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N Morgunov

Publications and source records attributed to N Morgunov.

6 recordsLinked to original sources
PubMed1987

Electrochemical analysis of renal Na+-glucose cotransport in salamander proximal tubules.

The changes in electrical membrane parameters and intracellular sodium activity associated with the absorption of D-glucose were studied in the isolated perfused proximal tubule of the Ambystoma tigrinum kidney. The addition of 10 mM D-glucose to a substrate-free luminal perfusate depolarized the basolateral and luminal membrane potentials by -16.2 +/- 0.9 mV and +20.4 +/- 0.9 mV, respectively (P less than 0.01), increased intracellular sodium activity (acellNa) by 5.1 +/- 0.8 mM (P less than 0.01) and significantly (P less than 0.01) decreased luminal membrane resistance from 2,859 +/- 454 to 1,483 +/- 120 omega X cm2. Both the electrogenic response and the change in acellNa induced by luminal glucose were a saturating function of luminal glucose and sodium concentrations. The electrogenic response to luminal glucose was sensitive to intracellular glucose concentration and the change in acellNa induced by luminal glucose was sensitive to intracellular sodium concentrations. Within the physiological range of membrane potentials and studied, the sodium-glucose cotransporter is more sensitive to a decrease in a favorable electrical gradient than to an increase in a favourable chemical gradient for sodium across the luminal membrane.

Ambystoma↗
PubMed1985

Vagal afferent activity and renal nerve release of dopamine.

To investigate the involvement of vagal afferents in renal nerve release of catecholamines, we compared norepinephrine, dopamine, and epinephrine excretion from innervated and chronically denervated kidneys in the same rat. The difference between innervated and denervated kidney excretion rates was taken as a measure of neurotransmitter release from renal nerves. During saline expansion, norepinephrine excretion from the innervated kidney was not statistically greater than from denervated kidneys. Vagotomy increased norepinephrine release from renal nerves. Thus vagal afferents participated in the suppression of renal sympathetic nerve activity during saline expansion. No significant vagal control of dopamine release by renal nerves was detected under these conditions. Bilateral carotid ligation stimulated renal nerve release of both norepinephrine and dopamine in saline-expanded rats. The effects of carotid ligation and vagotomy were not additive with respect to norepinephrine release by renal nerves. However, the baroreflex-stimulated renal nerve release of dopamine was abolished by vagotomy. Electrical stimulation of the left cervical vagus with a square wave electrical pulse (0.5 ms duration, 10 V, 2 Hz) increased dopamine excretion exclusively from the innervated kidney of hydropenic rats. No significant change in norepinephrine excretion was observed during vagal stimulation. Increased dopamine excretion during vagal stimulation was associated with a larger natriuretic response from the innervated kidney than from its denervated mate (p less than 0.05). We conclude that under appropriate conditions vagal afferents stimulate renal release of dopamine and produce a neurogenically mediated natriuresis.

Animals↗
PubMed1985

Submicron tip breakage and silanization control improve ion-selective microelectrodes.

Probable causes of failure of otherwise well-constructed liquid ion-exchanger (LIE) micro-electrodes of average tip size less than 0.15 micron were examined. The problem could be attributed to two major variables, both localized at the tip: partial tip occlusion during fabrication prevents the generation of an electromotive force (small or absent slope and/or selectivity, high resistance); or poor hydrophobicity of the tip permits water to displace the resin from the tip (small or absent slope and/or selectivity and low electrode resistance). Controlled dry tip breakage on paper coated with glassine to final tip sizes well below 0.5 micron (confirmed by scanning electron microscopy) improves the yield of usable electrodes severalfold. Adequate silanization of the tip and consequent retention of resin at the tip can be predicted from the contact angles observed at the glass-LIE-backfilling solution interface. Satisfactory silanization can be achieved despite high ambient humidity. No evidence of shunting of Na+-LIE microelectrodes by the glass wall was seen. In the isolated perfused proximal tubule of Ambystoma tigrinum, the mean intracellular Na+ activity recorded by broken-tip electrodes (13.7 +/- 1.9 meq, n = 4) was similar to that recorded by intact electrodes (15.5 +/- 1.1 meq, n = 31).

Adsorption↗
PubMed1981

Renal nerves and catecholamine excretion.

To determine which neurotransmitters are released into urine by renal nerves, we either acutely denervated one kidney or stimulated renal nerves by activation of the baroreflex. Acute denervation increased dopamine (DA) and decreased norepinephrine (NE) excretion from the denervated kidney. In contrast, DA excretion decreased and NE excretion increased progressively from the contralateral innervated kidney. Sodium excretion related directly to DA and inversely to NE excretion. In chronic denervation experiments, baroreceptor stimulation increased NE excretion by 25% more from the innervated kidney than from its contralateral denervated mate, while DA excretion increased by 50% only from the innervated kidney. Baroreflex-stimulated NE and DA excretion from innervated kidneys was reduced by prior feeding of a low salt diet. The response was completely abolished by a high salt diet. Sodium excretion increased by the same proportion from innervated and chronically denervated kidneys following baroreceptor stimulation. In conclusion, 1) renal nerves release both NE and DA, 2) after acute unilateral denervation sodium excretion related directly with DA and inversely with NE excretion, and 3) urinary excretion of NE and DA derived from renal nerves was influenced by dietary sodium intake.

Animals↗
PubMed1979

Tubular secretion and metabolism of dopamine, norepinephrine, methoxytyramine and normetanephrine by the rat kidney.

The fate of catecholamines released in rat kidneys was examined by microinjecting tritiated norepinephrine (NE), normetanephrine (NMN), dopamine (D) and 3-methoxytyramine (3MT) into proximal and distal tubule lumina and peritubular capillaries. [14C] Inulin included in the injectate served as a reference standard. After injection of NE, D, NMN and 3MT at 0.1 to 4.0 pg/min for 4 to 10 min into proximal tubules, 87 to 94% was recovered in the urine of the injected kidney. Less than 10% of the amines was chemically altered during passage through the nephron. After injection into capillaries, percentages secreted in the first passage through the kidney were: D, 25 +/- 5; 3MT, 47 +/- 3; NE, 13 +/- 2; and NMN, 4 +/- 3. After D capillary injections, excretion of 3MT and D from the microinjected was twice that from the contralateral kidney. Acidic metabolites, homovanillic acid and dihydroxyphenylacetic acid were excreted equally by both kidneys. There was no appreciable difference in the products excreted from left and right kidneys after NE injections. In summary, D released into the peritubular space is converted to 3MT and both compounds are secreted avidly. NE released into the peritubular circulation is converted to NMN and both compounds are secreted but to a much smaller extent than occurs with D and 3MT.

Animals↗