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PubMed1976

Differential effect of baroreceptor reflexes and clonidine on frequency components of sympathetic discharge.

The effects of the baroreceptor reflexes and clonidine on the 3 and 10 Hz components of spontaneously occurring renal sympathetic nervous discharge (SND) were studied in the cat. The proportion of 3 : 10 Hz SND was assessed by selective filtering and integration of activity in the 2-4 Hz and 9-11 Hz frequency bands. Baroreceptor denervation increased activity in both frequency bands while significantly lowering the 3 : 10 Hz ratio. Baroreceptor reflex activation (i.v. phenylephrine) decreased activity in both frequency bands while significantly increasing the 3 : 10 ratio. Clonidine (4-20 mug/kg, i.v.) affected the 3 : 10 Hz ratio of SND in a manner similar to baroreceptor reflex activation. These results indicate that the 3 and 10 Hz components of SND, both of which have been previously shown to be inherent to the central vasomotor system, are differentially affected by the baroreceptor reflexes and clonidine. It is concluded that it is possible to characterize certain cardiovascular states with respect to the 3 : 10 Hz ratio of SND.

Animals↗
PubMed1992

The integrative role of synaptic cotransmission in the bullfrog vasomotor C system: evidence for a synaptic gain hypothesis.

Understanding the integrative significance of synaptic cotransmission is a central problem in autonomic physiology. What are the functional roles of slow synaptic potentials in autonomic ganglia? This paper reviews the problem and its historical roots by focusing on work in the amphibian paravertebral sympathetic system. The phenotypic properties that distinguish the sympathetic B and C cell systems are summarized. Then, a synaptic gain hypothesis is proposed for the integrative function of muscarinic and peptidergic synapses in the vasomotor C system. The model states that the peripheral output of the vasomotor system is subject to synaptic amplification by two gain stages in series. The first gain stage is postulated to arise in ganglia from interactions between two slow postsynaptic potentials; the excitatory response mediated by luteinizing hormone releasing hormone, and the inhibitory response mediated by the muscarinic action of acetylcholine. The second gain stage is postulated to arise in arteries from interactions between two postganglionic cotransmitters: epinephrine and neuropeptide Y. A circuit with these properties would enable preganglionic patterns of electrical activity to regulate the system's output over a wider dynamic range than possible without cotransmitters.

Animals↗
PubMed1986

Methylprednisolone on circulating eicosanoids and vasomotor tone after endotoxin.

Acute pulmonary and systemic vasomotor changes induced by endotoxin in dogs have been related, at least in part, to the production of eicosanoids such as the vasoconstrictor thromboxane and the vasodilator prostacyclin. Steroids in high doses, in vitro, inhibit activation of phospholipase A2 and prevent fatty acid release from cell membranes to enter the arachidonic acid cascade. We, therefore, administered methylprednisolone (40 mg/kg) to dogs to see if eicosanoid production and the ensuing vasomotor changes could be prevented after administration of 150 micrograms/kg of endotoxin. The stable metabolites of thromboxane B2 (TxB2) and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) were measured by radioimmunoassay. Methylprednisolone by itself did not alter circulating eicosanoids but when given 2.5 h before endotoxin not only failed to inhibit endotoxin-induced eicosanoid production but actually resulted in higher circulating levels of 6-keto-PGF1 alpha (P less than 0.05) compared with animals receiving endotoxin alone. Indomethacin prevented the steroid-enhanced concentrations of 6-keto-PGF1 alpha after endotoxin and prevented the greater fall (P less than 0.05) in systemic blood pressure and systemic vascular resistance with steroid plus endotoxin than occurred with endotoxin alone. Administration of methylprednisolone immediately before endotoxin resulted in enhanced levels (P less than 0.05) of both TxB2 and 6-keto-PGF1 alpha but with a fall in systemic blood pressure and vascular resistance similar to the animals pretreated by 2.5 h. In contrast to the early steroid group in which all of the hypotensive effect was due to eicosanoids, in the latter group steroids had an additional nonspecific effect. Thus, in vivo, high-dose steroids did not prevent endotoxin-induced increases in eicosanoids but actually increased circulating levels of TxB2 and 6-keto-PGF1 alpha with a physiological effect favoring vasodilation.

Animals↗