PubMed Health⌕ Search

PubMed · 2211539

Blood pressure reduction with ECT response.

Abstract

A group of 48 male inpatients who responded to electroconvulsive therapy for major depression showed decreases in resting blood pressure along the course of treatment. Decreases occurred in both systolic (mean +/- SD = 8.0 +/- 17.3 mm Hg, p = .0025) and diastolic (7.4 +/- 13.2 mm Hg, p = .00030) pressures. Systolic pressure decreased by at least 20 mm Hg in 15 patients. These findings are consistent with reports that depressives show elevated plasma catecholamine levels, and that, with response to tricyclic antidepressants, their blood pressures decrease. Depression-associated blood pressure elevation might contribute to the excessive cardiac mortality of depressives; conversely, antidepressant treatment might control hypertension in some depressives.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

C M Swartz, A E Inglis. 1990. Blood pressure reduction with ECT response.. https://pubmed.ncbi.nlm.nih.gov/2211539/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Inhibition of astroglial inwardly rectifying Kir4.1 channels by a tricyclic antidepressant, nortriptyline.

The inwardly rectifying K(+) (Kir) channel Kir4.1 is responsible for astroglial K(+) buffering. We examined the effects of nortriptyline, a tricyclic antidepressant (TCA), on Kir4.1 channel currents heterologously expressed in HEK293T cells, using a whole-cell patch-clamp technique. Nortriptyline (3-300 microM) reversibly inhibited Kir4.1 currents in a concentration-dependent manner, whereas it marginally affected neuronal Kir2.1 currents. The inhibition of Kir4.1 channels by nortriptyline depended on the voltage difference from the K(+) equilibrium potential (E(K)), with greater potency at more positive potentials. Blocking kinetics of the drug could be described by first-order kinetics, where dissociation of the drug slowed down and association accelerated as the membrane was depolarized. The dissociation constant (K(d)) of nortriptyline for Kir4.1 inhibition was 28.1 microM at E(K). Other TCAs, such as amitriptyline, desipramine, and imipramine, also inhibited Kir4.1 currents in a similar voltage-dependent fashion. This study shows for the first time that nortriptyline and related TCAs cause a concentration-, voltage-, and time-dependent inhibition of astroglial K(+)-buffering Kir4.1 channels, which might be involved in therapeutic and/or adverse actions of the drugs.

Antidepressive Agents, Tricyclic↗