Rapid transcapillary exchange and unidirectional neuronal uptake of noradrenaline in the perfused rabbit heart.

Mann, Giovanni E.; Yudilevich, D. L.

doi:10.1113/jphysiol.1984.sp015127

Cited by 14 publications

(3 citation statements)

References 25 publications

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“…EVV did not vary significantly with flow and estimates for D-[14C]mannitol and [3H]dopamine were respectively 0 34 + 0 05 and 1P65 +0f26 ml/g (s.E., n = 16 values, 5 hearts). Capillary extraction and EVV measured for D-mannitol confirm earlier findings and, similar to noradrenaline (Mann & Yudilevich, 1984), the 'virtual' EVV for dopamine appeared to be reduced by inhibitors of neuronal reuptake.…”

Section: Psupporting

confidence: 72%

Proceedings of the Physiological Society, 22‐23 July 1988, Cambridge Meeting: Communications

1988

The Journal of Physiology

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Apical membrane sodium co-transport stimulation is associated with cell depolarization followed by partial recovery of potential over several minutes in a variety of lealky epithelia including amphibian and mammalian renal proximal tubules (Lang et al. 1986). Recent observations from this laboratory implicated the basolateral sodium bicarbonate transporter in the recovery of potential in the rabbit proximal tubule (Beck et al. 1987a). In the frog proximal tubule the recovery has been shown to be at least partly due to an increase in basolateral potassium conductance (Lang et al. 1986). We now report observations designed to examine the possibility that changes in the basolateral potassium conductance may also contribute to the recovery of cell potential in the rabbit proximal tubule.Grade IV specific pathogen free New Zealand White rabbits of either sex were anaesthetized with pentobarbitone (35 mg kg-' i.v.), the left kidney flushed with preservation fluid, removed and proximal convoluted tubule segments set up for microperfusion in vitro with measurement of VBL (Beck et al. 1986). Peritubular potassium was then briefly (< 5 s) stepped from 5 to 20 mm (in place of sodium) before, during and after stimulation of apical sodium co-transport by introduction of glucose and alanine (replacement of mannitol) into the lumen (Beck et al. 1987b). Initially, when VBL was -53-2 + 4-5 (S.E.M., n = 5) mV, potassium steps caused brief superimposed depolarizations of 86 + 25 mV. Introduction of glucose and alanine into the lumen caused the familiar transient change in PD consisting of a basolateral depolarization of 218 + 1P2 mV followed by a repolarization of 13-6 + 12 mV. At the peak of this slow depolarization, potassium steps caused depolarizations of 5-6 + 2-0 mV. However, after the slow repolarization, potassium steps caused larger depolarizations of 10-1 + 1P8 mV (P < 0 05, paired t test). When glucose and alanine were removed from the lumen the basolateral membrane hyperpolarized to -63 + 2-6 mV before return to -57 0 + 1P8 mV. Neither this final potential, nor the depolarization then elicited by potassium steps (9-8 +1 0 mV), were significantly different from control values.These results are consistent with an increase in relative basolateral potassium conductance during apical sodium cotransport stimulation in the rabbit proximal convoluted tubule.

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Section: Psupporting

confidence: 72%

Proceedings of the Physiological Society, 22‐23 July 1988, Cambridge Meeting: Communications

1988

The Journal of Physiology

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“…The NE overflow into the coronary sinus blood is a measure of the physical transport process; the overflow represents the difference between the rates of release and reuptake of the adrenergic neurotransmitter. Extraneuronal uptake plays a relatively minor role in the heart (Junstad et al, 1973;Langer and Rubio, 1973;Iversen, 1975;Matsuda et al, 1979;Masuda et al, 1980;Mann and Yudilevich, 1984). Hence, the overflow of NE mainly reflects the balance between the neuronal release and the subsequent neuronal reuptake of neurotransmitter.…”

Section: Discussionmentioning

confidence: 99%

Heart rate modulates the disposition of neurally released norepinephrine in cardiac tissues.

Masuda¹,

Levy²

1985

Circulation Research

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We determined the effect of heart rate on the disposition of neurally released norepinephrine from the cardiac tissues in open-chest, anesthetized dogs with complete atrioventricular block. After injecting desipramine to block the neuronal uptake of norepinephrine, we stimulated the cardiac sympathetic nerves supramaximally for about 3 minutes at a mean frequency of 2.7 Hz. In one series of experiments, we allowed coronary sinus blood flow to change spontaneously in response to cardiac pacing and sympathetic stimulation. The mean coronary sinus blood flows just before cessation of sympathetic stimulation were 67.4 +/- 4.2 (SE) and 37.4 +/- 2.7 ml/min during pacing at a high (150/min) and a low (60/min) frequency, respectively. The mean norepinephrine overflow into the coronary sinus blood during steady state sympathetic stimulation was 45.0 +/- 14.2% greater during high frequency pacing than during low frequency pacing. After cessation of neural stimulation, the norepinephrine overflow decayed more rapidly during high frequency pacing than during low frequency pacing. This difference in decay rates was mainly ascribable to the difference in coronary blood flows. In a second series of experiments, we adjusted the coronary sinus blood flow during sympathetic stimulation so that the flows were not significantly different during pacing at the two frequencies. During the initial 30-second period, after cessation of sympathetic stimulation, the mean decrements of norepinephrine overflow were 95.9 +/- 21.4 and 59.2 +/- 17.3 ng/min at the high- and low-pacing frequencies, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…125 I-T 4 and 125 I-T 3 uptake by the heart cells was measured relative to 3 H-mannitol, as a reference tracer. Mannitol is a marker molecule and its recovery in coronary venous effluent represents a simple diffusion into and out of the extracellular space (Mann & Yudilevich, 1984;Samuels, 1988;Preston & Segal, 1992a,b;Kostic et al 1995), whereas the lower values of thyroxine ( Fig. 1) and triiodothyronine (Fig.…”

Section: Discussionmentioning

confidence: 99%

Kinetics of Thyroxine (T₄) and Triiodothyronine (T₃) Transport in the Isolated Rat Heart

Rosić

Pantović

Lucic

et al. 2001

Experimental Physiology

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Thyroid hormones are the iodized derivatives of the amino acid tyrosine and are synthesized by the thyroid gland. Thyroxine (T 4 ) and triiodothyronine (T 3 ) regulate the processes of general metabolism (oxidative phosphorylation), growth, development and specific gene expression (Oppenheimer & Schwartz, 1987;Samuels, 1988). About 90 % of the thyroid production is T 4 while 10 % is T 3 . It is thought that T 4 has little, if any, biological activity, and it is considered as a prohormone, which becomes activated upon conversion into T 3 in peripheral tissues. About 80 % of the daily T 3 production is generated via this process while the remaining 20 % is directly secreted from the thyroid (Hennemann, 1987).To respond to thyroid hormone signals, cells have to contain specific thyroid hormone receptors (nuclear proteins) and thyroid hormone response elements (TRE) (specific DNA sequences upstream of regulated genes) (Brent et al. 1989). Thyroid hormone exerts its actions at a cellular level by binding to specific thyroid hormone receptor (TR) and binding of TR to TRE, in order to stimulate or inhibit the rate of transcription of specific genes (Franklyn & Gammage, 1996). Up to now, two major classes of thyroid hormone nuclear receptors have been described: thyroid hormone receptor-a (TRa) and thyroid hormone receptor-b (TRb) (Franklyn & Gammage, 1996;Nagaya et al. 1996). Several isoforms (a 1 , a 2 , a 3 , b 1 and b 2 ) are created by alternative splicing of TRa and TRb gene (Nagaya et al. 1996) and they display differences in terms of their tissue distribution and functional properties (Franklyn & Gammage, 1996). It has been shown that TRa 1 , TRa 2 and TRb 1 are expressed in the myocardium, and that TRa 1 and TRb 1 bind the ligand (thyroid hormone), while TRa 2 is non-ligand binding variant which may exert a 'dominant negative' influence on the action of a 1 and b 1 thyroid hormone receptor proteins (Brent et al. 1991;Franklyn & Gammage, 1996).Thyroid hormones have strong effects on the heart and circulation. It is considered that thyroid hormones perform direct and indirect actions on the heart. Thus, direct thyroid hormone actions on the heart involve regulation of transcription of a number of functionally relevant genes in the myocardium (nuclear mechanism). These include the myosin heavy chain contractile proteins (Ojamaa & Klein, 1993; Dubus et al. 1993), Na + ,K + -ATPase (Liu et al. 1993;Huang et al. 1994), Ca 2+ -ATPase and phospholamban (Kimura et al. 1994), which modulate the activity of calcium translocator (Klein & Ojamaa, 1996). But some effects, like the thyroid hormone effects on calcium uptake by the myocyte, are mediated by direct action on the plasma The dynamics and kinetics of thyroid hormone transport in the isolated rat heart were examined using the modified unidirectional paired tracer dilution method. The uptake of 125 Kinetics of thyroxine (T 4 ) and triiodothyronine (T 3 ) transport in the isolated rat heart

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Rapid transcapillary exchange and unidirectional neuronal uptake of noradrenaline in the perfused rabbit heart.

Cited by 14 publications

References 25 publications

Proceedings of the Physiological Society, 22‐23 July 1988, Cambridge Meeting: Communications

Proceedings of the Physiological Society, 22‐23 July 1988, Cambridge Meeting: Communications

Heart rate modulates the disposition of neurally released norepinephrine in cardiac tissues.

Kinetics of Thyroxine (T₄) and Triiodothyronine (T₃) Transport in the Isolated Rat Heart

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Rapid transcapillary exchange and unidirectional neuronal uptake of noradrenaline in the perfused rabbit heart.

Cited by 14 publications

References 25 publications

Proceedings of the Physiological Society, 22‐23 July 1988, Cambridge Meeting: Communications

Proceedings of the Physiological Society, 22‐23 July 1988, Cambridge Meeting: Communications

Heart rate modulates the disposition of neurally released norepinephrine in cardiac tissues.

Kinetics of Thyroxine (T4) and Triiodothyronine (T3) Transport in the Isolated Rat Heart

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Kinetics of Thyroxine (T₄) and Triiodothyronine (T₃) Transport in the Isolated Rat Heart