Reference

Tension development and associated calcium influx of control and reserpine pretreated rabbit aortae in response to norepinephrine, isoproterenol and acetylcholine

Tension development and associated calcium influx of control and reserpine pretreated rabbit aortae in response to norepinephrine, isoproterenol and acetylcholine. Hester, R. K.; Carrier, O., Jr. (Dep. Pharmacol., Univ. Texas Health Sci., San Antonio, Tex., USA). Arch. Int. Pharmacodyn. Ther., 233(1), 21-41 (English) 1978. CODEN: AIPTAK. ISSN: 0003-9780. DOCUMENT TYPE: Journal CA Section: 2 (Hormone Pharmacology) Section cross-reference(s): 1 The influence of reserpine (I) [50-55-5] (3 mg/kg) pretreatment on phasic and tonic components of the contractile responses of rabbit aortae to maximally effective concns. of l-norepinephrine bitartrate [51-40-1], acetylcholine bromide [66-23-9] and dl-isoproterenol-HCl [949-36-0] and on agonist-induced movements of 45Ca during these responses were studied. Four h after I administration, there were no histol. changes, no changes in extracellular space, and no change in tissue water, Na, Ca, or Mg. K contents were slightly decreased and the catecholamine content was depleted by 95%. The responses to the 3 agonists were enhanced in the I pretreated tissues. The absence of Ca eliminated the slow tonic component of the responses. I induced an increase in La3+-resistant 45Ca uptake. The 3 agonists induced an increase in La3+-resistant 45Ca uptake of equal magnitude in both I-pretreated and control tissues. La ion affected 45Ca efflux similarly in both I-pretreated and untreated tissues. Apparently, a major portion of the enhanced responsiveness of rabbit aortic strips following I administration is the result of a change in Ca retention in those tissue stores mobilized by these agonists to initiate the fast, phasic component, and is, therefore, a reflection of an increased agonist intrinsic activity.

Synaptic delay in the heart: an iontophoretic study

Synaptic delay in the heart: an iontophoretic study. Hill-Smith, Ian; Purves, Robert D. (Dep. Anat. Embryol., Univ. Coll., London, Engl.). J. Physiol. (London), 279 31-54 (English) 1978. CODEN: JPHYA7. ISSN: 0022-3751. DOCUMENT TYPE: Journal CA Section: 2 (Hormone Pharmacology) Iontophoretically applied acetylcholine bromide [66-23-9] or carbachol [51-83-2] to spontaneously beating clusters of cultured ventricular muscle cells isolated from neonatal rats, decreased the rate of spontaneous beating to responses with min. latencies of 250 ms and total durations of 6-12 s. Noradrenaline bitartrate [51-40-1], adrenaline bitartrate [51-42-3], or isoprenaline sulfate [299-95-6] increased the rate of spontaneous beating; the min. latency was 3-6 s and the rate remained elevated for 32 min. Chronotropic responses of intact atria from adult rats to stimulation of the autonomic nerves were of similar time course to responses of cultured muscle cells. Calcns. based on diffusion theories showed that access of drugs to their receptors was not rate-limiting for the obsd. responses.