Circulating catecholamine (CA) levels in the aortic blood did not change significantly in anesthetized dogs during a period of 60 min following the rapid intravenous injection of ouabain at a dose of 10 microgram/kg, but they did increase significantly after administration of a dose of 75 microgram/kg. After bilateral cervical vagotomy, the high dose of ouabain caused a greater and earlier elevation in circulating CA levels than in intact animals along with an increased cardiac index and a lower peripheral resistance. These findings suggest the existence of a vagal inhibitory mechanism upon liberation of CA following the administration of ouabain. Although ventricular arrhythmias did occur before the increase in circulating CA, preinjection CA levels were significantly higher in animals presenting ventricular fibrillation, suggesting that a high background adrenergic tone facilitates the production of ventricular arrhythmias by ouabain. Moreover, ventricular tachycardia occurred earlier in vagotomized dogs, in which the immediate elevation of circulating CA could have been a precipitating factor for this type of arrhythmia.

Anesthesia↗

PubMedDate not supplied

Effects of atenolol and hydrochlorothiazide on blood pressure and plasma catecholamines in essential hypertension.

The antihypertensive effects of atenolol and hydrochlorothiazide were compared with placebo in a randomized, double-blind crossover study, with the blood pressure responses related to sympathetic nervous system activity. Twelve patients with essential hypertension were given atenolol (100 mg), hydrochlorothiazide (50 mg), and placebo as single daily doses, each for 6 weeks. Mean supine, standing, and post-exercise blood pressures (mm Hg) on atenolol (155/94, 152/95, 177/93, respectively) and hydrochlorothiazide (154/99, 150/103, 172/96) were lower (p less than 0.01) than corresponding placebo values (172/109, 166/113, 204/111) at 6 weeks. The role of the sympathetic nervous system in the antihypertensive actions of atenolol and hydrochlorothiazide was examined. The supine plasma norepinephrine on placebo was used as an index of sympathetic activity to categorize each patient's "adrenergic status." The six "hyperadrenergic" patients with high resting norepinephrine values (mean, 302 pg/ml) exhibited a greater (p = 0.05) decrease in BP (-30/-20 mm Hg) on atenolol compared with the BP fall of -9/-11 mm Hg observed in the lower norepinephrine group (mean, 211 pg/ml). Resting plasma norepinephrine values did not predict the BP fall on hydrochlorothiazide. The "adrenergic status" of each patient as measured by the plasma norepinephrine concentration tended to be relatively constant regardless of therapy or the state of activity. In this study, atenolol was an effective antihypertensive agent comparable to hydrochlorothiazide in potency. Adrenergic status tended to predict the BP response to atenolol and was a relatively constant feature of the patients in all treatment phases.

Adult↗

PubMedDate not supplied

[Hypertension and the sympathetic nervous system: research to pursue. Interview by Robert Henry].

Explore the source record for details and available documents.

Animals↗

PubMedDate not supplied

Vasovagal syncope: management with atrioventricular sequential pacing and beta-blockade.

A case of vasovagal syncope in an otherwise healthy 74-year-old woman is described. Attempts to prevent symptoms with ventricular and atrioventricular sequential temporary pacing (documented by continuous monitoring of heart rate and intra-arterial recording of blood pressure during spontaneous episodes) proved inadequate. However, the addition of a beta-blocker to permanent DDD pacing was clinically successful in markedly diminishing symptoms. The mechanisms of action of this treatment modality is discussed.

Adrenergic beta-Antagonists↗

PubMedDate not supplied

6-hydroxydopamine, 6-hydroxydopa and degeneration of adrenergic nerves.

Explore the source record for details and available documents.

Animals↗

PubMedDate not supplied

[Interaction between the sympathetic and renin-angiotensin system].

The renin-angiotensin system is involved in the control of sodium and water balance, mitogenesis and the regulation of vascular tone as well as of the activity of the sympathetic nervous system. Many of these effects may be regulated at a local level by independent tissue renin-angiotensin systems. The renin-angiotensin and adrenergic nervous systems are cross-regulated by interactive compensatory mechanisms. Therefore, the activation of one of these systems induces the activation or induction of the other leading to a co-amplification of cellular mechanisms, for instance resulting in the facilitation of sympathetic neurotransmission. This paper describes the interactions between these systems in the central nervous system and at pre- and postsynaptic sites of the nerve endings in cardiovascular tissues. Since these systems are cross-regulated, the inhibition of one would attenuate the activity of the other. The drugs that inhibit specifically the various components of the renin-angiotensin system have proved powerful tools for studies of the physiology of this system as well as for the treatment of hypertension and heart failure.

Animals↗