PubMed · 11677898
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S Garnett, P Abrams. 2001. Managing benign prostatic hyperplasia.. https://pubmed.ncbi.nlm.nih.gov/11677898/
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We investigated a non-invasive measurement for changes in finger blood flow during wakefulness and sleep. Changes in finger blood flow, reflected by pulse wave amplitude (PWA) derived from finger plethysmography, were compared with changes in forearm vascular flow assessed by venous occlusion plethysmography after intra-arterial infusion of norepinephrine (NE), phentolamine, and isoproterenol (n=15, 15, 14 subjects, respectively). Moreover, PWA was assessed during obstructive breathing during sleep (n=8 patients). Vasoconstriction in the finger (PWA) was stronger than that obtained in the forearm vascular bed in the higher NE dose range both without (ANOVA, P=0.002) and with concomitant phentolamine-induced alpha-receptor blockade (P=0.02). Isoproterenol increased forearm blood flow but did not induce flow changes detectable by the finger plethysmographic technique (P<0.001). PWA was significantly reduced during arousal from obstructive sleep apnea (-37.5+/-16.1%, P=0.002, n=6 patients), suggesting vasoconstriction in the digital vascular bed. PWA derived from finger plethysmography allows continuous, non-invasive measurement of changes in finger blood flow during wakefulness and sleep. However, as may be expected from the anatomical and functional differences between the finger and forearm vascular beds and demonstrated by the lack of response to beta(2)-receptor stimulation, PWA does not mimic forearm vascular flow characteristics. Thus, finger plethysmography may be a useful complement to current vascular research techniques, in particular to monitor sympathetic influences on skin blood flow in the finger.
In recent decades the theory that amine transmitter release at nerve terminals is routinely regulated through negative feedback systems sensing and responding to the instantaneous perineuronal concentration of previously liberated transmitter has assumed pre-eminence. However, observations indicate a major drop off in per pulse transmitter release when only two or four stimulation pulses are administered, reflecting the unexpectedly prompt operation of feedback inhibition. We explored this quandary in our understanding of control of transmitter release by axonal depolarization versus terminal feedback using isotopic norepinephrine and in vitro slices of rabbit hippocampus. A technique of continuous collection of superfusate over a 30min cycle of stimulation utilizing a wide range of intervals between individual stimulation pulses was used. Following simulation with single pulses even 60s apart or pseudo one pulses 150s apart a marked decline in per pulse release was noted. The deficits in per pulse release were not related to the number of pulse delivered at any time over the course of a 30min stimulation period. The pulse decrements were independent of the activity of neuronal uptake and of superfusion flow rate or even individual pulse duration and frequency. Presynaptic receptor antagonists, potentiated efflux near maximally with the second of only two pulses. Potentiations were independent of pulse number, pulse duration, or frequency. No linkage between perineuronal transmitter concentrations and the antagonist potentiation of release was found. However, the decrements in per pulse release with multiple pulses and the potentiation by alpha presynaptic antagonists occurred under the same test conditions. We conclude that the pulse deficit can be looked at as largely attributable to an enhanced efflux with delivery of the first pulse in a train of pulses, rather then to a pattern of progressively declining efflux linked to increasing extracellular transmitter levels as frequency and pulse number increase.
The human alpha(2B)-adrenoceptor (alpha(2B)-AR) was mutated by substituting the D(3.49) aspartate in position 109 with an alanine (alpha(2B)-D109A) in the conserved DRY sequence at the cytoplasmic face of TM3. We studied the effects of the mutation on agonist binding and on receptor activation in CHO cells, including possible inverse agonism monitored by measuring intracellular Ca(2+) concentrations ([Ca(2+)](i)). The mutated receptor had increased binding affinity for agonists, especially dexmedetomidine (3.8-fold). The increased affinity was abolished by pretreatment of the cells with pertussis toxin. The mutation produced constitutive receptor activity evidenced as increased basal [Ca(2+)](i) and increased potency and efficacy of agonists to elicit Ca(2+) responses. The imidazoline derivative RX821002 functioned as an inverse agonist only through the alpha(2B)-D109A, reducing [Ca(2+)](i). The results thus indicate that this mutation causes constitutive receptor-G(i)-protein precoupling, and that the D(3.49) aspartate residue of the DRY motif is involved in controlling coupled and uncoupled conformations of alpha(2B)-AR.