Intrarenal site of action of calcium on renin secretion in dogs.
We studied the effects of intrarenal calcium infusion on renin secretion in sodium-depleted dogs in an attempt to elucidate the major site of calcium-induced inhibition of renin release. Both calcium chloride and calcium gluconate reduced renal blood flow and renin secretion while renal perfusion pressure was unchanged. These data indicate that calcium inhibition of renin secretion did not occur primarily at the renal vascular receptor; decreased renal blood flow is usually associated with increased renin secretion. Calcium chloride infusion increased urinary chloride excretion without affecting sodium excretion, and calcium gluconate failed to increase either sodium or chloride excretion. Also, the filtered loads of sodium and chloride were unchanged during the calcium infusions. These results give no indication that calcium inhibited renin secretion by increasing the sodium or chloride load at the macula densa. The effects of intrarenal calcium infusion on renin release were also assessed in dogs with a nonfiltering kidney in which renal tubular mechanisms could not influence renin secretion. The observation that calcium still suppressed renin release in these dogs provides additional evidence that the the major effect of calcium involved nontubular mechanisms. Thus, it appears likely that calcium acted directly on the juxtaglomerular cells to inhibit renin secretion. (+info)
Isolation and purification of rat mammary tumor peroxidase.
7,12-Dimethylbenz(a)anthracene-induced rat mammary tumors often contain high levels of the enzyme perioxidase, a putative marker of estrogen dependence. This enzyme can be effectively extracted with 0.5 M CaCl2, giving rise to a soluble peroxidase with a molecular weight of about 50,000 as determined by gel filtration. This is the same size as the estrogen-induced peroxidase of rat uterus but smaller than other mammalian peroxidases. Further purification of the rat mammary tumor peroxidase by concanavalin A-Sepharose chromatography and hydrophobic interaction chromatography on phenyl Sepharose provides a 640-fold purification of the enzyme. (+info)
Electrical and mechanical responses to diltiazem in potassium depolarized myocardium of the guinea pig.
Effects of diltiazem on the electrical and mechanical activities of guinea pig papillary muscle were investigated in K-rich Tyrode's solution (Kc1 12.7 mM). The electrical properties of cell membrane in K-rich solution were also examined in the ventricular muscle fibers. It was found that the overshoot as well as the maximum rate of rise (Vmax) of the action potential were highly sensitive to the extracellular concentration of CaC12 in K-rich solution. Vmax was also affected by NaC1. Diltiazem at a lower concentration (1.1 X 10(-7) M) caused a reduction in the contractile force of K-depolarized papillary muscle without producing significant changes in the resting and action potentials. In the presence of a higher concentration of diltiazem (1.1 X 10(-5) M), the contractile force decreased concurrently with the change in the action potential. Addition of CaC12 restored the original strength of contraction in parallel to the recovery of the action potential, especially in its overshoot and Vmax. From these results, it is inferred that diltiazem may decrease the contractile force of guinea pig papillary muscle either by interfering with the intrasmembrane calcium influx or by intracellularly reducing the free calcium ion concentration in the myoplasm. (+info)
Effect of salt addition on the fractal structure of aggregates formed by heating dilute BSA solutions.
The fractal dimension, Df, of aggregates in a dilute BSA system with added salt was evaluated by static light scattering (SLS). A fractal structure was observed for the system with NaCl addition. The values of Df increased with increasing heating time and ionic strength. The values of Df were larger than those (Df = 1.8 or 2.1) predicted by the conventional cluster-cluster aggregation model, probably due to a "restructuring" of aggregates during the aggregation process. On the other hand, a fractal structure was not apparent for the system with added CaCl2. (+info)
Effect of praeruptorin C on spontaneous [Ca2+]i transients in cultured myocardial cells of neonatal rats.
AIMS: To study the effects of praeruptorin C (Pra-C) on [Ca2+]i transients in cultured neonatal myocardiocytes. METHOD: Using Ca(2+)-sensitive fluorescent indicator, Fura 2-AM, spontaneous cytosolic Ca2+ transients were measured in cultured myocardial cells of neonatal rats. RESULTS: Pra-C 10, 30 mumol.L-1 caused a decrease in the peak of Ca2+ transients. Pra-C 30 mumol.L-1 and 10-30 mumol.L-1 inhibited partly the stimulatory effects of CaCl2 4.8 mmol.L-1 and Bay k 8644 100 nmol.L-1 on peak Ca2+ transients, respectively. Pra-C did not cause any marked change in the basal [Ca2+]i level between beats. Pra-C inhibited the reduced [Ca2+]i transients after inhibition of sarcoplasmic reticulum Ca2+ release in ryanodine pretreated cells. CONCLUSIONS: Pra-C inferred with the Ca2+ influx responsible for excitation-contraction coupling in myocardiocytes. (+info)
Effects of cycloprotobuxine-A on atrial fibrillation.
AIM: To study the effects of cycloprotobuxine-A (Cyc-A) on atrial fibrillation. METHODS: Atrial fibrillations in vivo and in vitro were induced by arrhythmogenic drugs. Action potentials were measured by the standard microelectrode technique. RESULTS: Cyc-A, similar to or slightly stronger than amiodarone (Ami), decreased incidences of atrial fibrillation elicited by CaCl2-acetylcholine in mice and increased doses of aconitine, ouabain, or adrenaline to elicit atrial fibrillation in isolated guinea pig atria. Cyc-A 0.3-100 mumol.L-1 decreased the normal automaticity and 0.3-30 mumol.L-1 attenuated or almost abolished the isoprenaline-induced abnormal increase in automaticity in sinus nodal cells. In isolated left atria, Cyc-A 0.3-30 mumol.L-1 inhibited the abnormal rhythmic activity elicited by adrenaline, prolonged action potential duration (APD) and effective refractory period, and reduced excitability. At 3-30 mumol.L-1, Cyc-A also decreased the maximal velocity of depolarization (Vmax). Cyc-A antagonized the acetylcholine-induced shortening of APD. These electrophysiologic effects were similar to those of amiodarone, but Ami did not affect the Vmax. CONCLUSION: Cyc-A produces a protective effect against experimental atrial fibrillation via a prolongation of repolarization, a decease of automaticity, and an inhibition of excitability. (+info)
Heparin influence on alpha-staphylotoxin formed channel.
The effects of heparin on ion channels formed by Staphylococcus aureus alpha-toxin (ST channel) in lipid bilayers were studied under voltage clamp conditions. Heparin concentrations as small as 100 pM induced a sharp dose-dependent increase in channel voltage sensitivity. This was only observed when heparin was added to the negative-potential side of lipid bilayers in the presence of divalent cations. Divalent cations differ in their efficiency: Zn2+>Ca2+>Mg2+. The apparent positive gating charge increased 2-3-fold with heparin addition as well as with acidification of the bathing solution. 'Free' carboxyl groups and carboxyl groups in ion pairs of the protein moiety are hypothesized to interact with sulfated groups of heparin through divalent cation bridges. The cis mouth of the channel (that protrudes beyond the membrane plane on the side of ST addition and to which voltage was applied) is less sensitive to heparin than the trans-mouth. It is suggested that charged residues which interact with heparin at the cis mouth of ST channels and which contribute to the effective gating charge at negative voltage may be physically different from those at the trans mouth and at positive voltage. (+info)
Modulation of calcium mobilization in aortic rings of pregnant rats: Contribution of extracellular calcium and of voltage-operated calcium channels.
Pregnancy is associated with decreased vascular responsiveness to vasopressor stimuli. We have tested the involvement of Ca2+ mobilization in myotropic responses of aortic rings obtained from pregnant and virgin rats. Contractions of the rings to phenylephrine, in the absence of calcium in the bathing medium, were lower in tissues from virgin than from pregnant rats. Concentration-response curves to CaCl2 that were measured after stimulation by phenylephrine in the absence of Ca2+ were shifted to higher levels of contraction. This was not observed when KCl was used to prestimulate the aorta. D-600, a phenylalkylamine calcium channel blocker, similarly inhibited these responses to CaCl2 in tissues from both pregnant and virgin animals. D-600 exerted a concentration-dependent inhibition of responses to phenylephrine and KCl. However, the calcium antagonist was less effective in aortic rings of pregnant than of virgin rats. Basal 45Ca2+ uptake was lower in aortic rings from pregnant than from virgin rats, and Bay K 8644 was unable to reverse this difference. The time course of basal and stimulated (KCl) 45Ca2+ influx was lower in aorta of pregnant rats at all times studied. Moreover, when the intracellular calcium pools were emptied with phenylephrine, the refilling of these pools was delayed in aortic rings of pregnant rats. These results indicate an altered extracellular calcium mobilization of aortic rings from pregnant rats. These changes may be due to a functional alteration of the voltage-operated calcium channels during pregnancy. (+info)