Adult↗
PubMed1979

Responsiveness to prazosin in renal failure.

1. The fall in blood pressure produced by a test dose of prazosin was greater in a group of patients with chronic renal failure than in a group with normal renal function. 2. This difference could not be attributed to increased reactivity, measured as the slope of the regression line relating mean blood pressure and plasma prazosin concentration, nor to retarded elimination of the drug. 3. The enhanced antihypertensive effect of prazosin in renal failure appears to reflect changes in the bioavailability or distribution of the drug, which result in higher drug concentrations for a given dose.

Adult↗
PubMed1979

False-negative saralasin responses in renovascular hypertension.

Blood pressure responses to the infusion of saralasin and plasma renin levels were measured in 31 hypertensive patients following preparation with frusemide. Five patients had unilateral renal artery stenosis, with renal vein ratios lateralising strongly to the affected side. Saralasin produced depressor responses in 3 of these but failed to evoke significant effects in the other 2, despite the fact that in both cases hypertension was subsequently alleviated by renal bypass surgery. A further period of more severe sodium depletion increased plasma renin levels and the depressor effect of saralasin, but did not help to differentiate renal artery stenosis from other forms of hypertension.

Adult↗
PubMed1978

Labetalol in hypertensive emergencies.

Labetalol, a combined alpha-blocking and beta-blocking agents, was administered by intravenous bolus to six severely hypertensive patients. The blood pressure response was unsatisfactory in every case. It is concluded that intravenous administration of labetalol is not useful in hypertensive emergencies which occur in patients who are already receiving other antihypertensive agents.

Adult↗
PubMed1978

The beta-adrenoceptor controlling renin release.

The beta-adrenoceptor antagonists, atenolol, metoprolol and propranolol, administered intravenously to anaesthetized rats in doses producing equal beta1-adrenoceptor blocking effects, caused comparable suppression of plasma renin activity (PRA) despite the fact that, at these doses, atenolol and metoprolol exhibited no beta2-adrenoceptor blocking properties. Practolol, an agent specific for beta1-adrenoceptors but possessing intrinsic sympathomimetic activity, caused less marked suppression of PRA. When doses of atenolol, metoprolol, propranolol and butoxamine were selected to achieve equal beta2-blocking effects, PRA was again significantly suppressed by atenolol and metoprolol but not by propranolol or butoxamine. These results do not support the concept that adrenergic release of renin is mediated by beta2-adrenoceptors, but are compatible with the involvement of a beta1-adrenoceptor-mediated mechanism.

Angiotensin II↗
PubMed1978

Withdrawal of clonidine: effects of varying dosage or duration of treatment on subsequent blood pressure and heart rate responses.

The influence of the dosage or duration of treatment on the incidence and severity of clonidine withdrawal responses was examined in normotensive rats. Clonidine (0.01 or 0.1 mg/kg i.m.) was administered either in single doses, or twice daily for 3 days or 3 weeks. Rats were then anesthetized and arterial catheters were inserted. Significant overshoots in blood pressure and heart rate, reaching peak values 16 to 26 hr after the last injection, occurred in all clonidine-treated rats, but in no control rats. The overshoots after single injections of clonidine were as great as those after suspension of sustained treatment. Moreover, withdrawal responses were as great after the low dose as they were after the 10-fold greater dose. Only plasma renin activity showed a significantly greater elevation during withdrawal of the high dose of clonidine. Since ganglionic blockade reduced blood pressures and heart rates to the same levels in rats with clonidine withdrawal hypertension as in control rats, the withdrawal overshoots appear to be nervously mediated. Neither the dosage nor the duration of treatment could be shown to determine the magnitude of the response to withdrawal of clonidine.

Animals↗
PubMed1978

Comparative haemodynamic effects of clonidine and guanfacine.

Dose-response relationships were established for the acute effects on arterial pressure and heart rate of the antihypertensive agents, clonidine and guanfacine, administered intravenously or intramuscularly to anaesthetized rats. The intramuscular route appeared to be preferable to the intravenous, for the direct pressor potency of each drug was thereby greatly reduced in relation to the hypotensive efficacy. The potency of clonidine was 10-20 times that of guanfacine, but the same maximal fall in blood pressure was obtained with either agent administered by either route. Both agents caused a marked, dose-related suppression of plasma renin activity. When either clonidine or guanfacine was administered twice daily for 3 weeks and then discontinued, a phase of blood pressure overshoot with tachycardia commenced within 24 hr of the last injection. These withdrawal effects were more evident in guanfacine-treated rats than in clonidine-treated rats.

Animals↗
PubMed1977

Influence of dosage and dietary sodium on the first-dose effects of prazosin.

The effects of the first dose of prazosin were assessed in hypertensive patients on different sodium intakes. Patients received 250, 100, or 30 mmol sodium per 24 hours for a week before taking 2 mg or 0-5 mg prazosin. The acute effects of prazosin on blood pressure and pulse rate were milder with a high sodium intake. On the 100-mmol intake symptomatic postural hypotension occurred in five out of seven patients given 2 mg prazosin and in two out of four given a 0-5-mg dose, whereas those taking 2 mg or 0-5 mg and a 250-mmol sodium intake experienced no postural symptoms. These findings indicate that particular care should be taken in starting prazosin treatment in sodium-depleted patients.

Adult↗
PubMed1977

The effect of mental arithmetic in normotensive and hypertensive subjects, and its modification by beta-adrenergic receptor blockade.

1 The effects of a 5-min period of sustained mental arithmetic upon blood pressure and heart rate were determined in several groups of healthy subjects and hypertensive patients. 2 The arithmetic produced significant increases in heart rate and blood pressure (both systolic and diastolic) in both normotensive and hypertensive subjects. 3 The blood pressure changes were neither attenuated nor enhanced by the prior administration of basis. 4 In subjects habituated to the test the heart rate increase was unaffected by the drugs, but in those less familiar with the test it was usually attenuated. 5 Although the beta1-adrenoceptor selective blocker, metoprolol, caused decreases in baseline values for blood pressure and heart rate similar to those observed with the use of the two non-selective blockrs, it was shown in a double-blind crossover comparison with propranolol that the haemodynamic changes provoked by the mental arithmetic were not less in the presence of beta1-receptor blockade than when both beta1- and beta2-receptors were blocked. 6 These findings suggest that, during beta2-adrenoceptor blockade, the haemodynamic effects of minor mental stress are not exaggerated because of uncompensated alpha-receptor mediated vasoconstriction, such as occurs following adrenaline infusion.

Adrenergic beta-Antagonists↗
PubMed1977

The use of clonidine by intramuscular injection in the treatment of hypertension.

Clonidine (Catapres) administered intramuscularly in a dose of 150 microng produced a satisfactory reduction in blood pressure in 13 of 16 hypertensive patients. Its effect occurred within five minutes, was maximal at 75 minutes and persisted for five hours. In six patients who received two doses (150 microng and 300 microng), the response was shown to be dose-related. No serious side effects were noted. Intramuscular administration of clonidine thus appears to be safe and effective. It has a place in the management of uncontrolled hypertension when a rapid reduction in blood pressure is undesirable and in the maintenance of blood pressure control when oral therapy cannot be tolerated.

Adult↗